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Year : 2022  |  Volume : 2  |  Issue : 1  |  Page : 78-80

Capsular bag distention syndrome in a child: A case report

1 Department of Paediatric Ophthalmology and Strabismology, Narayana Nethralaya, Narayana Health City, Bangalore, Karnataka, India
2 Department of Glaucoma Services, Narayana Nethralaya, Narayana Health City, Bangalore, Karnataka, India

Date of Submission05-Mar-2021
Date of Acceptance20-Aug-2021
Date of Web Publication07-Jan-2022

Correspondence Address:
Dr. Jyoti Matalia
Department of Paediatric Ophthalmology and Strabismology, Narayana Nethralaya 2, Narayana Health City, #258/A, Bommasandra Industrial Estate, Anekal Taluk, Hosur Road, Bangalore - - 560 099, Karnataka
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijo.IJO_101_21

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How to cite this article:
Matalia J, Tejwani S, Chandramouli A. Capsular bag distention syndrome in a child: A case report. Indian J Ophthalmol Case Rep 2022;2:78-80

How to cite this URL:
Matalia J, Tejwani S, Chandramouli A. Capsular bag distention syndrome in a child: A case report. Indian J Ophthalmol Case Rep [serial online] 2022 [cited 2022 Jan 19];2:78-80. Available from: https://www.ijoreports.in/text.asp?2022/2/1/78/334848

Capsular bag distension syndrome (CBDS), also known as capsular block syndrome or capsular bag hyperdistention, is a condition characterized by the accumulation of fluid between the posterior chamber intraocular lens (PCIOL) and the posterior capsule (PC), leading to distension of the capsular bag and forward displacement of the PCIOL. This condition has been reported in 0.73%–1% of the adult patients following cataract surgery but not commonly reported in the pediatric age group.[1],[2] We report an unusual case of CBDS in a child, describing its occurrence, course, and management.

  Case Report Top

A 14-year-old boy, a case of bilateral congenital glaucoma, came to us for his routine follow-up with drop in vision in his left eye (LE). He had undergone trabeculectomy and trabeculotomy (Trab-Trab) in both eyes at 1 month of age. Although the IOP remained controlled in the right eye (RE), the LE had an eventful course. He needed a repeat Trab-Trab in the LE at 4 months of age, then a trabeculectomy at 2 years of age, and an Ahmed glaucoma valve (AGV) implantation at 7 years of age. Two years later, he developed a posterior subcapsular cataract and an increase in IOP due to the formation of a fibrotic capsule around the body of the valve. In addition, the tube was abutting the cornea, resulting in a corneal opacity in the periphery [Figure 1]. For this, the child underwent lens aspiration with PCIOL implantation of +4D power with simultaneous repositioning of AGV tube and excision of the fibrotic capsule. Although the IOP was stable for 2 years, he eventually required another AGV implantation at 12 years of age. After this, his BCVA was 20/30p with − 5.50 DS in the RE and 20/80 with − 18.50 DS in the LE due to refractive amblyopia with a stable PCIOL in the bag and good IOP control. He also had low amplitude, high-frequency horizontal jerk nystagmus with a right face turn.
Figure 1: Snapshot of slit-lamp videography showing anterior segment picture of the left eye with two peripheral iridectomies and the Ahmed glaucoma valve (AGV) tube in the inferotemporal quadrant of the anterior chamber with a peripheral corneal opacity due to the AGV tube abutting the cornea

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Two years thereafter, he presented with a drop in his LE vision to 20/160 and retinoscopy revealed a dull glow. IOP was normal. Slit-lamp evaluation revealed a well-formed bleb superiorly and a patent peripheral iridectomy in the RE while in the LE there were well-formed blebs with AGV tubes in the well-formed AC. Due to the high-frequency nystagmus, multiple vigilant observations to look for the cause of drop in vision revealed the presence of turbid fluid sequestered between the PCIOL and the PC with bowing of PC into the anterior vitreous [Figure 2]a. These features were suggestive of late-onset CBDS. One consistent finding noted retrospectively in each visit after the second AGV surgery was the presence of pigments on the anterior surface of the PCIOL [Figure 2]b. The child then underwent Nd: Yag capsulotomy with cleaning of the anterior surface of IOL (22 shots of 1.6-J energy) under topical anesthesia using Abraham lens. Post capsulotomy, topical steroids were prescribed. The fluid disappeared and the capsular distension resolved [Figure 2]c and [Figure 2]d. Immediate BCVA was 20/80p.
Figure 2: (a) Snapshot of slit-lamp video showing pigment deposition on the anterior surface of the PCIOL. (b) Snapshot of slit-lamp video showing presence of white turbid fluid between the PCIOL (indicated by the yellow arrow) and the posterior capsule (indicated by the white arrow) using a narrow slit. (c) Snapshot of slit-lamp video showing absence of pigments on the PCIOL after polishing of the anterior surface of the PCIOL using broad beam illumination. (d) Snapshot of slit-lamp video after Nd: Yag capsulotomy opening with no turbid fluid using a narrow slit

