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reduction, 4 months after YAG capsulotomy. There was no change in the morphology of the cells. In case of WS with an already compromised cornea, we expected the cell loss to be more than the expected. The last follow-up 15 months postoperatively in the LE and 9 months postoperatively in the RE showed an 8.6% (174 cells/mm2) decrease in cells in LE and 7.3% (160 cells/mm2) decrease in RE, which is within the normal range of cell loss. We conclude that short-term results after cataract surgery and YAG capsulotomy were excellent with modern microsurgical techniques in a patient with WS. Through this case, we want to highlight that WS should be kept in mind when operating on any patient with features of premature aging and special precautions should be taken when doing the cataract surgery.
Acknowledgement The author would like to thank the patient for providing consent to use her photograph in this article.
References 1. Rosenthal G, Assa V, Monos T, Biedner B, Lifshitz T, Zirkin H, et al. Werner’s syndrome. Br J Ophthalmol 1996;80:576-7. 2. Ruprecht KW. Ophthalmological aspects in patients with Werner’s syndrome. Arch Gerontol Geriatr 1989;9:263-70. 3. Yamamoto K, Imakiire A, Miyagawa N, Kasahara T. A report of two cases of Werner’s syndrome and review of the literature. J Orthop Surg 2003;11:224-33.
Cataract surgery after Descemet stripping endothelial keratoplasty Sunita Chaurasia, Muralidhar Ramappa, Virender Sangwan Management of endothelial dysfunction in phakic patients is sometimes a dilemma for corneal surgeons. Phakic patients with visually significant cataract and endothelial dysfunction are Access this article online Quick Response Code:
Website: www.ijo.in DOI: 10.4103/0301-4738.103803 PMID: ***
Cornea and Anterior Segment Services, LV Prasad Eye Institute, Hyderabad, India Correspondence to: Dr. Sunita Chaurasia, LV Prasad Eye Institute, LV Prasad Marg, Banjara Hills, Hyderabad – 500034, India. E-mail:
[email protected] Manuscript received: 28.12.10; Revision accepted: 08.06.11
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4. Moghimi S, Soleimani M, Soltani R. UBM study in spontaneous bleb formation and blebitis after cataract surgery in Werner syndrome. Eye (Lond) 2009;23:1481-3. 5. Kocabora MS, Kürkçüoglu AR, Engin G, Yilmazli C, Arslan O. Cataract surgery by phacoemulsification in Werner’s syndrome. J Fr Ophtalmol 2000;23:1012-5. 6. Wollina U, Gruner M, Koch A, Köstler E, Hubl W, Hanson NB, et al. Topical PDGF BB results in limited healing in a patient with Werners syndrome and chronic leg ulcers. J Wound Care 2004;13:415-6. 7. Brien PD, Fitzpatrick P, Kilmartin DJ, Beatty S. Risk factors for endothelial cell loss after phacoemulsification surgery by a junior resident. J Cataract Refract Surg 2004;30:839-43. 8. Peng Q, Hennig A, Vasavada AR, Apple DJ. Posterior capsular plaque: A commom feature of cataract surgery in developing world. Am J Ophthalmol 1998;125:621-6. 9. Kraff MC, Sanders DR, Jampol LM, Lieberman HL. Effect of primary capsulotomy with extracapsular surgery on the incidence of pseudophakic cystoid macular edema. Am J Ophthalmol 1984;98:166-70. 10. Slomovic AR, Parrish RK 2nd, Forster RK, Cubillas A. NeodymiumYAG laser posterior capsulotomy. Central corneal endothelial cell density. Arch Ophthalmol 1986;104:536-8. Cite this article as: Kemmanu V, Nagappa S, Hegde K, Yadav NK, Shetty BK. Endothelial cell study in a case of Werner's syndrome undergoing phacoemulsification and Yettrium-Aluminum-Garnet laser capsulotomy. Indian J Ophthalmol 2012;60:570-2. Source of Support: Nil. Conflict of Interest: None declared.
preferably managed by performing combined cataract surgery with endothelial keratoplasty. However, combined surgery may be deferred in eyes with early incipient cataract, younger age and where anterior chamber is poorly visualized. As cataract formation may be accelerated after endothelial keratoplasty, these eyes may need cataract surgery subsequently. Surgical intervention in eyes with endothelial keratoplasty is of concern as this may affect the graft adversely and threaten graft survival. In this report, we describe the intraoperative surgical details and postoperative clinical course of a patient who underwent phacoemulsification with intraocular lens implantation after Descemet stripping automated endothelial keratoplasty (DSAEK). Key words: Cataract surgery, endothelial keratoplasty, phacoemulsification
The preferred approach to manage phakic patients with cataract and an endothelial disorder is to perform a combined procedure of cataract extraction along with endothelial keratoplasty. Simultaneous cataract surgery and endothelial keratoplasty is deferred when cataract is insignificant, anterior chamber cannot be properly visualized and in younger patients to preserve the accommodation. However, these patients may require cataract extraction later. Cataract surgery after endothelial keratoplasty is a challenging procedure. Care must be taken to prevent the potential complications such as graft dislodgement, endothelial trauma, and graft failure. There is limited literature on cataract extraction after endothelial keratoplasty.[1] We describe our observations of sequential phacoemulsification with intraocular lens (IOL) implantation
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performed after Descemet stripping automated endothelial keratoplasty (DSAEK).
