Intraocular Lens Dislocation



Cataract surgery is the most common operation performed by ophthalmologists. Although it has a very high success rate, certain complications may occur. Intraocular lens (IOL) malpositions range from simple IOL decentration to luxation into the posterior segment. Subluxated IOLs involve such extreme decentration that the IOL optic covers only a small fraction of the pupillary space. Luxation involves total dislocation of the IOL into the posterior segment. Decentration of an IOL may be the result of the original surgical placement of the lens, or it may develop in the postoperative period because of external (eg, trauma, eye rubbing) or internal forces (eg, scarring, peripheral anterior synechiae [PAS], capsular contraction, size disparity). Posterior dislocation of an intraocular lens (IOL) is an uncommon complication of cataract surgery and Nd:YAG posterior capsulotomy.

See What the Eyes Tell You: 16 Abnormalities of the Lens, a Critical Images slideshow, to help recognize lens abnormalities that are clues to various conditions and diseases.


IOL dislocation can be subdivided into early and late dislocation. Early dislocation refers to dislocation occurring within 3 months of cataract surgery, whereas late dislocation occurs more than 3 months after cataract extraction.[1]

Posterior dislocation of an IOL may occur during or shortly after cataract surgery. In these cases, posterior capsular rupture or zonular dialysis usually is present. It occurs because of improper fixation within the capsular bag and instability of the IOL–capsular bag complex.[2] The implementation of a continuous curvilinear capsulorrhexis (CCC) during phacoemulsification has decreased the rate of early IOL dislocation.[3] CCC gives support to the IOL optic for 360 degrees and permits excellent IOL fixation. Prior to CCC, most IOL dislocation occurred secondary to asymmetric IOL fixation or IOL malposition within the capsular bag. Rarely, it may occur following Nd:YAG capsulotomy or beyond the immediate postoperative period. Trauma may be a precipitant in these cases.

Late IOL dislocation has been noted to occur more frequently than previously thought.[1, 4, 5] Late IOL dislocation results from zonular weakness since the IOL is adequately fixed within the capsular bag. Several risk factors, including pseudoexfoliation syndrome,[6] trauma, prior vitreoretinal surgery, and connective tissue disorders, have been associated with zonular weakness. In a retrospective case series of 86 late IOL dislocations, the IOL dislocated on average 8.5 years after phacoemulsification and IOL implantation.[1] These same authors reported that patients with any type of IOL were at risk for late in-the-bag IOL dislocation. A population-based study of patients by Pueringer et al found that after cataract extraction, the long-term risk of late IOL dislocation was low and had no significant change over the almost 30-year study period.[7]

The IOL rarely dislocates completely onto the retinal surface. It usually lies meshed into the anterior vitreous with one haptic still adherent to the capsule or iris. It may cause a vitreous hemorrhage by mechanical contact with ciliary body vessels. The IOL may be related to retinal detachment or cystoid macular edema secondary to vitreous changes and may cause pupillary block or corneal contact with secondary corneal edema. On many occasions, it does not cause any complications and may be left alone if the patient is able to use aphakic spectacles or contact lenses.



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Clinically insignificant decentration occurs in at least 25% of cases. Clinically significant decentration occurs in about 3% of the cases. The frequency of IOL dislocation ranges from 0.2-1.8%. The rate is lower in eyes with posterior chamber IOLs (PCIOL) than with anterior chamber IOLs (ACIOL) or iris-supported lenses. However, since posterior chamber IOLs constitute most lenses implanted, decentered and dislocated posterior chamber IOLs have become more prevalent.

The frequency appears to have increased in the past few years because of the following reasons: (1) phacoemulsification has a steep learning curve, and, as it becomes more popular, more complications are occurring; (2) anterior segment surgeons are becoming more reluctant to place anterior chamber intraocular lenses (ACIOLs); (3) aggressive placement of posterior chamber IOL in the presence of capsular tears has become more common; and (4) silicone plate IOLs have become popular.

A longitudinal study reported that, in 85% of posterior chamber IOL exchange cases, the indication was decentration/dislocation of the lens.


