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 Table of Contents    
CASE REPORT
Year : 2023  |  Volume : 16  |  Issue : 1  |  Page : 126-132  

Secondary open-angle pigmentary glaucoma resulting from a single-piece hydrophobic intraocular lens in the sulcus


1 Sun Eye Hospital and Lasik Laser Centre, Cataract and Refractive Unit, Lucknow, Uttar Pradesh, India
2 Sun Eye Hospital and Lasik Laser Centre, Lucknow, Uttar Pradesh, India

Date of Submission08-Oct-2020
Date of Decision02-Apr-2022
Date of Acceptance02-Aug-2022
Date of Web Publication21-Feb-2023

Correspondence Address:
Sudhir Srivastava
57-B, Singar Nagar, Alambagh, Lucknow - 226 005, Uttar Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ojo.ojo_391_20

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   Abstract 


The case report of a 68-year-old man with a single-piece hydrophobic intraocular lens (IOL) implanted in the sulcus with posterior capsular rent in the right eye inducing secondary open-angle pigmentary glaucoma without individual hereditary steroid susceptibility. The clinical and diagnostic evaluations of the patient were thoroughly and specifically carried out. The unilateral pseudophakic open-angle pigmentary glaucoma developed in the long course in the context of rubbing of the haptics and optic of a hydrophobic IOL implanted in the sulcus, against the posterior surface of the iris, resulting in pigment dispersion, trabecular inflammation, and aqueous outflow obstruction. Although the clinical findings of our case were very similar to that of pigmentary glaucoma, the distinction between the two conditions was still quite easy, considering that pigmentary glaucoma is a bilateral disorder predominantly affecting young myopic men with Krukenberg's spindle and increased incidence of steroid responsiveness. It has been clearly distinguished from steroid-induced glaucoma based on the pigmented trabecular meshwork.

Keywords: Pseudophakia, IOL Induced secondary open-angle pigmentary glaucoma, steroid responsiveness, Sulcus Fixation Single Piece Intraocular lens, Posterior capsular rent with IOL, Hydrophobic IOL in sulcus


How to cite this article:
Srivastava S, Gupta A, Fatima T, Dubey S, Srivastava S. Secondary open-angle pigmentary glaucoma resulting from a single-piece hydrophobic intraocular lens in the sulcus. Oman J Ophthalmol 2023;16:126-32

How to cite this URL:
Srivastava S, Gupta A, Fatima T, Dubey S, Srivastava S. Secondary open-angle pigmentary glaucoma resulting from a single-piece hydrophobic intraocular lens in the sulcus. Oman J Ophthalmol [serial online] 2023 [cited 2023 Mar 26];16:126-32. Available from: https://www.ojoonline.org/text.asp?2023/16/1/126/370056




   Introduction Top


The implantation of an intraocular lens (IOL) in the sulcus after uneventful or complicated cataract surgery may initiate the development of some additional mechanisms for secondary glaucoma such as pupillary block, inflammatory reactions, hemorrhage, and pigment dispersion.[1] Secondary glaucoma due to IOL in the sulcus can be early onset or late onset.[2] Early onset can occur due to pupillary block, vitreous incarceration or could be steroid induced. Delayed onset can occur due to pigment dispersion or due to prolonged steroid use. Ultrasound biomicroscopy is a helpful diagnostic tool to evaluate the causes of pseudophakic glaucoma through adequate visualization of different angle structures.[3]

This article presents a case of unilateral open-angle pigmentary glaucoma secondary to sulcus fixation of single-piece hydrophobic IOL after posterior capsular rent during surgery, considering the establishment of the differential diagnosis and pathogenesis of the disease.


   Case Report Top


A 68-year-old man presented to the hospital with complaints of gradual loss of vision with intermittent irritation and redness in the right eye for the past 2 years after cataract surgery was performed elsewhere in January 2018. The patient also reported fluctuations in vision since then. No medical records were available with the patient. He was not aware of any complications occurring during surgery. However, upon taking a detailed history, he explained about slow postoperative recovery and prolonged use of postoperative drugs for 2 months. He was hypertensive for the past 3 years and was on antihypertensive medications with a history of good blood pressure control. The family history was noncontributory.

On his first visit, his best-corrected distance visual acuity on the Snellen visual acuity chart was 6/12P in the right eye and 6/9 in the left eye. His corrected intraocular pressure (IOP) was 30 mmHg in the right eye and 14 mmHg in the left eye.

Anterior segment evaluation revealed mild conjunctival congestion and clear cornea with few pigments on the endothelium. The anterior chamber was deep, and the pupil was normal in size but sluggish on light reflex. An IOL was present with moderate-size posterior capsular rent with pigments floating in the anterior vitreous.

Dilated examination showed that a single-piece hydrophobic IOL was placed centrally but haptics was positioned in the sulcus [Figure 1].
Figure 1: Single-piece IOL present in sulcus & pigments in anterior vitreous

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The fundus examination was performed. The right eye fundus showed a cup–disc ratio of 0.9 with a notch, attenuated arteries, and tessellated background [Figure 2].
Figure 2: Right Eye Fundus Photo

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The left eye fundus showed a cup/disc ratio of 0.3 and similar attenuated vessels [Figure 3].
Figure 3: Left Eye Fundus photo

