March-April 2025 (Vol 30 No 6)

Table of ContentsFrom the President’s DESK 07From the Editors 08Ophthalmic History 10 Masseuse For Eyes: A Walk Down the Historical Lanes PG Corner 13 Capsular Devices in Complicated Phacoemulsification Tools & Techniques in Ophthalmology 17 Optical Coherence Tomography Angiography - Applications in Ophthalmology Drugs in Ophthalmology 29Ophthalmic History 32FDA Approved Ophthalmic Drugs in 2023Unusual Occurrence of Granular Dystrophy Even in Nonrelated Spouses of the Affected Family Members Cornea & External Eye Diseases 33 Arborizing Dendrites: The Art of Clinical DiagnosisSubspecialty Articles 35 Firecracker-Associated Ocular InjuriesCase Report - Intrastromal Voriconazole for Post Phacoemulsification Incision Site Fungal KeratitisRole of Dyslipidaemia and Effect of Lipid Lowering Drugs on Meibomian Gland Disease - A Prospective Study 38 42A Rare Case of Bilateral Congenital Lacrimal Fistula 58Strabismus 48 Overview of Visual Assessment in ChildrenOculoplasty 55 Lessons Learnt the Hard WayAssociations of Post MSICS IntraocularBleed: A Retrospective Observational StudyDiabetic Retinopathy Studies: OverviewPostoperative Endophthalmitis: Basic Concepts of its Management 63 67 76Retina 60 Retinopathy of Prematurity - RBSK Guideline and a Medicolegal PerspectiveRetina & Uvea 74 Unilateral Granulomatous Uveitis: AnUnusual Culprit

04 05PresidentJoint Secretary Editor DJO Library OfficerVice President Secretary Treasurer Prof. Rohit SaxenaDr. R. P. SinghDr. Ankur SinghDr. Pranita SahayDr. Rajendra PrasadDr. Anu MalikDr. Rakesh GuptaDr. Jatinder SinghBhallaDr. Deepa SharmaDr. Ritin GoyalDr. AlkeshChaudharyDr. Ikeda LalDr. Siddharth MadanDr. Rahul Mayor Dr. Bhupesh SinghProf. Rajesh Sinha Dr. Prafulla Kumar Maharana Prof. Kirti SinghDOS Office BearersDOS Executive Committee (2024-2026)Executive MemberDOS Representatives to AIOS Ex-Officio MemberDOS Times - Volume 30, Number 6, March-April 2025 04 www.dosonline.org

04 DOS Times - Volume 30, Number 6, March-April 2025 05 www.dosonline.orgSection InchargesManaging EditorsThe Editorial BoardDr. Prafulla Kumar MaharanaEditor in ChiefDr. Prashant BawankuleOphthalmic QuizDr. Amit MehtaniWhat’s New?Dr. Arpan GandhiOphthalmology:Basic SciencesDr. Jatinder BaliInteresting Facts inOphthalmologyDr. Pranita SahayPG CornerDr. Neha GulianiOphthalmic HistoryDr. Arshi SinghDebates in OphthalmologyDr. Ritu Nagpal Dr. Anu MalikDr. Siddharth MadanLatest ArticlesDr. Deepali SinghalPhacoemulsification:From Basics to AdvancedDr. Ankur SinghDebates in OphthalmologyDr. Ashish MarkanDr. Ikeda LalOphthalmicImagingDr. Vineet SehgalDrugs inOphthalmologyDr. Digvijay SinghYO UpdatesDr. Karan BhatiaYO UpdatesDr. Amar PujariTools & Techniquesin Ophthalmology

DOS Times - Volume 30, Number 6, March-April 2025 06 www.dosonline.org 07Section EditorsRetina & UveaUvea & Ocular Inflammatory DisordersCornea & External Eye DiseasesOcular SurfaceDr. Abhishek JainDr. Avnindra GuptaDr. Daraius ShroffDr. Gagan BhatiaDr. Sandhya MakhijaDr. Tinku BaliDr. Anurag NarulaDr. Naginder VashishtDr. Parul JainDr. Sarita AggarwalDr. Supriya DharDr. Tulika ChauhanDr. Aastha SinghDr. Abhishek DaveDr. Rajat JainCataract & IOLDr. Aman MalikDr. Ritin GoyalDr. Shweta GaurRefractive SurgeryDr. Raghav MalikDr. Shilpi DiwanDr. Sridevi NairDr. Tushar GroverOculoplasty & AestheticsDr. Hina kauserDr. Poonam JainDr. Rwituja GroverDr. Sahil AgarwalGlaucomaDr. Annu JoonDr. Kiran BhanotDr. Suneeta DubeyNeuro-OphthalmologyStrabisumsCommunity OphthalmologyOcular OncologyComprehensive OphthalmologyDr. Rebika DhimanDr. Sumit MongaDr. Varshini ShankarDr. Anita GangerDr. Smita KapoorDr. Puneet JainDr. Shaloo BagejaDr. Sima DasDr. Sumit GroverDr. Harinder Singh SethiDr. R.K. DuveshDr. Utsav BansalDr. Suraj SenjamDr. Anil TanwarDr. Anuj MehtaDr. Ashish KumarDr. Ashok Grover Dr. Col. Ranjit GoenkaDr. G K DasDr. Jatinder Singh BhallaDr. Jeewan Singh TitiyalDr. Kirti SinghDr. M. VanathiDr. Mahipal SachdevDr. Manavdeep SinghDr. Namrata SharmaDr. OmprakashDr. Radhika TandonDr. Rishi MohanDr. Sanjay ChaudhryDr. Sanjay MishraDr. Sarita BeriDr. Subhash Dadeya Dr. Sudhank BhartiDr. Taru DeewanDr. Uma SridharDr. V P GuptaDr. Vinay GarodiaDr. Virender SangwanAdvisory Board

From The President’s Desk06 DOS Times - Volume 30, Number 6, March-April 2025 07 www.dosonline.orgProf. Rohit SaxenaIt gives me great pleasure to present this issue of the DOS Times, which encapsulates a diverse and clinically pertinent selection of topics at the forefront of contemporary ophthalmic care. With a careful blend of pediatric vision science, surgical innovation, diagnostic advancement, and postoperative care, this edition aims to provide our readership with both depth and practical insight.We open with a comprehensive discussion on Visual Assessment in Children: When, Why and How. The article highlights standardised approaches tailored to various developmental stages, while addressing common challenges in clinical evaluation and screening. Retinopathy of Prematurity (ROP) remains a major cause of preventable childhood blindness worldwide. This issue integrates evolving screening protocols, the role of telemedicine, and the importance of timely intervention, emphasising the need for multidisciplinary coordination and vigilance in neonatal care settings.In the realm of diagnostic imaging, OCT Angiography: An In-Depth Look offers a state-of-the-art overview of this non-invasive modality. The article Capsular Devices for Complicated Phacoemulsification: At a Glance succinctly summarises current innovations, ranging from capsular tension rings to segmental devices, highlighting their indications, intraoperative handling, and outcomes in challenging scenarios such as zonular weakness or trauma.The article on Post-Operative Endophthalmitis: Basics of Management outlines a pragmatic and evidence-based approach to early diagnosis, empiric therapy, surgical intervention, and long-term management, serving as an essential reference for both general and subspecialty ophthalmic practitioners.Each contribution in this edition reflects our ongoing commitment to scientific rigor, clinical relevance, and the advancement of ophthalmic knowledge. We extend our gratitude to all authors and reviewers whose expertise has enriched the content herein.A major highlight among this year’s initiatives is the forthcoming 75th Annual DOS Conference, scheduled to be held from June 13th to 15th, 2025, at the prestigious Bharat Mandapam - Convention Centre, New Delhi. This landmark event represents a historic milestone, as it will be the first time the conference convenes at this newly inaugurated, world-class venue - an architectural and technological exemplar designed to support high-level academic exchange and interdisciplinary collaboration.Equipped with cutting-edge infrastructure and optimized for large-scale scientific gatherings, the venue provides an ideal platform to facilitate meaningful dialogue, disseminate advancements in ophthalmology, and strengthen professional networks.We extend a cordial invitation to all members of the ophthalmic community to participate in this significant occasion. Your valued presence and active engagement will undoubtedly enhance the quality of discourse and contribute to the enduring success of this commemorative conference.We hope this issue serves not only as a source of knowledge but also as a catalyst for continued dialogue, research, and innovation within the ophthalmology community.Prof Rohit Saxena MD, PhDPresident, DOS