Pseudoexfoliation syndrome, by virtue of its weakening effect on the zonules, is one of the most common conditions associated with late IOL dislocation.[1] The pseudoexfoliation syndrome is commonly seen in people with Scandinavian heritage.


No gender preference exists in IOL dislocation.


Age is not related to this condition.


See the list below:


ACIOL decentration

In patients with ACIOL decentration, slit lamp examination and gonioscopy may reveal iris tuck, which can cause uveal inflammation.

The eye may be red and tender.

A peaked or oval pupil can be found.

Inappropriate ACIOL size may cause a mobile lens.

ACIOL malposition may produce ongoing mechanical trauma to the cornea, iris, ciliary body, or anterior chamber angle.

Chronic inflammation may lead to corneal endothelial cell loss, cystoid macular edema (CME), glaucoma, microhyphema, and pain.

PCIOL decentration

Visual acuity can be compromised by optical aberrations and refractive changes. Slit lamp examination usually does not reveal evidence of inflammation unless contact of a portion of the IOL with the cornea or vitreous prolapse is present.

Corneal edema from IOL or vitreous touch can be found. In these cases, CME may be a complication.

Vitreous traction can increase the risk of a retinal detachment, while vitreous to the wound can be implicated in endophthalmitis.

IOL dislocation

The posterior capsule usually has an obvious defect.

Zonular dialysis may be present.

The IOL may be freely mobile in the vitreous cavity; it may be in apparent contact with the retina; or it may have one haptic attached to the posterior capsule, iris, or ciliary body.


IOL decentration may occur as a result of factors during the original surgery and lens implantation, or it may develop at a later time as a result of either outside forces, such as trauma, or internal forces related to capsular dynamics.

ACIOL decentration

Inadequate size: A lens that is too small may be too mobile and cause intermittent damage to the cornea and iris.

Improper placement during surgery: An improperly placed ACIOL may be associated with iris tuck and uveal inflammation and PAS.

Prolapse of a haptic into either wound or iridectomy: This usually requires repositioning at a different angle to avoid recurrences.

PCIOL decentration

The pathogenesis of PCIOL malposition may be related to a variety of locations of haptic fixation, to the forces of capsular contraction, or to a combined mechanism. In a study by Tappin et al, early decentration of the injected IOLs occurred in eyes without a continuous capsulorrhexis. In contrast, late decentration was due to subluxation associated with capsular fibrosis.[8]

Asymmetric haptic placement: Before the development of capsulorrhexis, it was common for the surgeon to place the inferior IOL haptic within the capsule, while releasing the superior haptic into the ciliary sulcus producing asymmetric haptic fixation. Because significant decentration was expected, PCIOLs had large optics (7 mm) and long length (13-14 mm). Subsequent healing from capsular fusion and contraction potentially caused the inferior haptic to exert forces on the optic unopposed by forces from the superior haptic within the sulcus. Migration of the optic as a result is termed sunrise syndrome.

Inadequate zonular or capsular support: This can be due to posterior capsular rupture or zonular dialysis both of which are more prevalent in patients with pseudoexfoliation. A disruption of the superior zonules when the inferior haptic is in the bag and the superior haptic is through the disinsertion also causes a sunrise syndrome as contraction of the bag forces the superior haptic through the disinsertion. Inferior dislocation of a PCIOL through an unrecognized zonular dialysis is a serious malposition termed sunset syndrome and is usually clinically evident within the first 6 weeks after surgery. A tear in the anterior capsule may allow one or both IOL haptics to migrate out of the capsular bag under the forces of capsular contraction. This has been referred to as "pea-podding."

Capsular contraction syndrome: Capsulorrhexis is a major surgical advance that contributes to long-term IOL stability and centration. Despite an intact capsulorrhexis, IOL decentration may still occur due to capsular contraction syndrome. Too small a capsulorrhexis has been implicated. Silicone-plate IOL design is particularly susceptible to the forces of capsular contraction and may decenter, rotate, tilt, or buckle. A survey by Mamalis et al cited IOL decentration as the most frequent reason for plate-type silicone IOL removal.[9] Plate-design lenses have a smaller arc of contact with the capsular fornix, reducing anchoring forces that normally reduce potential for rotation and decentration.

