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, Joobin Khadamy, MD, FEBO, FEBOS-CR, 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 Up to Date
 by Derek W DelMonte, MD on April 6, 2026.


Clinical and imaging findings in posterior capsule opacification (PCO). A. Retroillumination image showing multiple Elschnig pearls involving the optical zone and visual axis; the yellow arrow indicates pearl-type PCO. B. Appearance after Nd:YAG laser posterior capsulotomy with a central cruciate opening, outlined by the dashed black line. C. Anterior segment photograph showing an open posterior capsule with residual Elschnig pearls; the dashed white circle marks the capsulotomy opening. D. Anterior segment OCT showing cystic hyporeflective spaces consistent with Elschnig pearls; the yellow arrow indicates Elschnig pearls and the white arrow indicates the rolled posterior capsule at the edge of the capsulotomy. Courtesy of Joobin Khadamy, MD, FEBO. Previously published in: Khadamy J. Efterstarr (Posterior Capsule Opacification, PCO). Internetmedicin. Revised April 12, 2026. Available at: https://www.internetmedicin.se/ogonsjukdomar/efterstarr-posterior-capsule-opacification-pco
Clinical and imaging findings in posterior capsule opacification (PCO). A. Retroillumination image showing multiple Elschnig pearls involving the optical zone and visual axis; the yellow arrow indicates pearl-type PCO. B. Appearance after Nd:YAG laser posterior capsulotomy with a central cruciate opening, outlined by the dashed black line. C. Anterior segment photograph showing an open posterior capsule with residual Elschnig pearls; the dashed white circle marks the capsulotomy opening. D. Anterior segment OCT showing cystic hyporeflective spaces consistent with Elschnig pearls; the yellow arrow indicates Elschnig pearls and the white arrow indicates the rolled posterior capsule at the edge of the capsulotomy. Courtesy of Joobin Khadamy, MD, FEBO. Previously published in: Khadamy J. Efterstarr (Posterior Capsule Opacification, PCO). Internetmedicin. Revised April 12, 2026.[1] Available at: https://www.internetmedicin.se/ogonsjukdomar/efterstarr-posterior-capsule-opacification-pco

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.[2] 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,[3] and the reported decrease may represent only a later onset of PCO.[3][4][5][6] 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%.[5][7]

Risk Factors

Younger age is a significant risk factor for PCO.[8] Other potential risk factors include the presence of conditions such as diabetes, uveitis, myotonic dystrophy, retinitis pigmentosa, and traumatic cataract.[9][10][11][12][13]

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.[2] 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.[14]

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.[15] 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.[3]

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.

Pre-treatment evaluation before Nd:YAG: compare with postoperative best-corrected VA, assess red reflex/retroillumination, exclude macular/retinal causes, consider OCT if symptoms and PCO severity do not match.

History and Symptoms

Most patients present from months to up to several years following uneventful cataract extraction.[2] 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

Differential diagnosis / masqueraders of PCO:

  • IOL opacification
  • Late capsular bag distension / liquefied after-cataract
  • Retrolental membrane

Ancillary Testing and Imaging

The diagnosis of posterior capsule opacification (PCO) is usually clinical and is based on history, visual symptoms, retroillumination, and slit-lamp biomicroscopy. Ancillary testing is not routinely required in straightforward cases, but it may be useful when symptoms are disproportionate to the apparent PCO, when the opacity is difficult to localize, or when another cause of post-cataract visual decline is suspected.

Macular OCT should be considered when visual decline cannot be fully explained by the degree of PCO, particularly to exclude cystoid macular edema, epiretinal membrane, vitreomacular traction, diabetic macular edema, age-related macular degeneration, or other macular pathology.[1]

Anterior segment OCT (AS-OCT) can be useful in selected cases to assess the relationship between the intraocular lens (IOL), posterior capsule, retrolental space, and capsular bag. It may help distinguish true PCO from IOL opacification, retrolental fibrotic membrane, capsular bag distension syndrome, or liquefied after-cataract.[1][16]

Ultrasound biomicroscopy (UBM) may be considered when AS-OCT visualization is limited or when more detailed assessment of the capsular bag, IOL position, zonules, ciliary body, or retrolental space is required.

Anterior chamber paracentesis is not part of routine PCO evaluation, but aqueous sampling may be considered in atypical cases with capsular plques and persistent or recurrent low-grade inflammation, hypopyon, capsular plaque, or suspicion of chronic postoperative endophthalmitis before Nd:YAG capsulotomy is performed.[17]

Management

PCO causing visual disturbance is most commonly treated in older children and adults with neodymium:YAG (Nd:YAG) laser capsulotomy.[18] 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.[5] Rarely, patients may develop reopacification and require a second laser treatment.[19][20] The annual cost of Nd:YAG capsulotomy in the United States alone has been estimated at $250 million (for 1 million patients with PCO).[3]

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.[4][21]

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.