Case Report A 37-year-old male underwent endothelial keratoplasty in the right eye for primary graft failure following large diameter (11.5 mm) therapeutic penetrating keratoplasty. The therapeutic penetrating keratoplasty was done for advanced fungal keratitis 6 months prior to DSAEK. Following therapeutic keratoplasty, there was no recurrence infection. The graft was edematous with 10 intact sutures covered by conjunctiva, the anterior chamber was deep with few peripheral anterior synechiae, pupil showed posterior synechiae, and lens showed early nuclear sclerosis. The intraocular pressure was within normal range throughout the postoperative period. Figure 1: Slit-lamp photograph of the right eye after DSAEK (Day 1 post op)
Figure 2: Post-op Day 1 anterior segment OCT image showing well-attached, compact graft 2500
A superior scleral incision approach was used. Synechiolysis was done and phacoemulsification was performed by the stop and chop technique. Irrigation was kept off while inserting the phaco handpiece into the anterior chamber to avoid dislodging the graft. During surgery, a dispersive ophthalmic viscosurgical device (hydroxypropyl methylcellulose 2%, Viscomet, Sun Pharmaceuticals Industries Ltd., India) was used to protect the endothelium. A foldable, acrylic IOL was implanted in- the bag. The phaco time used was 15 seconds.
Discussion Cataract surgery following penetrating keratoplasty is a safe and effective procedure, with a low but definite risk of corneal
1500 1000 500
Po eop st -o p 1 Po w ee st k -o p 1 Po m on st -o th p 1 m on th s
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On the first postoperative day, vision was 20/160, improving to 20/80, and the graft was compact [Figs. 1 and 2]. He was treated with ofloxacin 0.3% eyedrops 6 times/day for a week and prednisolone acetate 1% eyedrops 8 times/day for the initial 1 week, followed by tapering of one drop a week and finally maintained on 3 times/day. One month after the cataract surgery, his vision was 20/50. At the last visit, 3 months later, the graft was compact and the best corrected visual acuity was 20/30 with a −0.75 D Sph/−1.50 D Cyl at 160°. Table 1 shows the visual acuity, donor thickness [assessed by anterior segment Optical Coherence Tomography (OCT), Visante: Carl Zeiss, Germany] and visual acuity pre- and post-cataract surgery. Fig. 3 shows the changes in the endothelial cell density.
Endothelial cell density (cells/mm2)
2000
Pr
DSAEK was done using Moria microkeratome system (Moria/Microtek Inc., Doylestown, PA, USA) with a 350- mm head. Considering the patient’s age and the absence of significant cataract, simultaneous cataract surgery was deferred. The endothelial cell density of the donor cornea was of 2272 cells/mm2. The posterior lamellar graft was inserted by the push-in technique using the sheet IOL glide (BD MedicalOphthalmic Systems, Franklin Lakes, NJ USA) protecting the endothelium with sodium hyaluronate 1%. The graft clarity recovered in 1 month after the surgery. At 3 months postoperative visit, the graft was clear; however, a significant progression of cataract was noted. The vision was 20/400 due to a nuclear cataract of grade 2+. The patient underwent uneventful phacoemulsification with IOL implantation 3 months after DSAEK. Pre-operative evaluation by confocal microscopy (Nidek, Confoscan 4) revealed an endothelial count of 1937 cells/mm.[2] Biometry was performed using the keratometry readings obtained from Orbscan II (Bausch and Lomb’s, Florida, USA) and IOL power was calculated for a postoperative targeted refraction of −0.5 diopters of myopia.