Capsular fusion: An eccentric capsulorrhexis may allow one of its edges to be more peripheral than the optic in one area, with fusion developing, producing decentration away from the area of contact. A large, symmetric, round, central capsulorrhexis is recommended to reduce significant decentration.

Postoperative trauma

In general, the main cause of dislocation is lack of capsular support for the IOL. This may be caused by any of the following:


IOL dislocations may lead to various postoperative complications, including rhegmatogenous retinal detachment, glaucoma, cystoid macular edema bullous keratopathy, and uveitis.[10, 11]

Imaging Studies

If a vitreous hemorrhage or severe corneal edema is present, B-scan ultrasonic imaging should be used to determine the position of the IOL and the presence or absence of retinal detachment.

Histologic Findings

Studies in cadaver eyes indicate that transscleral sutures must exit the sclera 0.8 mm posterior to the limbus in the vertical meridian and 0.46 mm posterior to the limbus in the horizontal meridian to be within the true ciliary sulcus.

Postmortem studies disclosed that scarring does not occur in the vicinity of the sutured IOL. The haptics are surrounded by a thin fibrous capsule at their attachment site. The transscleral portion of the suture is characterized by the lack of inflammation. In addition, the suture tip usually is exposed externally. If the fixation sutures were cut, the IOL would dislocate back into the vitreous cavity. It was concluded that the stability of the IOL was primarily a result of intact transscleral sutures and not fibrous encapsulation or ciliary sulcus placement of the haptics.

Medical Care

Selection of treatment in the case of a decentered IOL should be based on the patient's symptoms, needs, and expectations.

Observation: In the absence of symptoms and no evidence of inflammatory sequelae, observation is an option. In the case of an ACIOL associated with a peaked or oval pupil, careful observation is warranted if there are no signs or symptoms of intraocular inflammation.

Miotics: If symptoms from a decentered PCIOL are infrequent and limited to evening, due to a dilated pupil, these patients may be treated conservatively by using a topical miotic such as pilocarpine 0.5-1% qhs. A trial of miotic agents may be warranted prior to removing or repositioning an implant.

Observation may be recommended in dislocated IOLs if the following conditions are met:

Surgical Care

When more severe and disabling symptoms or if inflammation is present with the potential for further complications in the future, treatment should include either repositioning, explanting, or exchanging the decentered IOL.[12] Selection of treatment is based on the patient's symptoms, visual needs, and expectations, and an assessment of which option is likely to provide the best long-term benefit with the least risk.

Several indications for surgical intervention exist for a dislocated IOL. If the patient is not satisfied or cannot tolerate aphakic spectacle correction or contact lenses or if there is concomitant retinal pathology, such as a retinal detachment, surgery must be considered.

Several surgical options are available. These options include removal, exchange, or repositioning of the IOL. A multitude of techniques has been described on how to grasp, suture, and place the IOL. Repositioning of the IOL into the ciliary sulcus or over capsular remnants with less than a total of 6 clock hours of inferior capsular support is not a stable situation, as many of those repositioned IOLs will end up dislocating again. Transscleral suturing or IOL exchange (removal of the dislocated IOL and placement of a flexible open loop ACIOL) is recommended in these cases.


A vitreoretinal specialist should be consulted whenever this complication occurs.

Medication Summary

Pilocarpine hydrochloride sometimes can be used as a trial medication to evaluate symptoms related to edge glare and optical aberrations secondary to IOL decentration.

Pilocarpine HCL (Akarpine, Ocusert Pilo-40, Pilostat, Piloptic, Salagen)

Clinical Context:  Pilocarpine, with a chemical name of (3S-cis)-2(3H)-Furanone, 3-ethyldihydro-4-[(1-methyl-1H -imidazol-5-yl)methyl], monohydrochloride, has a molecular weight of 244.72. Pilocarpine HCl ophthalmic solution is a sterile solution for ophthalmic administration having the following composition: a direct-acting cholinergic parasympathomimetic agent, which acts through direct stimulation of muscarinic neuroreceptors and smooth muscle such as the iris and secretory glands. Pilocarpine produces miosis through contraction of the iris sphincter, causing increased tension on the scleral spur and opening of the trabecular meshwork spaces to facilitate outflow of aqueous humor. Outflow resistance is thereby reduced, lowering intraocular pressure.