Nd:YAG technique pearls:

  • Lowest effective energy
  • Posterior focus offset to reduce IOL pitting
  • Avoid overly large opening
  • Adjust size to photopic pupil/premium IOL/zonular status
  • Release residual strands
  • Reconsider surgery for dense fibrotic membranes

When to delay or avoid Nd:YAG capsulotomy:

  • Active inflammation
  • Recent CME
  • Unstable retinal disease
  • Recent symptomatic PVD
  • Possible future IOL rotation/exchange
  • Suspected chronic Cutibacterium acnes endophthalmitis with capsular plaque and longstanding inflammation in A/C [22]

High-risk groups requiring caution:

  • Glaucoma/ocular hypertension
  • Advanced optic nerve damage
  • High myopia in younger patients before complete PVD
  • Prior retinal tear/RD, ERM, VMT, previous CME, uveitis, active nAMD

Postoperative medication and follow-up should be individualized:

  • IOP-lowering prophylaxis and early IOP check for glaucoma/OHT/high-energy cases
  • Steroids for dense fibrotic PCO, high energy, uveitis, prior CME
  • NSAID mainly for CME-risk patients[1]

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.[6] 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:[4][5][8][6]

  • 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

IOL design is one of the most important modifiable factors in PCO prevention. A sharp posterior square-edge optic creates a mechanical barrier that inhibits migration of lens epithelial cells across the posterior capsule and has been associated with lower PCO scores and reduced Nd capsulotomy rates compared with round-edge optic designs.[23]

A continuous 360-degree square edge is preferable to an interrupted edge, because discontinuities at the optic–haptic junction may permit lens epithelial cell migration. Posterior optic angulation and broad contact between the posterior optic surface and the posterior capsule may further support the barrier effect by promoting early posterior capsular apposition. Although IOL material may influence capsular biocompatibility and lens epithelial cell behavior, available evidence suggests that optic geometry, particularly a sharp posterior edge, is more consistently associated with reduced PCO than material alone.[24]

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.[25][26][27]

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.[28]

References

  1. ↑ 1.0 1.1 1.2 1.3 Khadamy J. Efterstarr (Posterior Capsule Opacification, PCO). Internetmedicin. Revised April 12, 2026. Accessed June 30, 2026.
  2. ↑ 2.0 2.1 2.2 Wormstone IM. Posterior capsule opacification: a cell biological perspective. Exp Eye Res. 2002;74(3):337-347.
  3. ↑ 3.0 3.1 3.2 3.3 Apple DJ, Solomon KD, Tetz MR, et al. Posterior capsule opacification. Surv Ophthalmol. 1992;37(2):73-116.
  4. ↑ 4.0 4.1 4.2 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.
  5. ↑ 5.0 5.1 5.2 5.3 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
  6. ↑ 6.0 6.1 6.2 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.
  7. ↑ 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.
  8. ↑ 8.0 8.1 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.
  9. ↑ 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.
  10. ↑ 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.
  11. ↑ 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.
  12. ↑ 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.
  13. ↑ Krishnamachary M, Rathi V, Gupta S. Management of traumatic cataract in children. J Cataract Refract Surg. 1997;23(Suppl 1):681-687.
  14. ↑ 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
  15. ↑ 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.
  16. ↑ Tan YL, Mohanram LS, Ti SE, Aung T, Perera SA. Imaging late capsular bag distension syndrome: an anterior segment optical coherence tomography study. Clin Ophthalmol. 2012;6:1455-1459.
  17. ↑ Clark WL, Kaiser PK, Flynn HW Jr, Belfort A, Miller D, Meisler DM. Treatment strategies and visual acuity outcomes in chronic postoperative Propionibacterium acnes endophthalmitis. Ophthalmology. 1999;106(9):1665-1670.
  18. ↑ 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.
  19. ↑ 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.
  20. ↑ McPherson RJ, Govan JA. Posterior capsule reopacification after neodymium:YAG laser capsulotomy. J Cataract Refract Surg. 1995;21(3):351-352.
  21. ↑ 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
  22. ↑ Khadamy J. Expert pearls in posterior capsule opacification after cataract surgery. touchOPHTHALMOLOGY. Published June 25, 2026. Accessed June 30, 2026.
  23. ↑ Maedel S, Evans JR, Harrer-Seely A, Findl O. Intraocular lens optic edge design for the prevention of posterior capsule opacification after cataract surgery. Cochrane Database Syst Rev. 2021;8(8).
  24. ↑ Findl O, Buehl W, Bauer P, Sycha T. Interventions for preventing posterior capsule opacification. Cochrane Database Syst Rev. 2010;2010(2).
  25. ↑ Born CP, Ryan DK. Effect of intraocular lens optic design on posterior capsular opacification. J Cataract Refract Surg. 1990;16(2):188-192. 
  26. ↑ 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.
  27. ↑ 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
  28. ↑ Gurnani B, Kaur K, Rajendran P. An after-after-cataract. Indian J Ophthalmol Case Rep. 2021;1(3):456.
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