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There was a history of treatment with steroids and a combination of timolol 0.5% and dorzolamide 2% in the right eye but there was no visual field analysis and glaucoma evaluation done. We added prostaglandin analogs along with timolol and the patient was kept on oral carbonic anhydrase inhibitors to control the initial high IOP. Following this, the patient was called for a detailed glaucoma assessment after 3 days. On the second visit, the patient's Humphrey field analysis was done and retinal nerve fiber assessment was done on swept-source optical coherence tomography (SS-OCT). IOP came down with medications to 12 mmHg in the right eye. On gonioscopy, angles were evaluated and the right eye showed sparse anterior synechiae [Figure 4] and pigmentation dispersion at the trabecular meshwork area was found but all angle structures were clearly visible. Left eye gonioscopy revealed comparatively clearer trabecular meshwork with open angles all around [Figure 5].
Figure 4: Right eye Gonioscopy showing sparse Peripheral Anterior Synechiae and pigmentation

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Figure 5: Gonioscopy of left eye showing relatively clear angle structures

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Humphrey field analysis showed advanced glaucomatous damage in 24–2 and 10–2 strategies in the right eye [Figure 6] and [Figure 7]. Humphrey field analysis of the left eye showed reduced retinal sensitivity due to nuclear cataract [Figure 8].
Figure 6: Right eye showing advanced glaucomatous damage

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Figure 7: Right eye 10-2 showing advance glaucomatous damage

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Figure 8: Reduced generalised retinal sensitivity due to nuclear sclerosis

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SS-OCT highlighted advanced nerve fiber loss in the right eye [Figure 9].
Figure 9: RNFL showing marked retinal fibre layer loss

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   Discussion Top


Positive findings of examination confirmed pigmentary glaucoma in the right eye, whereas the left eye examination ruled out any evidence of primary pigment dispersion glaucoma. The differential diagnosis of our case included all the forms of open-angle glaucoma with increased pigment deposition at angles. This fact did not necessarily imply that the angle was free of obstructive elements. The possibility of steroid-induced glaucoma was also kept in mind.

We evaluated the differential diagnosis of this case as follows:

  1. Primary pigmentary glaucoma
  2. Secondary glaucoma


    1. Pretrabecular membrane formation
    2. Trabecular forms accumulation of extracellular material structural changes
    3. Posttrabecular forms


The primary open-angle glaucoma and developmental glaucoma were easy to diagnose and were differentiated by taking into account past medical history and thorough clinical and functional evaluations. Pigment dispersion glaucoma was ruled out as the patient was elderly with the unilateral presentation. All the forms of secondary open glaucoma, i.e., the pretrabecular, trabecular, and posttrabecular glaucoma had to be considered and accounted for.

The analysis of the pathogenesis of this case showed that this glaucoma may be included among the pretrabecular and trabecular forms of secondary open-angle glaucoma. Of the multiple causes implicated in the pathogenesis of the pretrabecular and trabecular forms, three of them, i.e., implantation in the sulcus of a single-piece hydrophobic posterior chamber IOL, subsequently initiated inflammation of the trabecular meshwork, and the trabecular clogging by pigment and inflammatory cells (macrophages) creating an obstruction in the aqueous outflow. The haptic part of the IOL placed in the sulcus enhanced the back and forth mechanical rubbing of the posterior peripheral iris surface against the anterior surface of IOL resulting in pigment dispersion in the anterior chamber. These facts point toward the liberation and shedding of the melanin granules from the pigmented epithelium of the iris, particularly in the mid-peripheral region into the aqueous humor, its dispersion by aqueous currents, and deposition on all the anterior segment structures, including the trabecular meshwork. This was the reason for the presence of pigments in the vitreous cavity through the posterior capsular rent. The elevation of IOP appeared to be caused by the accumulation of pigment in the aqueous outflow system with an obstruction of the intertrabecular spaces and damage to the trabecular meshwork secondary to denudation, collapse, and sclerosis. In addition, inflammatory cells (macrophages), present due to the associated edema and inflammation of the trabecular meshwork, contributed to increased resistance of the aqueous outflow by trabecular clogging.


   Conclusion Top


Although the clinical picture of our case was very similar to that of pigmentary glaucoma, the distinction between the two conditions was still quite easy, considering that pigmentary glaucoma is a bilateral disorder predominantly affecting young myopic men with Krukenberg's spindle and increased incidence of steroid responsiveness. In this case, the reason for pigment dispersion was the presence of thick haptics and optic hydrophobic IOL in the sulcus which created erosion of the posterior surface of the iris.

To conclude, it is not advised to implant hydrophobic single-piece IOL in the sulcus. Instead, to avoid such late complications, one should select multipiece IOL for sulcus fixation. If haptics of a hydrophobic IOL is detected lying in the sulcus, one should try to fix the problem to prevent complications in future.[4]

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.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
   References Top

1.
Woodhams JT, Lester JC. Pigmentary dispersion glaucoma secondary to posterior chamber intra-ocular lenses. Ann Ophthalmol 1984;16:852-5.  Back to cited text no. 1
    
2.
Călugăru D, Mang A, Călugăru M. Secondary open-angle pigmentary glaucoma resulting from pseudophakia. Case report. Rom J Ophthalmol 2016;60:125-30.  Back to cited text no. 2
    
3.
Ragab IT, Abdelkader AM, Kishk HM, Elshal AA. Assessment of post-operative pseudophakic glaucoma by ultrasound Bio microscopy. Clin Ophthalmol 2020;14:1495-501.  Back to cited text no. 3
    
4.
Kohnen T, Kook D. Solving intraocular lens-related pigment dispersion syndrome with repositioning of primary sulcus implanted single-piece IOL in the capsular bag. J Cataract Refract Surg 2009;35:1459-63.  Back to cited text no. 4
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9]



 

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