Figure 3: Endothelial cell density changes
Table 1: Pre and post-cataract surgery parameters Parameters
Pre-op
1 week
1 month
3 months
Visual acuity
20/400
20/50
20/30
20/30
90
90
90
90
1937
2012
2078
1562
Donor thickness (in μm) Endothelial cell density (cells/mm2)
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graft failure.[2] However, the safety and efficacy of intraocular intervention in eyes that have undergone DSAEK is not well established. Post-DSAEK surgical interventions may be fraught with the risk of endothelial cell damage or donor graft detachment or subsequent endothelial rejection. Therefore, patients with visually significant cataract often undergo cataract surgery at the time of endothelial keratoplasty. [3] It may be deferred in eyes where the anterior chamber cannot be properly visualized. In eyes with crystalline lens or early nuclear sclerosis that have undergone only endothelial keratoplasty, cataract formation may be hastened due to surgical manipulation, air tamponade at the time of surgery and use of postoperative steroid medications.[4] It is likely that all the mentioned factors might have led to accelerated cataract progression in this case. The specific surgery-related issues to be considered in these eyes are: the site of internal incision in relation to the edge of the lamellar graft, turbulence during insertion of the phaco handpiece with irrigation, which can potentially lead to graft dislodgement, reduced working space in the anterior chamber, and endothelial cell loss during surgery. The main postoperative concern is to prevent graft rejection secondary to surgical intervention. The case described here had an uneventful intraoperative and postoperative course. Appropriate surgical measures were taken to protect the graft throughout surgery. Intraoperatively, no deformation or detachment of the donor graft was noticed. The graft remained compact and well apposed. There was no noticeable corneal edema in the postoperative period. An endothelial cell loss of 14.7% was noted at 3 months after DSAEK and an additional loss of 19.3% was noted from the time of cataract surgery to 3 months later. The overall cell loss at 6 months post-DSAEK was 31.2%, which is comparable to
Progressive multifocal leukoencephalopathy presenting as homonymous hemianopia in a patient with acquired immunodeficiency syndrome Amit Pandey, Karishma Bandivdekar, Suresh Ramchandani1, Sushama Ramchandani1 Access this article online Quick Response Code:
Website: www.ijo.in DOI: 10.4103/0301-4738.103804 PMID: ***
Residents in Ophthalmology, MGM Hospital, Kamothe, 1Private Practice at Nerul, Navi Mumbai, India Correspondence to: Dr. Suresh Ramchandani, Shivam Eye Foundation, Plot no 14, Sector 25, Nerul, Navi Mumbai – 400706, Maharashtra, India. E-mail:
[email protected] Manuscript received: 20.02.11; Revision accepted: 11.09.11
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the endothelial cell density changes reported after DSAEK in various series.[5,6] This case shows that subsequent intraocular surgery with appropriate precautions can be performed safely in postDSAEK eyes. However, the long-term effect on the endothelium and graft survival needs to be better understood.
References 1. Price MO, Price DA, Fairchild KM, Price FW Jr. Rate and risk factors for cataract formation and extraction after Descemet stripping endothelial keratoplasty. Br J Ophthalmol 2010;94:1468-71. 2. Nagra PK, Rapuano CJ, Laibson PL, Kunimoto DY, Kay M, Cohen EJ. Cataract extraction following penetrating keratoplasty. Cornea 2004; 23:377-9. 3. Covert DJ, Koenig SB. New triple procedure: Descemet’s stripping and automated endothelial keratoplasty combined with phacoemulsification and intraocular lens implantation. Ophthalmology 2007;114:1272-7. 4. Price MO, Price FW Jr. Cataract progression and treatment following posterior lamellar keratoplasty. J Cataract Refract Surg 2004;30:1310-5. 5. Terry MA, Chen ES, Shamie N, Friend DJ. Endothelial cell loss after Descemet’s stripping endothelial keratoplasty in a large prospective series. Ophthalmology 2008; 115:488-96. 6. Lee WB, Jacobs DS, Musch DC, Kaufman SC, Reinhart WJ, Shtein RM. Descemet’s stripping endothelial keratoplasty: Safety and outcomes: A report by the American Academy of Ophthalmology. Ophthalmology 2009;116:1818-30. Cite this article as: Chaurasia S, Ramappa M, Sangwan V. Cataract surgery after Descemet stripping endothelial keratoplasty. Indian J Ophthalmol 2012;60:572-4. Source of Support: Nil, Conflict of Interest: None
We present a case of a Human Immunodeficiency Virus (HIV) positive patient who was referred for retinal evaluation to rule out ophthalmic manifestations of Acquired Immunodeficiency Syndrome (AIDS). She complained of some disturbance in vision in both eyes. Fundus examination showed no abnormality. Perimetry, done to rule out optic nerve pathology, showed a left homonymous hemianopia. Magnetic Resonance Imaging (MRI) scan showed features of Progressive Multifocal Leukoencephalopathy (PML). She had no other neurological symptoms or signs. Key words: Acquired Immunodeficiency Syndrome, demy elination, homonymous hemianopia, perimetry, progressive multifocal leukoencephalopathy
Progressive multifocal leukoencephalopathy (PML), also known as progressive multifocal leukoencephalitis, is a rare and usually fatal viral disease[1] that is characterized by progressive damage or inflammation of the white matter of the brain at multiple locations. It occurs almost exclusively in people with severe immune deficiency, such as transplant patients on immunosuppressive medications, patients receiving certain kinds of chemotherapy, patients receiving natalizumab (Tysabri) [1] for multiple sclerosis, psoriasis patients on long-term efalizumab (Raptiva) or AIDS patients. It is caused by a virus, the James Canyon (JC) virus, which
