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| CASE REPORT |
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| Year : 2023 | Volume
: 3
| Issue : 1 | Page : 45-47 |
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Deep anterior lamellar keratoplasty in advanced secondary lipid keratopathy
Anupama Kalwad1, Satish G Agraharam2, Sowmya Polisetty1
1 Department of Cornea, Anand Eye Institute, Hyderabad, Telangana, India
2 Vitreo Retina Services, Anand Eye Institute, Hyderabad, Telangana, India
| Date of Submission | 19-Apr-2022 |
| Date of Acceptance | 19-Sep-2022 |
| Date of Web Publication | 20-Jan-2023 |
Correspondence Address:
Anupama Kalwad
Department of Cornea, Anand Eye Institute, Habsiguda, Hyderabad, Telangana
India
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/ijo.IJO_996_22
A 33-year-old male presented with progressive diminution of vision in his right eye for the past ten years following an alkali injury. Examination revealed diffuse, central, advanced, secondary lipid keratopathy (LK) with best-corrected visual acuity (BCVA) of counting fingers-one meter (CF-1 m). Anterior segment optical coherence tomography (AS-OCT) revealed a thin and scarred cornea. Due to the advanced stage of the condition, a manual deep anterior lamellar keratoplasty (DALK) with argon laser photocoagulation (ALPC) to feeder vessels (500 m, 200 ms, 300 mv) combined with intraoperative needle thermal cautery was performed. A reasonably clear cornea with a good visual outcome with complete surface epithelization was achieved postoperatively and documented on AS-OCT at follow-up.
Keywords: Argon laser photocoagulation, DALK, lipid keratopathy, needle thermal cautery
How to cite this article:
Kalwad A, Agraharam SG, Polisetty S. Deep anterior lamellar keratoplasty in advanced secondary lipid keratopathy. Indian J Ophthalmol Case Rep 2023;3:45-7 |
How to cite this URL:
Kalwad A, Agraharam SG, Polisetty S. Deep anterior lamellar keratoplasty in advanced secondary lipid keratopathy. Indian J Ophthalmol Case Rep [serial online] 2023 [cited 2023 Feb 7];3:45-7. Available from: https://www.ijoreports.in/text.asp?2023/3/1/45/368230 |
Alkali burns cause severe inflammation that promote neovascularization (NV) due to hypoxia, mechanical injury, and, or limbal stem cell deficiency.[1] Lipid keratopathy (LK) is usually associated with this abnormal vascularization of the cornea, and the lipid classically deposits adjacent to these vessels. Secondary LK typically presents unilaterally as cream-colored irregular stromal opacification adjacent to neovascularization.[2]
Management of this condition usually aims to eliminate or prevent abnormal vessel formation but options in advanced cases narrow down to the surgical replacement of scarred cornea along with additional treatment modalities like argon laser photocoagulation (ALPC) of feeder vessels and intraoperative needle thermal cautery[3],[4] to limit neovascularization. The reported reduction in the extent and density of LK with these modalities are 62% and 49%, respectively.[5]
We report a case of successfully managed advanced secondary LK with deep anterior lamellar keratoplasty (DALK) and repeated ALPC to neovascularization with good postoperative outcomes. To the best of our knowledge, there are limited publications on DALK in the management of advanced secondary LK.