DOS Times - Volume 30, Number 6, March-April 2025 08 www.dosonline.orgFrom the EditorsDear Readers This issue, is delightfully diverse, a reflection of many minds and many paths. It holds no single theme, but rather offers a mosaic of thoughts, educational insights, creative expressions, social reflections, and academic explorations. This issue aims to be more engaging and diverse with a broader coverage across major sections and subspecialties. Content that caters to the needs and interests of both young residents as well as professionals has been included with a blend of personal experiences as well as published literature. As always we have tried to present the content in a clear, easy to understand language, enhanced with flow charts and clinical photographs wherever appropriate to support better comprehension. A Spark Ahead: As you journey through this issue, we want you to know that something special is on its way. On the eve of our Diamond Jubilee, we are preparing a special edition to celebrate 75 glorious years of leadership, legacy and achievements of our society. This upcoming issue will share memorable stories of our society right from its foundation to the present days achievements. It will be more than just a magazine, but a tribute to our journey and a symbol of hope and progress. Inviting you to share your work, reflections, words, and wisdom for the journeys yet to come.Warm Regards,Dr. Ritu Nagpal, MD (AIIMS, New Delhi)Former Fellow; Cornea and Anterior segment, LVPEI HyderabadManaging Editor, DOS TimesDr. Prafulla Kumar Maharana Dr. Ritu Nagpal Dr. Anu Malik Dr. Ashish MarkanIn the quiet rustle of these pages,you’ll find not just articlesbut echoes of questions asked in classrooms,passions sparked in library corners,and dreams shaped by chalk, code, and conversation.

Ophthalmic HistoryDOS Times - Volume 30, Number 6, March-April 2025 10 www.dosonline.orgMasseuse For Eyes: A Walk Down the Historical Lanes Surbi Taneja[1] MBBS, DNB | Swati Singh[2] MBBS, MD1. Junior Consultant Glaucoma and Cataract Services, Ahooja Eye and Dental Institute, Gurgaon, Haryana2. Senior Consultant Glaucoma and Cataract Services, Centre for Sight, New Delhi Ophthalmic HistoryOcular massage, a therapeutic technique dating back millennia across various cultures, represents a fascinating intersection of ancient wisdom and modern medical practice. Techniques involving gentle manipulation around the eyes were noted in medical texts of the time, although these were often part of broader treatments rather than specific therapies focused solely on massage.From early times the benefits of ocular massage for eyehealth have been recognized. Ancient civilizations such as the Egyptians and Mesopotamians practiced various forms of eye care, including rudimentary forms of eye massage and manual techniques to alleviate eye discomfort and promote healing.In Traditional chinese medicine, which dates back thousands of years, eye massage techniques were developed as part of overall health practices which included Gentle acupressure around the eyes and temples aiming to improve circulation, relieve eye strain, and enhance overall vision health.[1]Massage of the eyes seems not to have originated with the intellectuals, for the early natives of Africa and America used it intuitively. Paul of Aegina of ancient Greece, best known for writing medical encyclopedia “Medical Compendium in Seven Books” recommended compresses of sponges soaked in hot water along with using an egg with rosewater or goose fat at bedtime as a treatment for dry eyes.[2] Pagenstecher in 1871 reported Abstract: Ocular massage has been an ongoing practice since ancient times. Rooted in diverse medical traditions, its evolution reflects a continuum of care aimed at alleviating eye strain, managing intraocular pressure in conditions like glaucoma, and enhancing tear production in dry eye syndrome. This article delves into the historical foundations, clinical applications, and current research, highlighting ocular massage as a complementary therapy.Keywords: ocular massage, bleb massage, lid massage, accupressure“magnificent results” obtained by ocular massage even when other agents failed.[3] Donders in 1872 presented his achievements with ocular massage before the International Congress of Ophthalmology at London. Heiberg in 1874, Pedraglia in 1880 and Damalix in 1881 highlighted benefits of massage.[3] Ancient indian medical records prescribed warm compresses for treating diseases of wind known as Xerokollyria along with other compresses such as pap, goat’s milk cooked with the roots and leaves of the castor oil plant.[4]As the time advances, technology advances. With the roaring benefits of ocular massage, instruments were developed for providing the therapy in easier and efficient manner. Hoffmann was the first to design an instrument for mechanically massaging the eye[5]which has been described in detail in the “Encyclopedie francaise d’ophtalmologie[6]” stating:“Pneumatic massage conceived by Hoffmann, of Ulm, was practiced with the aid of an eyecup well fitted to the globe. To the bottom of the cup a syringe was attached. By up and down movement of the piston the pressure on the globe is increased or diminished.”An ocular massager developed by victor company consisted of glass cups through which operator could watch the action taking place (Figure-1A).[3] Another ocular corneal massager made by the same company included elastic material stretched across the circular mouth of the appliance, held in place by a knurled collar

