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.


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.



United States

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.




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.

Imaging Studies

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 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.[10] 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





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

Disclosure: Heidelberg Engineering None Speaking and teaching


Rafael Alberto García, MD, Chief of Outpatient Services, Department of Ophthalmology, Hospital México of San José, Costa Rica

Disclosure: Nothing to disclose.

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

Disclosure: Medscape/WebMD Salary Employment

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

Disclosure: Nothing to disclose.

Specialty Editors

Brian A Phillpotts, MD, Former Vitreo-Retinal Service Director, Former Program Director, Clinical Assistant Professor, Department of Ophthalmology, Howard University College of Medicine

Disclosure: Nothing to disclose.

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; Adjunct Professor of Ophthalmology, Columbia College of Physicians and Surgeons; Clinical Professor Ophthalmology, Chinese University of Hong Kong

Disclosure: Alcon Laboratories Consulting fee Consulting

Lance L Brown, OD, MD, Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri

Disclosure: Nothing to disclose.

Chief Editor

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

Disclosure: Nothing to disclose.


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