| Case Report | |  |
A 33-year-old healthy male presented with a history of progressive diminution of vision in his right eye (RE) for the past ten years. On examination, his best-corrected visual acuity (BCVA) in RE was counting fingers-one meter (CF-1 m) and slit lamp evaluation revealed advanced secondary LK with corneal neovascularization, obscuring visual axis [Figure 1]a. Anterior segment optical coherence tomography (AS-OCT) image of RE showed an irregularly thinned and scarred cornea [Figure 1]b. Due to the advanced stage of the condition, a manual DALK with perioperative topical steroids (1% prednisolone acetate 6 times daily) and pre-operative ALPC to feeder vessels (500 m, 200 ms, 300 mv) was planned. His fasting serum lipid profile was within normal limits. | Figure 1: (a) Pre-operative image showing advanced secondary lipid keratopathy and ALPC burns. (b) Pre-operative AS-OCT
Click here to view |
After the surface inflammation was controlled with topical steroids, a manual dissection DALK was performed under peribulbar anesthesia. After painting with povidine iodine 5% and draping, an adequate trephine size was chosen to encompass as much scar tissue as possible. The appropriate depth of corneal lamella to be dissected was judged using a blunt-tipped instrument. The superficial lamella was dissected using a crescent blade and further deeper layers were identified and dissected out using a blunt-tipped DALK dissector until the pre-Descemetic layer was reached. Needle thermal cautery was applied intraoperatively to corneal vessels to curtail interface lipid deposition, possibly to limit interface haze in the future. A micro-perforation of about one clock hour was encountered but a successful DALK was still performed by continuous air injection into the anterior chamber and dissecting away from the region of micro-perforation. A double anterior chamber was encountered on the first postoperative day, which required air injection into the anterior chamber. Postoperatively, the patient was put on topical steroids and antibiotics in tapering doses. A reasonably clear cornea was achieved postoperatively, with BCVA - 20/40 and complete surface epithelization at 6 months follow-up [Figure 2]a and [Figure 2]b. ALPC was repeated at 4 months postoperatively to address the residual neovascularization. | Figure 2: (a) Postoperative image after manual DALK showing a relatively clear cornea with complete epithelialization and minimal ocular surface inflammation. (b) Postoperative AS-OCT image
Click here to view |
| Discussion | | |
LK is characterized by corneal opacification due to lipid deposition. LK may be idiopathic or secondary to an ocular infection, inflammation, or trauma. Lipid deposition occurs majorly in regions around corneal neovascularization. If this process becomes progressive due to continued surface inflammation, opacification can threaten the visual axis.
Treatment modalities for LK vary widely in terms of approach and effectiveness, most of which aim to eliminate neovascularization. Steroids can be of use if the primary etiology is inflammatory, but these agents do not inhibit angiogenesis directly and neovascularization can progress in the absence of inflammation[4] also. Multiple steroid-sparing modalities have also been proposed, which include photodynamic therapy (PDT), anti-vascular endothelial growth factor (VEGF) antibodies, argon laser treatment, needlepoint cautery, and finally keratoplasty. Of these, argon laser treatment causes heat-induced vessel occlusion by directing a beam of light onto the pathologic vessels leading to a reduction in the extent and density of lipids to 62% and 49%, respectively.[5]
Primarily for secondary LK, the underlying condition should be treated first. If there is no resolution, then various modalities as mentioned earlier, including surgery, i.e., keratoplasty, should be explored to provide good vision to the patient. However, outcomes of keratoplasty are less favorable when compared to the idiopathic form.
To the best of our knowledge, there are limited publications on DALK in the management of advanced LK. DALK is a rarer choice for managing LK when compared to penetrating keratoplasty (PK) due to its demerits of suboptimal visual outcomes and surgical challenges faced during manual dissection. DALK was chosen, in our case, to preserve the structural and immunologic integrity of the globe, considering the patient's age and phakic status.
As vascularization of the recipient cornea[6] remains one of the most important factors in long-term graft survival, a combination of ALPC and needle thermal cautery was employed in our procedure, to curtail neovascularization and also limit further interface lipid deposition. The rationale for combining two anti-angiogenic treatments was to attain an additive effect and minimize future interface haze. Anti-VEGF is not employed in our treatment as maintenance of chronic NV appears to be less dependent on VEGF.
| Conclusion | | |
DALK is a more promising modality of intervention in stromal opacification. In addition, ALPC and needle thermal cautery address corneal neovascularisation. However, poor visibility during lamellar dissection remains a challenge.
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 | | |
| 1. | Hamill CE, Bozorg S, Peggy Chang H-Y, Lee H, Sayegh RR, Shukla AN, et al. Corneal alkali burns. Int Ophthalmol Clin 2013;53:185-94.  |
| 2. | Hall MN, Moshirfar M, Amin-Javaheri A, Ouano DP, Ronquillo Y, Hoopes PC. Lipid keratopathy: A review of pathophysiology, differential diagnosis, and management. Ophthalmol Ther 2020;9:833-52. |
| 3. | Wertheim MS, Cook SD, Knox-Cartwright NE, Van D Le, Tole DM. Electrolysis-needle cauterization of corneal vessels in patients with lipid keratopathy. Cornea 2007;26:230-1. |
| 4. | Chang J-H, Gabison EE, Kato T, Azar DT. Corneal neovascularization. Curr Opin Ophthalmol 2001;12:242-9. |
| 5. | Marsh RJ. Argon laser treatment of lipid keratopathy. Br J Ophthalmol 1988;72:900-4. |
| 6. | Zheng Y, Lin H, Ling S. Clinicopathological correlation analysis of lymphangiogenesis and corneal graft rejection. Mol Vis 2011;17:1694-700. |
[Figure 1], [Figure 2]
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