Posterior Capsule Opacification

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Article initiated by:
Caroline Awh, Jeffrey M Goshe
All contributors:
Jordan Scott Masters, MD, Derek W DelMonte, MD, Kourtney Houser, MD, Caroline Awh, Jeffrey M Goshe, Bharat Gurnani MBBS,DNB,FCRS,FICO(UK), FAICO (Cornea, AIIMS, AIOS), FAICO (Refractive Surgery, AIIMS, AIOS), MRCS (Ed), MNAMS
Assigned editor:
Derek W DelMonte, MD
Review:
Assigned status Update Pending
 by Derek W DelMonte, MD on March 24, 2025.


Posterior capsule opacification (PCO) is the most common complication of cataract surgery. PCO can cause significant visual symptoms and is effectively treated with laser capsulotomy. Greater understanding of the underlying pathophysiology has led to modifications in surgical technique and intraocular lens design with the potential to decrease the incidence of PCO.

Disease Entity

Posterior capsule opacification after cataract

Disease

Posterior capsule opacification (PCO), often referred to as secondary cataract, is the most common postoperative complication of cataract extraction. In PCO, the posterior capsule undergoes secondary opacification due to the migration, proliferation, and differentiation of lens epithelial cells (LECs). PCO can cause significant visual symptoms, particularly when it involves the central visual axis.[1] Despite advances in surgical technique and intraocular lens (IOL) design and the development of therapeutic agents to inhibit PCO, this condition continues to impose a significant burden on patients and the health care system.

Epidemiology

PCO occurs in 20%-50% of patients within 2 to 5 years of cataract surgery. Although the incidence of PCO is reported to have declined in recent years, there are no definitive data,[2] and the reported decrease may represent only a later onset of PCO.[2][3][4][5] Children and infants have a significantly higher incidence and earlier onset of PCO, along with the potential for associated amblyopia. In children, reported rates of PCO reach 100%.[4][6]

Risk Factors

Younger age is a significant risk factor for PCO.[7] Other potential risk factors include the presence of conditions such as diabetes, uveitis, myotonic dystrophy, retinitis pigmentosa, and traumatic cataract.[8][9][10][11][12]

Etiology and Pathophysiology

The pathophysiology of PCO is multifactorial. During routine phacoemulsification surgery, the surgeon excises a portion of the anterior capsule (capsulorrhexis), removes the cataractous lens material, and implants a synthetic lens into the intact capsular bag. PCO occurs when residual LECs on the residual anterior capsule undergo 3 phenomena: proliferation, migration toward the posterior capsule, and normal and abnormal differentiation.[1] The accumulated LECs result in opacification of the intact posterior lens capsule, with resultant negative effects on vision.

Multiple cytokines and growth factors, including transforming growth factor β (TGF-β), fibroblast growth factor 2 (FGF-2), and hepatocyte growth factor (HFG), and matrix metalloproteinases (MMOs) have been implicated in the pathogenesis of PCO. Exogenous hyaluronic acid (HA), a component of some viscoelastic substances used during cataract surgery, may result in increased rates of ex vivo PCO.[13]

PCO has 2 forms: fibrous and pearl (also referred to as proliferative). Fibrous PCO occurs due to abnormal proliferation of LECs, and it presents as wrinkles and folds on the posterior capsule at the site of fusion of the anterior and posterior capsules. Histological examination reveals extracellular matrix (ECM) accumulation and elongated fibroblast cells.[14] Pearl PCO is responsible for the majority of PCO-related visual loss. Pearl PCO is composed of normally differentiated LECs that line the equatorial lens region. Examination shows clusters of swollen, opacified, and differentiated LECs called bladder or Wedl cells.[2]

Diagnosis

The onset of blurry vision or visual acuity decline after cataract extraction should prompt the examiner to look for signs of PCO. The diagnosis of PCO is clinical, based on history and slit-lamp examination of the eye.

History and Symptoms

Most patients present from months to up to several years following uneventful cataract extraction.[1] Patients may complain of decreased vision, blurred vision, glare, light sensitivity, impaired contrast sensitivity, halos around lights, or difficulty reading.