Ophthalmic HistoryDOS Times - Volume 30, Number 6, March-April 2025 11 www.dosonline.orgwith the handle was connected to an ear pump which vibrated the diaphragm pneumatically transmitting the vibrations to the corneal surface (Figure-1B).[3] Dimitry created a device similar to Hoffman’s for ocular massage which consisted of a small cup, a syringe and a light (Figure-2).[7] The cup is placed on the eye which grips the cornea under the magnified visualization by the flashlight as the plunger of the 2cc syringe connected to the cup is released. Alternate movement of thumb on the plunger provided the massage to the cornea. The device was shown to benefit in decreasing intraocular pressures in glaucoma and rapid clearing of keratitis as it increased blood flow A study by Hayashi et al concluded that shortterm periocular massage with accupressure and automated eye massager can improve ocular blood flow and visual acuity.[9]Figure 1: (A) The Victor Company glass eye cup pneumo massager. The glass cups allowed direct observation of the eyes being massaged. (B) Corneal Ocular Massager.Figure 2: The Dimitry luminous ocular massage instrument.Ocular massage remains part of modern day interventions for specific conditions. Focal digital ocular pressure is a commonly used as adjunct in the post-operative care of patients who have undergone trabeculectomy.[8] Another use of ocular massage is in acute state of central retinal artery occlusion to dislodge the emboli thus improving retinal perfusion.[10] Ocular massage in form of lid massage has been used to treat meibomian gland dysfunction (MGD) which releases the pent up mebum and provides relief to the patient.With the advent of time, many devices have been developed to provide relief for dry eye symptoms in MGD. LipiFlow (Johnson & Johnson Vision; Santa Ana, California) is a Thermal Pulsation System consisting of a console and a single-use sterile device that uses sensor-regulated heat and peristaltic motion to evacuate obstructed meibum.[11] IPL (Intense Pulsed Light) provides brief, powerful bursts of light at specific wavelengths (in this case, between 500 and 800 nm) causing changes in blood vessels near the surface of the skin, raising skin temperature and eliminate problematic flora on the skin and eyes, all of which may have a beneficial effect on meibomian gland dysfunction.[12]Apart from treating eye diseases, ocular massage helps in relieving eye strain, relaxes sore ocular muscles, improves tear production and has a calming effect.It would be appropriate to say that from the early techniques documented in ancient civilizations to the sophisticated approaches studied today, ocular massage stands as a testament to the enduring quest for effective treatments in vision care.Advancements in technology and clinical research methodologies continue to shed light on the mechanisms by which ocular massage may influence intraocular pressure dynamics, improve tear film stability, and enhance overall eye health. However, challenges such as standardization of techniques, patient variability, and the need for rigorous clinical trials underscore the complexity of integrating ocular massage into mainstream practice.In conclusion, ocular massage is a simple yet a powerful tool in the armamentarium of an ophthalmologist which has been passed down through centuries.References1. Rosenfarb, A. (2007). Healing Your Eyes with Chinese Medicine: Acupuncture, Acupressure, & Chinese Herbs. Berkeley, California: North Atlantic Books. 2. Hirschberg, J. (1982). The History of Ophthalmology, Vol. 1: Antiquity. Bonn: Verlag J. P. Wayenborgh. 3. Keeler, Richard; Singh, Arun D; Dua, Harminder S.  British Journal of Ophthalmology; London Vol. 96, Iss. 10, (Oct 2012): 1283. DOI:10.1136/bjophthalmol-2012-302532.4. Hirschberg, J. (1982). The History of Ophthalmology,

Ophthalmic HistoryDOS Times - Volume 30, Number 6, March-April 2025 12 www.dosonline.orgVol. 1: Antiquity. Bonn: Verlag J. P. Wayenborgh. 5. Domec, S.: Anjou med. 6:185 and 220, 1899; cited by Lagrange and Valude.6. Lagrange, F., and Valude, E.: Encyclopedie francaise d’ophtalmologie, Paris, O. Doin, 1909, vol. 8, p. 1013.7. DIMITRY TJ. VACUUM MASSAGE OF THE EYEBALL. Arch Ophthalmol. 1940;23(5):926–929. doi:10.1001/archopht.1940.00860131050004.8. Gouws P, Buys YM, Rachmiel R, et al. Finger massage versus a novel massage device after trabeculectomy. Can J Ophthalmol 2008;43:222-4.9. Hayashi N, Du L. Acute and Chronic Periocular Massage for Ocular Blood Flow and Vision: a Randomized Controlled Trial. Int J Ther Massage Bodywork. 2021 Jun 1;14(2):5-13. PMID: 34079599; PMCID: PMC8133878.10. McIlraith I, Buys Y, Campbell RJ, et al. Ocular massage for intraocular pressure control after Ahmed valve insertion. Can J Ophthalmol 2008;43:48-52. 11. Pucker AD, Rueff E, Ngo W, Tichenor AA, Conto JE. LipiFlow for the treatment of dry eye disease. Cochrane Database Syst Rev. 2022 Dec 15;2022(12):CD015448. doi: 10.1002/14651858.CD015448. PMCID: PMC9754914.12. Toyos R, McGill W, Briscoe D. Intense pulsed light treatment for dry eye disease due to meibomian gland dysfunction; a 3-year retrospective study. Photomed Laser Surg. 2015 Jan;33(1):41-6. doi: 10.1089/pho.2014.3819. PMID: 25594770; PMCID: PMC4298157.Surbi Taneja MBBS, DNBJunior Consultant Glaucoma and Cataract ServicesAhooja Eye and Dental Institute, Gurgaon, HaryanaCorresponding Author:

PG CornerDOS Times - Volume 30, Number 6, March-April 2025 13 www.dosonline.orgCapsular Devices in Complicated PhacoemulsificationPushpa Kumari MSAdditional CMO, Ispat General Hospital, RourkelaIntroductionCapsular support devices are important management tools for eyes with zonulopathy.It facilitate safe and successful cataract surgery by improving capsular bag stability and centration both intra-operatively and post-operatively.[1] It avoid capsular contraction and opacification. Indications[2]a. Pseudoexfoliation syndromb. Traumatic/Iatrogenic zonular dialysisc. Hypermature cataractd. High axial lengthe. Vitrectomized eyeFour Types of Capsular Devicesa. Capsular Ring (Figure-1)b. Modified capsular ring (Cionni) (Figure-2)c. Capsular Segment (Figure-3 and 4)d. Capsular retractor hook (Figure-5 to 7) e. Assi anchor (Figure-8)Indicated in mild diffuse zonulopathy and zonular dialysis <3 to 4 o’clock. Contraindicated in irregularity in capsulorrhexis posterior capsular tear and scleral inflammation.Figure 1: (A) Capsular Ring (B) Modified capsular ring (Cionni)(C) Capsular Segment (D) Capsular retractor hook.Figure 2: Model1-L Single fixation hook away from insertion end. Model2-C Single fixation hook near insertion end.Model2-L Two fixation hook on both end.Figure 3: Ahmed capsular segment.

PG CornerDOS Times - Volume 30, Number 6, March-April 2025 14 www.dosonline.orgFigure 4: Morcher capsular segment.Figure 7: Iris retractor.Figure 8: Assi anchor.Figure 5: Mackool hook.Figure 6: Nylon capsular hook.

PG CornerDOS Times - Volume 30, Number 6, March-April 2025 15 www.dosonline.orgPrinciple of Action of Capsular Support1. CTR- Circumferential support which redistributes zonular support from intact to weak area.[3]2. Modified CTR- Transverse support by anchoring capsule to sclera.3. Capsular hook- Antero posterior support to capsular bag. Advantages of CTS Over CTRa. Can be placed in bag atraumaticaly as it does not require dialingb. Can be used in presence of incomplete capsulorrhexis & PCR. Can be used for bag stabilization both intra and post operativeCapsular Tension Ring Specification:Morcher Ring-3 Types[4]a. Type 14-12.3mm diameter, compresses to 10.0mm. b. Type 14C-13.0mm diameter, compresses to 11.0mm.c. Type 14A-14.5mm diameter, compresses to 12mm.Optech Ring-2 Typesa. Model 275-12.0mm diameter, compresses to 10mm.b. Model 276-13.0mm diameter, compresses to 11.0mm.Sizing of Capsular Support1. Axial Length of Eye:a. < 24mm-Type14-12.3-10mmb. 24-28mm-Type14C-13-11mmc. >28mm-Type14A-14.5-12mm2. White to white corneal diameter:a. WTW11.5-12.5mm-Mediumb. WTW <11.5mm-Smallc. WTW>12.5mm-LargeInsertion Methods: (Figure-9)1. Manual2. Using inserter3. Fish tail4. Suture guidedTiming of InsertionEarly after hydrodissection and late before IOL implantation.Complications of Capsular SupporterFaulty technique can result in loss of capsular support Figure 9: Preloaded capsular tension ring.Figure 10: Suture guided capsular tension ring insertion.in wrong place like anterior chamber angle and vitreous cavity.ConclusionCTRs have proven to be useful devices for cataract surgery. Although CTRs can stabilize the eye for successful surgical completion, implantation of these rings should be carefully planned and properly executed. Additional improvements and information may further improve CTR performance and efficacy.