Class Summary

For temporary pupillary constriction to relieve symptoms of optical aberrations.

Further Outpatient Care

Patients should receive follow-up care as needed.


A study by Tappin et al examined some of the intraoperative and postoperative factors leading to IOL decentration in patients requiring IOL exchange in an attempt to identify avoidable causes of IOL decentration.[8] They concluded that significant postoperative subluxation of injected silicone IOLs may be minimized by implanting only into a lens capsule bag with an intact capsulorrhexis. The risk of decentration of a small optic (5.5 mm) PMMA IOL may be minimized by positioning the haptics at 90° to any capsulorrhexis tear. After cataract surgery complicated by posterior capsular rupture or zonular dehiscence, it is important to assess the remaining capsular support and, if sufficient, implant a large optic diameter (7 mm) PCL in the ciliary sulcus.

The anterior segment surgeon should be advised to avoid implantation of a flexible silicone plate IOL if there is a break in the posterior capsule, radial notch, or tear in the anterior capsular rim or zonular dialysis.

Small capsulorrhexis openings should be avoided.

Current models of ACIOLs often do not result in the same types of complications as older models. These lenses should be considered if adequate capsular support is lacking rather than risking a posterior dislocation of an IOL.


Complications from a decentered IOL

Complications associated with ACIOL, iris-fixated IOLs, and older PCIOLs are much more severe than those encountered with modern PCIOL decentration. Corneal edema and inflammatory consequences such as uveitis-glaucoma-hyphema syndrome and chronic CME were common reasons for explanation in the above cases.

Complications from a dislocated IOL

Complications associated with dislocated IOL include the following:

Complications from transscleral suture fixation

Late endophthalmitis through the suture track has been reported.

IOL torque may occur. In addition, to place the IOL truly in the sulcus, the suture must be placed 0.8 mm posterior to the limbus in the vertical meridian and 0.46 mm in the horizontal meridian. The effective lens power is probably less than the desired one.

Vitreous hemorrhage may occur if the major arterial circle of the iris is pierced inadvertently during the maneuvers required to suture the IOL. In addition, these maneuvers also may raise the risk of a postoperative retinal detachment.

Erosion of the suture through the conjunctiva also has been reported in cases where scleral flaps were used. An attempt to melt the eroded sutures with the argon laser has been recommended. The sutures cannot be removed because the IOL haptics do not scar into place if placed in the ciliary sulcus. Once the sutures are removed, the IOL will redislocate.


With proper vitreoretinal techniques, excellent visual results and a low complication rate is possible. Long-term prognosis is highly dependent on the prevention of retinal detachment and choroidal hemorrhage secondary to surgical manipulation.


Lihteh Wu, MD, Consulting Surgeon, Department of Ophthalmology, Vitreo-Retinal Section, Instituto De Cirugia Ocular, Costa Rica

Disclosure: Received honoraria from Bayer Health for speaking and teaching; Received honoraria from Quantel Medical for speaking and teaching.


Rafael Alberto García, MD,

Disclosure: Nothing to disclose.

Robert H Graham, MD, Consultant, Department of Ophthalmology, Mayo Clinic, Scottsdale, Arizona

Disclosure: Partner received salary from Medscape/WebMD for employment.

Specialty Editors

Simon K Law, MD, PharmD, Clinical Professor of Health Sciences, Department of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine

Disclosure: Nothing to disclose.

Steve Charles, MD, Director of Charles Retina Institute; Clinical Professor, Department of Ophthalmology, University of Tennessee College of Medicine

Disclosure: Received royalty and consulting fees for: Alcon Laboratories.

Chief Editor

Hampton Roy, Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Disclosure: Nothing to disclose.

Additional Contributors

Brian A Phillpotts, MD, MD,

Disclosure: Nothing to disclose.


Teodoro Evans, MD Consulting Surgeon, Vitreo-Retinal Section, Clinica de Ojos, Costa Rica

Disclosure: Nothing to disclose.


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