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  Discussion Top

To the best of our knowledge, CBDS has previously reported in the pediatric population only by Medsinge and Nischal[3] in a 7-year-old girl with juvenile idiopathic arthritis who underwent cataract surgery with PCIOL implantation. However, this was seen 4 months after surgery, unlike in our case where it was seen almost 5 years post-surgery.

Various causes have been reported for late-onset CBDS, the commonest being a small anterior capsulorhexis sealing the posterior chamber following adhesion with the PCIOL preventing the escape of intracapsular fluid, residual cortical matter which undergoes metaplasia and further proliferation producing numerous types of collagen and extracellular matrix in the capsular bag,[4],[5] severe post-operative inflammation[6] and P. acne infection.[6],[7]

Another infrequently reported risk includes combined cataract and glaucoma surgery.[8],[9] Aqueous drainage procedures for glaucoma causes disparity in the anterior and posterior chamber pressure, resulting in the forward displacement of the IOL against the anterior capsule. This constant movement of the IOL and the fluctuation of pressure displaces the fluid into the capsular bag.[8]

After the child underwent the second AGV implantation, we observed deposition of pigments on the PCIOL at every visit, which indicated an ongoing low-grade inflammation within the eye. The reason for this being breakdown of the blood–aqueous barrier, which could have incited a chronic low-grade inflammation.[9] Hence, in our case, the cause for CBDS could be a combination of the two abovementioned factors, that is, the fluctuation in the chamber pressure following AGV and the chronic low-grade inflammation.

Although the treatment of CBDS may be just a YAG capsulotomy, it is a challenge to evaluate a child with nystagmus. The drop in vision with the absence of posterior capsular opacification with a dull retinoscopic reflex arose the suspicion of the CBDS. Hence, in such situations, where imaging techniques such as ASOCT cannot be performed, preliminary examination, such as vision, refraction, and slit-lamp evaluation, plays a vital role in arriving at a diagnosis of CBDS.

  Conclusion Top

Possibility of CBDS in the pediatric population should be well thought out if there is a poor retinoscopic reflex due to the presence of turbid fluid between the PCIOL and PC in the late postoperative period, particularly in children who have undergone multiple surgeries. In children with nystagmus, where examination is a challenge and imaging is not always possible, it becomes important to rely on signs such as a drop in vision and a dull glow on retinoscopy as an indicator of an underlying change.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Kim HK, Shin JP. Capsular block syndrome after cataract surgery: Clinical analysis and classification. J Cataract Refract Surg 2008;34:357-63.  Back to cited text no. 1
Holtz SJ. Postoperative capsular bag distension. J Cataract Refract Surg 1992;18:310-7.  Back to cited text no. 2
Medsinge A, Nischal K. Capsular blockage syndrome in a child: A case report. Eye 2013;27:1333-4.  Back to cited text no. 3
Miyake K, Ota I, Ichihashi S, Miyake S, Tanaka Y, Terasaki H. New classification of capsular block syndrome. J Cataract Refract Surg 1998;24:1230-4.  Back to cited text no. 4
Bhattacharjee H, Bhattacharjee K, Bhattacharjee P, Das D, Gogoi K, Arati D. Liquefied after cataract and its surgical treatment. Indian J Ophthalmol 2014;62:580-4.  Back to cited text no. 5
[PUBMED]  [Full text]  
Kollias AN, Vogel MA, de Kaspar HM, Lackerbauer CA, Grueterich M. Propionibacterium acnes in capsular bag distension syndrome. J Cataract Refract Surg 2010;36:167-9.  Back to cited text no. 6
Dhaliwal DK, Farhi P, Eller AW, Kowalski RP. Late capsular block syndrome associated with propionibacterium acnes. Arch Ophthalmol 2011;129:246-7.  Back to cited text no. 7
Muñoz-Negrete FJ, Rebolleda G. Capsular bag distension syndrome after combined cataract and glaucoma surgery. Acta Ophthalmol Scand 2005;83:252-5.  Back to cited text no. 8
Kanclerz P, Wang X. Postoperative capsular bag distension syndrome-Risk factors and treatment. Semin Ophthalmol 2019;34:409-19.  Back to cited text no. 9


  [Figure 1], [Figure 2]


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