PG CornerDOS Times - Volume 30, Number 6, March-April 2025 16 www.dosonline.orgReferences1. Chang DF. Phaco strategies with zonulopathy. InAdvanced IOL fixation techniques 2024 Jun 1 (pp. 5-16). CRC Press.2. Lanzetta P, Chiodini RG, Polito A, Bandello F. Use of capsular tension ring in phacoemulsification. Indications and technique. Indian Journal of Ophthalmology. 2002 Jan 1;50(4):333-7.3. Hasanee K, Butler M, Ahmed II. Capsular tension rings and related devices: current concepts. Current opinion in ophthalmology. 2006 Feb 1;17(1):31-41.4. Liu CS, Eleftheriadis H. Multiple capsular tension rings for the prevention of capsular contraction syndrome. Journal of Cataract & Refractive Surgery. 2001 Mar 1;27(3):342-3.Pushpa Kumari MSAdditional CMO, Trained in Phaco, Oculoplasty & Comprehensive OphthalmologyIspat General Hospital, Rourkela.Corresponding Author:

Tools & Techniques in OphthalmologyDOS Times - Volume 30, Number 6, March-April 2025 17 www.dosonline.orgOptical Coherence TomographyAngiography - Applications in Ophthalmology Sonal Praveen Paliwal [1] MBBS, DNB, FVRS | Swati Singh[2] MBBS, MDDepartment of Ophthalmology, Consultant Vitreoretina Services, Sewa Sadan Eye Hospital, BhopalAbstract: Optical coherence tomography angiography is a new, non-invasive imaging modality to study the microvasculature of retina and choroid. Compared to the previous imaging modalities like florescence angiography and Indocyanine angiography which are still considered the gold standard, OCTA is time efficient and provides ‘3D’ imaging information with detailed volumetric data analysis. It can specifically localize and delineate pathology with both structural and blood flow information of the various layers of retina and choriocapillaris. In this article we will discuss the technical principles of OCTA, image processing and artifacts and its clinical applications in ophthalmology including both anterior and posterior segment pathologies.Keywords: Optical coherence tomography angiography, age related macular degeneration, diabetic retinopathy, glaucoma, cornea IntroductionVarious ocular pathologies have been directly or indirectly linked to vascular abnormalities. For a through and extensive understanding of various retinal vascular pathologies, imaging of the retinal and choroidal vasculature in detail was needed. Optical coherence tomography angiography has emerged as a novel, non-invasive imaging technique for visualizing the retinal and choroidal microvasculature in detail.[1] It provides in vivo 3D vascular information by analyzing the movement of flowing red blood cells and thereby enabling the visualization and quantification of functional vessel networks within microcirculatory tissue beds in a noninvasive manner without the use of dye injection.[2]Anatomy of Retinal and Choroidal Vasculature (Figure-1)Retinal MicrovasculatureThere are four vascular networks at the macula which are divided into 2 vascular plexuses superficial and deep.[3] The superficial vascular plexus (SVP) supplied by the central retinal artery consists of the superficial capillary plexus which lies in the ganglionic cell layer and radial peripapillary capillary plexus in the nerve fibre layer. The deep vascular plexus (DVP) consists of two capillary networks, located above and below the inner nuclear layer (INL) referred to as the “intermediate or middle” and “deep” capillary plexuses, respectively, and are supplied by vertical anastomoses from the SVP.[4,5]The DVP has a lobular configuration when compared to the superficial capillary and radial peripapillary capillary plexuses which run parallel to the retinal nerve fibre and ganglion cell layers.[6,7]Figure 1: Microvasculature of retina and choroid.(Source - Campbell, J., Zhang, M., Hwang, T. et al. Detailed Vascular Anatomy of the Human Retina by Projection Resolved Optical Coherence Tomography Angiography. Sci Rep 7, 42201 (2017). )

Tools & Techniques in OphthalmologyDOS Times - Volume 30, Number 6, March-April 2025 18 www.dosonline.orgChoroidal Microvasculature Adjacent to Bruch’s membrane is a layer of choriocapillaris in the choroid which is densely located at macular region. The choriocapillaris form a single layer of anastomosing, fenestrated capillaries having wide lumen. The other layers are Haller’s layer which of larger diameter and Sattler’s layer of medium diameter. Principles of OCT-AngiographyOCTA technology uses laser light reflectance of the surface of moving red blood cells. In contrast to the static tissue, flowing RBCs cause more variation in the OCT signals. Repeated B-scans are performed through the area of interest and evaluated for certain parameters. OCTA compares the differences in these backscattered OCT signal intensity or amplitude (decorrelation signals) between successive OCT B scans captured at the identical cross-section at very high speed to map the retinal and choroidal circulation. This technology needed a very high speed which was not possible on earlier OCT models. OCT-A technology is available on spectral-domain and swept-source OCT platforms. In spectral-domain OCT, the light of 810nm wavelength is used while in swept- source OCT, a light of 1050nm wavelength is used. Longer wavelengths have a deeper tissue penetrance, but a slightly lower axial resolution. OCTA AlgorithmsOCT-A employs two methods for detecting the motion of red blood cells: A) Speckle variance (amplitude or intensity-based): Varying degrees of speckles occur with OCT, based on interference and reflections of light within the tissues. The changes in these speckles are compared in consecutive B-scans at identical pixel locations. The amount of similarity (correlation) or dissimilarity (decorrelation) between these pixels is calculated. B) Phase variance: These algorithms rely on the change in phase of reflected light that occurs between successive OCT B-scans.[8]C) Complex variance (both phase and amplitudebased): These are hybrid algorithms that combine both phase variance and speckle variance. Optical Microangiography (OMAG) is based on complex variance. [9,10]To improve visualization and reduce background noise from normal small eye movements and finally to improvise the signal to noise ratio, two averaging methods are applied - 1) Split spectrum amplitude decorrelation technique (SSADA) - OCT spectrum is split into several narrower bands. Inter-B-scan decorrelation is computed using the spectral bands separately and then averaged. SSADA improves the signal-to-noise ratio of flow detection at the cost of axial resolution.[11]2) Volume averaging methods (OCTARA) - OCTA Ratio Analysis, in which the full spectrum is kept intact and therefore the axial resolution is preserved.[12]Performing an OCTATo improve the quality of the scan’s different machines, have a different algorithms as patient cooperation is very crucial to achieve quality image. The signal strength index (SSI) provided by the RTVue system is used to define scan quality. Higher SSI values improved the repeatability of OCTA parameters and should be considered for image comparisons during follow-ups to avoid misinterpretation of data.[13] Newer machines also have software to compensate for the patient’s involuntary eye movements and help acquire better angiograms with minimum artifacts. Segmentation of the retinal B-scan image can be done at different levels. It is usually preset by the manufacturer or by the physician at 4 different levels - The superficial vascular layer, the deep vascular layer, the outer retina, and the choriocapillaries (Figure-2).[14] The machine automatically detects the four segmentation layers or else it can also be manually moved on the OCT B-scan by the physician to scan the area of interest. OCT B-scans are simultaneously recorded with OCT angiograms so that the pathology can precisely be localized on the B-scan and the corresponding angiogram. Scans of different sizes ranging from 3x3mm, 4.5x4.5mm and 12x12mm are taken.[15] Smaller angiogram scans have better resolution and can pick up minute pathologies that cannot be picked up on a larger scan. 12x12mm scans can be used to pick up extrafoveal pathologies. With the advent of newer software, multiple angiograms can be taken, and a montage image can be made to produce wide field angiogram images. Parameters that can be measured on OCTA[16]1. Vessel density: It is defined as the percentage area occupied by vessels in the segmented area. 2. Flow area: It is defined as the average flow signal (which is correlated with flow velocity) in a selected area.