Signs

If PCO involves the visual axis, patients typically present with decreased visual acuity. Slit-lamp examination reveals a semiopaque membrane with variable levels of fibrosis forming on the posterior capsule. Other notable signs include the following:

  • Elschnig pearls: In pearl-type PCO, clusters of residual LECs can appear as round, clear “pearls” that shine on retroillumination. If these accumulate on the visual axis, they can cause decreased visual acuity.
  • Soemmering rings: These rings of residual LECs and cortical fibers may form between the posterior capsule and the edges of the anterior capsule remnant. They are often too peripheral to cause visual symptoms, but they can cause glare and visual loss if severe.
  • Capsular wrinkling

Management

PCO causing visual disturbance is most commonly treated in older children and adults with neodymium:YAG (Nd:YAG) laser capsulotomy.[15] Rarely, it is treated with surgical capsulotomy. Although Nd:YAG capsulotomy is noninvasive, quick, and effective, it is not without significant risk and expense and may not be available in large parts of the developing world. Complications are uncommon but may include retinal detachment, IOL damage, cystoid macular edema, increased intraocular pressure, iris hemorrhage, corneal edema, IOL subluxation, iritis, macular hole, corneal endothelial cell loss, and exacerbation of localized endophthalmitis.[4] Rarely, patients may develop reopacification and require a second laser treatment.[16][17] The annual cost of Nd:YAG capsulotomy in the United States alone has been estimated at $250 million (for 1 million patients with PCO).[2]

In younger children who cannot be safely treated with Nd:YAG capsulotomy, visual axis obscuration due to PCO can be treated with pars plana vitrectomy and capsulectomy.[3][18]

Various pharmacological and immunological methods to treat PCO are under investigation, but in vivo studies have not yet shown conclusive efficacy or safety of these modalities.

Prevention

Despite the ability to effectively treat PCO with Nd:YAG laser capsulotomy, the potential complications and significant cost of treatment make PCO prevention an important goal. Additionally, as new, accommodating IOLs that rely on flexible and intact posterior capsules become available, the prevention of PCO formation will gain further importance. Many studies have attempted to identify interventions that delay or inhibit PCO formation.[5] These interventions include surgical techniques, IOL design and material, and pharmacological interventions.

Surgical Technique

Several surgical techniques have been studied with the aim of decreasing the incidence of PCO. These techniques include the following:[3][4][7][5]

  • Thorough cortical cleanup with irrigation, aspiration, and/or manual polishing of the capsule: This is an attempt to remove all LECs remaining in the capsule bag, and in some studies, it has been shown to have a significant effect on the development of PCO.
  • Hydrodissection-enhanced cortical cleanup: Hydrodissection is a technique that weakens capsular-cortical connections in order to enhance cortical cleanup.
  • In-the-bag capsular fixation of the optic and haptic: This enhances the barrier effect of the IOL optic.
  • Continuous circular capsulorrhexis diameter slightly smaller than the IOL optic; capsulorrhexis edge on the IOL surface: This technique creates a “shrink-wrap” effect of the anterior capsule over the IOL optic. This sequesters the optic from the aqueous humor surrounding the capsule, preventing the potentially harmful effect of macromolecules and inflammatory mediators within the aqueous.
  • Broad adhesion of the IOL to the posterior capsule: This is another form of the “shrink-wrap” effect to minimize LEC migration by creating a tight fit of the posterior capsule against the back of the IOL optic.

IOL Design and Material

A square, truncated optic edge IOL design has demonstrated decreased PCO rates and improved visual outcomes compared to a soft, round optic edge IOL design. This is thought to be due to a mechanical barrier effect of the optic edge, preventing LEC growth over the posterior capsule. At this time, it is unclear whether differences in IOL loop (haptic) design play a role in PCO development.

Widely used IOL materials include high-water-content hydrophilic acrylic, low-water-content hydrophobic acrylic, and hydrophobic silicone hydrogel. Some studies have suggested that the use of hydrophobic IOL material decreases PCO formation, but meta-analysis has not demonstrated such an effect.[19][20][21]

Pharmacologic Intervention

Pharmacologic methods are being studied with the goal of depleting or inhibiting the regeneration of remaining LECs without exerting toxic side effects on the surrounding intraocular tissues. These methods include the use of antimetabolites, anti-inflammatory agents, hypo-osmolar drugs, and immunological agents. Two studies observed lower rates of PCO with the use of immunotoxin MDX-A, but there is no evidence of a significant effect from any other drug on PCO development. Recurrence after Nd:YAG laser capsulotomy has also been reported; therefore, patients should undergo regular and timely follow-up at 6 months.[22]

References

  1. ↑ 1.0 1.1 1.2 Wormstone IM. Posterior capsule opacification: a cell biological perspective. Exp Eye Res. 2002;74(3):337-347.
  2. ↑ 2.0 2.1 2.2 2.3 Apple DJ, Solomon KD, Tetz MR, et al. Posterior capsule opacification. Surv Ophthalmol. 1992;37(2):73-116.
  3. ↑ 3.0 3.1 3.2 Raj SM, Vasavada AR, Johar SR, Vasavada VA, Vasavada VA. Post-operative capsular opacification: a review. Int J Biomed Sci. 2007;3(4):237-250.
  4. ↑ 4.0 4.1 4.2 4.3 Awasthi N, Guo S, Wagner BJ. Posterior capsular opacification: a problem reduced but not yet eradicated. Arch Ophthalmol. 2009;127(4):555-562. doi:10.1001/archophthalmol.2009.3
  5. ↑ 5.0 5.1 5.2 Apple DJ, Peng Q, Visessook N, et al. Eradication of posterior capsule opacification: documentation of a marked decrease in Nd:YAG laser posterior capsulotomy rates noted in an analysis of 5416 pseudophakic human eyes obtained postmortem. Ophthalmology. 2001;108(3):505-518.
  6. ↑ Dholakia SA, Vasavada AR, Singh R. Prospective evaluation of phacoemulsification in adults younger than 50 years. J Cataract Refract Surg. 2005;31(7):1327-1333.
  7. ↑ 7.0 7.1 Pandey SK, Apple DJ, Werner L, Maloof AJ, Milverton EJ. Posterior capsule opacification: a review of the aetiopathogenesis, experimental and clinical studies and factors for prevention. Indian J Ophthalmol. 2004;52(2):99-112.
  8. ↑ Ebihara Y, Kato S, Oshika T, Yoshizaki M, Sugita G. Posterior capsule opacification after cataract surgery in patients with diabetes mellitus. J Cataract Refract Surg. 2006;32(7):1184-1187.
  9. ↑ Rahman I, Jones NP. Long-term results of cataract extraction with intraocular lens implantation in patients with uveitis. Eye (Lond). 2005;19(2):191-197.
  10. ↑ Garrott HM, Walland MJ, O’Day J. Recurrent posterior capsular opacification and capsulorhexis contracture after cataract surgery in myotonic dystrophy. Clin Exp Ophthalmol. 2004;32(6):653-655.
  11. ↑ Auffarth GU, Nimsgern C, Tetz MR, Krastel H, Volcker HE. Increased cataract rate and characteristics of Nd:YAG laser capsulotomy in retinitis pigmentosa. Ophthalmologe. 1997;94(11):791-795.
  12. ↑ Krishnamachary M, Rathi V, Gupta S. Management of traumatic cataract in children. J Cataract Refract Surg. 1997;23(Suppl 1):681-687.
  13. ↑ Sinha R, Shekhar H, Sharma N, Titiyal JS, Vajpayee RB. Posterior capsular opacification: a review. Indian J Ophthalmol. 2013;61(7):371-376. doi:10.4103/0301-4738.115787
  14. ↑ Shirai K, Saika S, Okada Y, Oda S, Ohnishi Y. Histology and immunohistochemistry of fibrous posterior capsule opacification in an infant. J Cataract Refract Surg. 2004;30(2):523-526.
  15. ↑ Stager DR Jr, Wang X, Weakley DR Jr, Felius J. The effectiveness of Nd:YAG laser capsulotomy for the treatment of posterior capsule opacification in children with acrylic intraocular lenses. J AAPOS. 2006;10(2):159-163.
  16. ↑ Jones NP, McLeod D, Boulton ME. Massive proliferation of lens epithelial remnants after Nd-YAG laser capsulotomy. Br J Ophthalmol. 1995;79(3):261-263.
  17. ↑ McPherson RJ, Govan JA. Posterior capsule reopacification after neodymium:YAG laser capsulotomy. J Cataract Refract Surg. 1995;21(3):351-352.
  18. ↑ Aslam TM, Dhillon B, Werghi N, Taguri A, Wadood A. Systems of analysis of posterior capsule opacification. Br J Ophthalmol. 2002;86(10):1181-1186. doi:10.1136/bjo.86.10.1181
  19. ↑ Born CP, Ryan DK. Effect of intraocular lens optic design on posterior capsular opacification. J Cataract Refract Surg. 1990;16(2):188-192. 
  20. ↑ Meacock WR, Spalton DJ, Boyce JF, Jose RM. Effect of optic size on posterior capsule opacification: 5.5 mm versus 6.0 mm AcrySof intraocular lenses. J Cataract Refract Surg. 2001;27(8):1194-1198.
  21. ↑ Findl O, Buehl W, Bauer P, Sycha T. Interventions for preventing posterior capsule opacification. Cochrane Database Syst Rev. 2010;2010(2):CD003738. doi:10.1002/14651858.CD003738.pub3
  22. ↑ Gurnani B, Kaur K, Rajendran P. An after-after-cataract. Indian J Ophthalmol Case Rep. 2021;1(3):456.
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