Tools & Techniques in OphthalmologyDOS Times - Volume 30, Number 6, March-April 2025 19 www.dosonline.orgFigure 2: OCTA images segmented at different levels of the retina; a) superficial capillary plexus b) deep capillary plexus c) outer retina and d) choriocapillaris.Conventional Angiography OCTA Procedure It is an Invasive procedure, with a contrast dye It is a dye less non-invasive procedure Time Taken Whole procedure takes over a period of 10-30 minutes Angiograms obtained within 5-6 seconds Leakage Patterns of dye leakage, staining and pooling can be identified Cannot identify leaking vesselsField of View Up to 200 degrees Maximum-12x12mm Location of Lesion Pathology cannot be delineated Can identify boundaries of the pathology and its location En-face Images with Segmentation Only 1 composite image Multiple en face images segmented at various levels can be obtained Systemic Adverse Effects Present (e.g. Nausea, vomiting, anaphylaxis) Not present Contra-Indication Known allergy to contrast agent, renal disease, liver dysfunction, pregnancy No contraindications Device OCT Platform Motion Algorithm Optovue AngioVue® (Optovue, Inc., Freemont, CA) Spectraldomain Split-spectrum amplitude-decorrelation angiography (SSADA) ZEISS AngioplexTM Spectraldomain OCT- microangiography complex algorithm (OMAG) Spectralis OCT2 (Heidelberg Engineering, Germany) Spectraldomain Full-spectrum amplitude-decorrelation angiography (SADA) Topcon DRI OCT Triton Swept-source OCTA Swept Source OCTA Ratio Analyses (OCTARA) Zeiss Plex Elite 9000 Swept Source OCT-microangiography complex algorithm (OMAG)Table 1: Comparison of OCTA with conventional angiography.Table 2: Currently, available commercial OCT-A devices[17]3. Non flow area: It corresponds to the area where there is no flow as in the foveal avascular zone or in the region of capillary loss. Comparison of OCTA with conventional angiography: Table-1 Currently, available commercial OCT-A devicesTable-2[17]

Tools & Techniques in OphthalmologyDOS Times - Volume 30, Number 6, March-April 2025 20 www.dosonline.orgImage Artifacts[18-20]1. Machine specifications leading to image acquisition artifacts: OCT machines with low number of A-scans/second produce more noise and attenuate the signal quality. This can be corrected by having devices that produce a greater number of A-scans/second as in spectral-domain or swept-source OCT. 2. Motion artifacts: Patient movements, breathing and micro saccades during the acquisition of OCTA scans create motion artefacts seen as dark or bright lines (white line artefact) on OCTA images. Effects of eye movement can be minimized using eye-tracking software. 3. Projection artifact: As the OCT light falls on the superficial vessels, part of it gets reflected and part of it is transmitted and subsequently reflected from a highly reflective RPE. Subtraction software can help in removing the projections of vessels in deeper zones. 4. Masking and unmasking artifacts: Pigment epithelial detachment, sub retinal and intraretinal fluid, blood, dense cataracts, vitreous opacities can cause loss of signals obscuring visualizing of retinal and choroidal vessels. Increased reflectivity in the areas of retinal atrophy or pigment epithelium atrophy causes increased visibility of retinal vessels. 5. Segmentation artifacts: In pathologies like high myopia (staphyloma), atrophy, oedema retinal thickness gets altered which causes errors in segmentation. This can be avoided by manual segmentation. Clinical Applications1. Non Neovascular Age Related Macular DegenerationHistopathological studies of age-related macular degeneration have revealed significant loss of choriocapillaris, even in the early stages of the disease.[21] OCTA scans in cases of non-neovascular age related macular degeneration shows decrease in vascular density of the choriocapillaris layer.[22] Retinal pigment epithelium (RPE) elevation maps are used, to obtain more accurate choriocapillaris vascular density measurements. As a result, it was discovered that there was a significant flow signal loss in choriocapillaris compared with healthy controls, even in areas without drusen in non-neovascular AMD cases.[23]In geographic atrophy, flow abnormalities are observed at the borders of the atrophy which has been reported to be directly proportional to the growth rate of geographic atrophy.[24]2. Neovascular Age Related Macular Degeneration One of the important applications of OCTA is in visualizing the exact boundaries of choroidal neovascular membranes (CNVM) in a non-invasive manner. Type 1 CNVM is the most common type of neovascular AMD located between RPE and Bruch’s membrane. These lesions, which are observed as fibrovascular pigment epithelial detachments (PED) or late leakage of an undetermined source on fluorescein angiography, can be visualized in the choriocapillaris section of OCTA. The COFT-1 study group said that the rate of OCTA imaging, supported by structural OCT to detect type 1 CNVM, was 85.7%.[25] Type 2 CNVMs are located above the RPE and are usually seen as smaller but sharper vascular structures than type 1 CNVM in the outer retinal section of OCTA.[26] Type 3 neovascularization originates from the deep capillary plexus. Eyes with unilateral type 3 CNVM were also reported to have decreased choriocapillaris perfusion versus fellow non-neovascular eyes, and therefore, it was suggested that outer retinal ischemia might play a role in the type 3 CNVM pathogenesis.[27]A disadvantage of OCT-A is its inability to detect leaks. This difficulty can be overcome by combining OCT-A with OCT for the detection of intra-retinal or sub-retinal fluid. Pattern of neovascular membrane (medusa, sea fan, glomerular, lacy wheel, etc.), the branching characteristics, anastomosis and loop formation have been studied to determine the lesion activity criteria. The pattern of medusa or sea fan, thin capillary structures with numerous branching, the formation of anastomosis and loops, the vessel termini forming peripheral arcades, and the hypo intense halo appearance around the lesion, were accepted as activity criteria.[28] In particular, the existence of a thin capillary structure and arcade formation were identified as the most related criteria with the possibility of exudation.[29]According to latest terminology, maturity of the CNVM lesion was categorized as immature, mature, and hypermature, according to the density of the capillaries.[30] The CNVM lesion was defined as immature in the presence of a dense network of capillary vessels (Figure-3). Mature CNVM lesions are those which have a reduced density of

Tools & Techniques in OphthalmologyDOS Times - Volume 30, Number 6, March-April 2025 21 www.dosonline.orgcapillaries with a well-developed network of vessels. If the CNVM lesion was composed of well-delineated vessels with almost no capillaries, it was categorized as hypermature. The central trunk was defined as a single large vessel, located anywhere within the lesion, branching into smaller vessels. Figure-3 Classification of the maturity of type 1 CNVM. (A) An immature type 1 CNVM with abundant number of capillaries. (B) A mature type 1 CNVM with reduction in the number of capillaries with a well-developed network. (C) A hyper-mature type 1 CNVM with almost no capillaries. (Source - Batıoğlu, Figen, Özge Yanık, Sibel Demirel, and Emin Özmert. 2023. “Clinical Use of Optical Coherence Tomography Angiography in Retinal Diseases” The presence of subclinical CNVMs has been demonstrated in 14.4% of patients with nonexudative AMD.[31] It was observed that these quiescent CNVM detected only by OCTA had 13.6 times increased risk of exudation compared with eyes without subclinical CNVM after 24 months.[32]OCTA scans after intravitreal antiVEGF injections showed a change in neovascular network of CNVM from a homogeneous structure with a small branching network to a heterogeneous structure with the loss of capillaries.[33]Figure 3: Classification of the maturity of type 1 CNVM. (A) An immature type 1 CNVM with abundant number of capillaries. (B) A mature type 1 CNVM with reduction in the number of capillaries with a well-developed network. (C) A hyper-mature type 1 CNVM with almost no capillaries. (Source - Batıoğlu, Figen, Özge Yanık, Sibel Demirel, and Emin Özmert. 2023. “Clinical Use of Optical Coherence Tomography Angiography in Retinal Diseases” 3. Pachychoroid Spectrum Classical pachychoroid features with a type 1 choroidal neovascular membrane in the absence of characteristics age related macular degeneration features is called as pachychoroid neovasculopathy.[34] Polypoidal choroidal neovasculopathy is characterised by aneurysmal dilations of the internal choroidal network. Polyps are observed as round structures with hyper or hypo flow in OCTA and the branching vascular network can be visualized better than polypoidal lesions on OCTA.[35] The limitations of ICGA in detecting CNVM in presence of choroidal hyperpermability and RPE alterations have been overcome by OCTA. Demirel et al. stated higher sensitivity of OCTA in detecting type 1CNVM compared to conventional angiography in pachychoroid spectrum.[36] OCTA is not only useful in diagnosing but also in knowing the cases which have higher chances of recurrence. Cheung et al postulated that the presence of the flow signals in the vascular network, in spite of inactive lesions may be a risk factor for recurrence.[37] Figure-4Figure 4: (A,B) Polypoidal structures and branching vascular network on the early and late phases of indocyanine green angiography. (C,D) Hypo reflective polyps on the choriocapillaries slab of the en-face OCTA and an inverted V shaped polyp with intrinsic flow signal on corresponding flow signal superimposed horizontal B -scan OCT. (E,F) Branching vascular network on choriocapillaries slab of en-face OCTA and flat irregular pigment epithelial detachment appearance corresponding to branching vascular network on the flow signal superimposed on horizontal B scan OCT.

Tools & Techniques in OphthalmologyDOS Times - Volume 30, Number 6, March-April 2025 22 www.dosonline.org4. Secondary CNV OCT-A is also useful in diagnosis of CNV due to other causes such as Myopia, Central Serous Chorioretinopathy, Adult-onset vitelliform disorder, and best disease. In pathological myopia OCTA helps to differentiate lacquer crack bleeds from CNV related hemorrhage as the bleed may obscure the CNV on FFA. OCT-A has been reported to have high sensitivity (80-100%) in diagnosing BEST disease-related CNV.[38,39] As the vitelliform material masks the neovascularization on FFA, OCTA is superior to FFA in diagnosing CNV in such cases. Similar observations of FAZ abnormalities, vascular rarefaction in the retinal capillary plexuses as well as choriocapillaris have also been made in patients of adult-onset vitelliform dystrophy.[40]OCT-A shows high sensitivity in diagnosing CSC related CNV.[41] Irregular PEDs in eyes with CSC may harbour CNV that can be diagnosed with high sensitivity using OCT-A.[42]5. Diabetic RetinopathyMicro aneurysms, capillary non-perfusion areas, choriocapillaris abnormalities, IRMA, enlargement of the foveal avascular zone (FAZ), increase in the perifoveal inter capillary space, and retinal and disc neovascularization can be visualized with OCTA in a non-invasive manner. Various quantitative measures like FAZ area helps us in understanding the severity of diabetic retinopathy and macular ischemia.[43] In cases of Proliferative diabetic retinopathy, OCTA may be useful in the differentiation of IRMA and NVE. The flow signal on the superimposed B scan is located under the internal limiting membrane in IRMA.[44] SS-OCTA B scan was comparable in diagnosing NVE similar to FFA (p = 0.92.[45] Couturier et al. observed that the detection rate of non-perfusion areas was higher with swept-source, wide-field OCTA than with UWF FA.[46]Limitations of OCTA includes inability to diagnose microaneurysms with reduced blood flow below the threshold of OCTA and segmentation errors due to macular edema. OCTA provides a field of view of 80 degree significantly less than the 200° provided by ultra-wide field (UWF) FA systems. Wide-field OCTA imaging can be considered an alternative technique for the near future. 6. Venous OcclusionsIn retinal venous occlusive diseases, OCTA has been used to identify areas of capillary non-perfusion, foveal and perifoveal vascular density and the morphology of the foveal avascular zone (FAZ). Other findings like microvascular abnormalities, collateral vessels, capillary telangiectasia, micro aneurysms, neovascularization and areas of vascular congestion can be isolated in different levels of the retinal capillary plexus by OCTA.[47] In patients of CRVO, FAZ was enlarged in both the superficial and the deep capillary plexus in OCTA which showed a significant correlation with visual acuity in cases without macular oedema.[48]However, the segmentation errors due to presence of macular oedema and its inability to scan the peripheral retina with high resolution is a limitation of OCTA in eyes with retinal vascular occlusions since these pathologies majorly affect the peripheral retinal vasculature. 7. Retinal Artery Occlusion Studies related to utility of OCTA in retinal artery occlusion are limited. In acute retinal perfusion limitations, OCTA imaging has been proven to reveal the precise boundary of the ischemic retinal area, especially on the deep capillary plexus.[49]8. UveitisOCTA is emerging as a valuable tool for evaluation of uveitis, mainly posterior uveitis and white dot syndromes. It can detect reduced vascular density in superficial and deep vascular plexus of the retinal and choriocapillaris.[50]In Behcet’s retinal vasculitis, the deep capillary plexus is more affected than the superficial plexus and shows microvascular changes like perifoveal capillary telangiectasia.[51] Anterior segment OCTA can detect iris hyperemia and subtle iris neovascularization. Subtle microvascular flow loss areas that are not detected by fluorescein angiography can be visualized on OCTA which helps to prevent the risk of early visual loss. OCTA has been widely used in the study of white dot syndromes and its complications. Acute posterior multifocal placoid pigment epitheliopathy (APMPPE) and serpiginous choroiditis showed perfusion defects at the level of choriocapillaries which suggests that choriocapillaries is the primary focus of the disease.[52] In contrary to this, the choriocapillaries is normal in multiple evanescent white dot syndrome (MEWDS) which suggests that the primary injury is at the photoreceptors and outer retina.[53]9. Idiopathic Macular Telangiectasia Idiopathic macular telangiectasia type 2 (MacTel 2 or perifoveal telangiectasia) is a macular disorder characterized by dilation and ectasia of perifoveal capillaries, muller cell

Tools & Techniques in OphthalmologyDOS Times - Volume 30, Number 6, March-April 2025 23 www.dosonline.orgdegeneration and loss which may be complicated by neovascularization.An OCTA-based staging system was described by Toto et al based on lateral extent of vascular anomalies.[54] The right-angled retinal venules, extending from the epiretinal surface to the deep capillary plexus, is also an additional imaging feature described with OCTA.[55]In the advanced stages, neovascularization develops in the sub-retinal space. Anastomosis may occur between sub retinal neovascularization and choroidal circulation. Epiretinal neovascularization is another newly defined OCTA finding.[56]10. Other Retinal Vascular Disorder If deep capillary ischemia affects the inner nuclear and inner plexiform layers, it is called paracentral acute middle maculopathy (PAMM). If it influences the outer plexiform and the outer nuclear layers, then it is called acute macular neuroretinopathy (AMN). The deep vascular complex consists of two different capillary networks: the intermediate and the deep capillary plexus. If the intermediate plexus is affected, PAMM develops; if the deep capillary plexus is affected, AMN develops. These two clinical pictures are differentiated from each other according to the retinal layer, where the hyper reflective band is seen in the structural B-scan images, or where nuclear atrophy develops. In OCTA, vascular density reduction is observed in the deep capillary plexus.[57]Microvascular abnormalities in both superficial and deep plexus can be observed in patients with sickle cell disease on OCTA.[58]11. Hereditary Retinal Disorders OCTA has also been evaluated in some retinal dystrophies. Microvascular density in both superficial and deep retinal capillary plexus is reduced in retinitis pigmentosa.[59]In Stargardt Disease there is vascular rarefaction in the choriocapillaris layer that corresponds to decreased retinal sensitivity on microperimetry.[60] Patients of choroideremia exhibit a significant impairment of vessel density in the choriocapillaris, outer retina as well as inner retina. [61] X-linked retinoschisis shows perifoveal microvascular alterations like telangiectasia.[62]12. GlaucomaStudies have shown that OCTA allows for early detection of microvascular changes that precede structural damage which is crucial for early diagnosis and progression in glaucoma monitoring. OCTA can identify decreased vessel density in peripapillary, and macular regions as compared to healthy controls.[63] A vascular attenuation as well as focal capillary dropout is also evident.[64] OCTA helps in identification of areas with microvascular dropouts often seen inferotemporally within the beta zone in glaucoma.[65]A few studies have also evaluated the response of vessel density to glaucoma surgery using OCTA where an increase in vessel density was observed.[66] However more research is needed to determine whether OCTA can replace traditional methods of glaucoma imaging. 13. Neuro-Opthalmology OCTA has also been evaluated to study the optic disc vasculature. Optic disc oedema shows vessel tortuosity and dilated pre-laminar capillary network on OCTA localized in the nerve fiber layer.[67]OCTA has also been evaluated to study the peripapillary microvasculature of eyes in patients of Non arteritis anterior ischaemic optic neuropathy (NAION).[68]However, it is yet to establish its role as a modality to diagnose and monitor disc pathologies. 14. Anterior Segment OCTA has also been studied for imaging of conjunctiva, cornea and the iris. OCTA can delineate corneal vessels, limbal and conjunctival vascularisation, pre and post inflammatory changes. OCTA allows analysis of iris vasculature and 3-D reconstruction of iris vessels. OCTA can also show iris filling defects, qualitative vessel density and fine iris vessels seen in different inflammatory pathologies.[69]Quantitative AnalysisVarious quantitative parameters on OCTA are described below. Blood vessel density (BVD)- Ratio of image area occupied by the blood vessels. This is important in vascular diseases that have areas of ischemia and vascular dropouts.[70]Blood vessel calibre (BVC)- It is used to measure the amount of vascular dilation or constriction in vascular disorders like DR and sickle cell retinopathy. It is the ratio of vessel area to the vessel length.[70]Blood vessel tortuosity (BVT)- It is a degree of vessel distortion in conditions where there is turbulent blood flow to disturbances in the vessel wall.[71] Vessel perimeter index (VPI)- It is the ratio between the total length of blood vessel boundaries and total blood vessel area in a segmented vessel map. VPI can detect vessel dropouts and early ischemia.[72]Foveal vascular zone area (FAZ)- The area of the avascular

Tools & Techniques in OphthalmologyDOS Times - Volume 30, Number 6, March-April 2025 24 www.dosonline.orgzone can be manually segmented or there is an inbuilt algorithm to detect the area in both the superficial and deep avascular zones.[70]Foveal vascular zone- Contour irregularity (FAZ-CI)- measures the structural irregularity of the FAZ. It is calculated as the ratio of the perimeter of FAZ-A to a reference circle of an ideal FAZ. Vessel complexity index (VCI)- It is used to quantify changes in the vascular complexity.[73]Branch point analysis (BPA)- It helps to quantify changes in the vascular bifurcation.[74]Differential artery-vein (A-V) analysis- Compares changes in arteries relative to the veins.[75]CNV Analysis- used to assess morphological distortions like sea fan, medusa, tangled and dead tree in choroidal vasculature. Future DirectionsDue to limited view of OCTA in comparison to FFA significant research is being done towards enhancing the field of view of OCT-A. Research-oriented platforms like the PLEX Elite 9000 device (Carl Zeiss Meditec, Inc., Dublin, CA) offer an in-built montage module that can stitch together an OCT-A image covering an area equivalent to the 7-standard field (7SF) images.[76] Software to decrease the projection artefacts and create images with less speckle and noise disturbances are being developed.[77] Deep learning algorithms are being tested to increase the accuracy of automated segmentation protocols and improving the quality of scans by denoising captured images.[78,79,80] In the future, artificial intelligence may completely bypass the need for specialised OCT-A algorithms by directly generating flow images from OCT B-scans.[81]References1. Fingler J, Readhead C, Schwartz DM, et al. Phasecontrast OCT imaging of transverse flows in the mouse retina and choroid. Invest Ophthalmol Vis Sci 2008; 49: 5055-5059. 2 Koustenis A, Harris A, Gross J, et al. Optical coherence tomography angiography: an overview of the technology and an assessment of applications for clinical research. Br J Ophthalmol 2017; 101: 16-20. 3 Stone J, van Driel D, Valter K, et al. The locations of mitochondria in mammalian photoreceptors: relation to retinal vasculature. Brain Res 2008; 1189: 58-69. 4. Provis JM. Development of the primate retinal vasculature. Prog Retin Eye Res 2001; 20: 799-821. 5. Snodderly DM, Weinhaus RS, Choi JC. Neuralvascular relationships in central retina of macaque monkeys (Macaca fascicularis). J Neurosci Off J Soc Neurosci 1992; 12: 1169–1193. 6. Henkind P. Radial peripapillary capillaries of the retina. I. Anatomy: human and comparative. Br J Ophthalmol 1967; 51: 115-123. 7. Alterman M, Henkind P. Radial peripapillary capillaries of the retina. II. Possible role in Bjerrum scotoma. Br J Ophthalmol 1968; 52: 26-31. 8. Chen C-l, Wang Rk. Optical Coherence Tomography Based Angiography [Invited]. Biomed Opt Express. 2017;8(2):1056-1082. 9. Reif R, Wang Rk. Optical Microangiography Based On Optical Coherence Tomography. In: Drexler W, Fujimoto Jg, Eds. Optical Coherence Tomography. Springer International Publishing; 2015:1373-1397. 10. Jia Y, Tan O, Tokayer J, Et Al. Split-spectrum Amplitude-decorrelation Angiography With Optical Coherence Tomography. Opt Express. 2012;20(4):47104725. 11. Jia Y, Tan O, Tokayer J, Et Al. Split-spectrum Amplitude-decorrelation Angiography With Optical Coherence Tomography. Opt Express. 2012;20(4):47104725. 12. Stanga Pe, Tsamis E, Papayannis A, Stringa F, Cole T, Jalil A. Swept-source Optical Coherence Tomography Angiotm (Topcon Corp, Japan): Technology Review. In: Bandello F, Souied Eh, Querques G, Eds. Developments In Ophthalmology. Vol 56. S. Karger Ag; 2016:13-17. 13. Yu, Jeffrey J Et Al. Signal Strength Reduction Effects In Oct Angiography 14. De Carlo, T.E., Romano, A., Waheed, N.K.et Al; A Review Of Optical Coherence Tomography Angiography (Octa).int J Retin Vitr1,5 (2015). 15. Spaide Rf, Curcio Ca. Evaluation Of Segmentation Of The Superficial And Deep Vascular Layers Of The Retina By Optical Coherence Tomography Angiography Instruments In Normal Eyes. Jama Ophthalmol. 2017;135(3):259 16. Jia Y, Bailey St, Hwang Ts, Mcclintic Sm, Gao Ss, Pennesi Me, Et Al. Quantitative Optical Coherence Tomography Angiography Of Vascular Abnormalities In The Living Human Eye. Proc Natl Acad Sci Usa. 2015 May 5;112(18):E2395-2402.

Tools & Techniques in OphthalmologyDOS Times - Volume 30, Number 6, March-April 2025 25 www.dosonline.org17. Munk MR, Giannakaki-Zimmermann H, Berger L, et al. OCT-angiography: A qualitative and quantitative comparison of 4 OCT-A devices. PLOS ONE 2017; 12: e0177059. 18. Spaide RF, Fujimoto JG, Waheed NK. IMAGE ARTIFACTS IN OPTICAL C O H E R E N C E TOMOGRAPHY ANGIOGRAPHY. Retina Phila Pa 2015; 35: 2163– 2180. 19. Chen FK, Viljoen RD, Bukowska DM. Classification of image artefacts in optical coherence tomography angiography of the choroid in macular diseases. Clin Experiment Ophthalmol 2016; 44: 388–399. 20. Enders C, Lang GE, Dreyhaupt J, et al. Quantity and quality of image artifacts in optical coherence tomography angiography. PloS One 2019; 14: e0210505. 21. Seddon, J.M.; McLeod, D.S.; Bhutto, I.A.; Villalonga, M.B.; Silver, R.E.;Wenick, A.S.; Edwards, M.M.; Lutty, G.A. Histopathological Insights Into Choroidal Vascular Loss in Clinically Documented Cases of Age-Related Macular Degeneration. JAMA Ophthalmol.2016, 134, 1272–1280. 22. Alten, F.; Lauermann, J.L.; Clemens, C.R.; Heiduschka, P.; Eter, N. Signal reduction in choriocapillaris and segmentation errors in spectral domain OCT angiography caused by soft drusen. Graefes Arch. Clin. Exp. Ophthalmol. 2017, 255, 2347–2355. 23. Borrelli, E.; Uji, A.; Sarraf, D.; Sadda, S.R. Alterations in the Choriocapillaris in Intermediate Age-Related Macular Degeneration.Investig. Ophthalmol. Vis. Sci. 2017, 58, 4792–4798. 24. Nassisi, M.; Baghdasaryan, E.; Borrelli, E.; Ip, M.; Sadda, S.R. Choriocapillaris flow impairment surrounding geographic atrophy correlates with disease progression. PLoS ONE 2019, 14, e0212563. 25. Inoue, M.; Jung, J.J.; Balaratnasingam, C.; Dansingani, K.K.; Dhrami-Gavazi, E.; Suzuki, M.; de Carlo, T.E.; Shahlaee, A.; Klufas,M.A.; El Maftouhi, A.; et al. A Comparison Between Optical Coherence Tomography Angiography and Fluorescein Angiography for the Imaging of Type 1 Neovascularization. Investig. Ophthalmol. Vis. Sci. 2016, 57, OCT314–OCT323. 26. Farecki, M.L.; Gutfleisch, M.; Faatz, H.; Rothaus, K.; Heimes, B.; Spital, G.; Lommatzsch, A.; Pauleikhoff, D. Characteristics of type 1 and 2 CNV in exudative AMD in OCT-Angiography. Graefe’s Arch. Clin. Exp. Ophthalmol. 2017, 255, 913–921. 27. Borrelli, E.; Souied, E.H.; Freund, K.B.; Querques, G.; Miere, A.; Gal-Or, O.; Sacconi, R.; Sadda, S.R.; Sarraf, D. Reduced Choriocapillaris Flow in Eyes with Type 3 Neovascularization and Age-Related Macular Degeneration. Retina 2018. 28. Coscas, G.J.; Lupidi, M.; Coscas, F.; Cagini, C.; Souied, E.H. Optical Coherence Tomography Angiography Versus Traditional Multimodal Imaging in Assessing the Activity of Exudative Age-Related Macular Degeneration: A New Diagnostic Challenge. Retina 2015, 35, 2219–2228. 29. Coscas, F.; Lupidi, M.; Boulet, J.F.; Sellam, A.; Cabral, D.; Serra, R.; Francais, C.; Souied, E.H.; Coscas, G. Optical coherence tomography angiography in exudative age related macular degeneration: A predictive model for treatment decisions. Br. J.Ophthalmol. 2019, 103, 1342–1346. 30. Mendonca, L.S.M.; Perrott-Reynolds, R.; Schwartz, R.; Madi, H.A.; Cronbach, N.; Gendelman, I.; Muldrew, A.; Bannon, F.;Balaskas, K.; Gemmy Cheung, C.M.; et al. Deliberations of an International Panel of Experts on OCT Angiography Nomenclatureof Neovascular Age-Related Macular Degeneration. Ophthalmology 2021, 128, 1109–1112. 31. de Oliveira Dias, J.R.; Zhang, Q.; Garcia, J.M.B.; Zheng, F.; Motulsky, E.H.; Roisman, L.; Miller, A.; Chen, C.L.; Kubach, S.; de Sisternes, L.; et al. Natural History of Subclinical Neovascularization in Nonexudative AgeRelated Macular Degeneration Using Swept-Source OCT Angiography. Ophthalmology 2018, 125, 255–266. 32. Yang J., Zhang Q., Motulsky E.H., Thulliez M., Shi Y., Lyu C., de Sisternes L., Durbin M.K., Feuer W., Wang R.K., et al. Two-Year Risk of Exudation in Eyes with Nonexudative Age-Related Macular Degeneration and Subclinical Neovascularization Detected with Swept Source Optical Coherence Tomography Angiography. Am. J. Ophthalmol. 2019;208:1–11. doi: 10.1016/j.ajo.2019.06.017. 33. Coscas G.J., Lupidi M., Coscas F., Cagini C., Souied E.H. Optical Coherence Tomography Angiography Versus Traditional Multimodal Imaging in Assessing the Activity of Exudative AgeRelated Macular Degeneration: A New Diagnostic Challenge. Retina. 2015;35:2219–2228. doi: 10.1097/IAE.0000000000000766. 34. Pang C.E., Freund K.B. Pachychoroid neovasculopathy. Retina. 2015;35:1–9. doi: 10.1097/IAE.0000000000000331.

Tools & Techniques in OphthalmologyDOS Times - Volume 30, Number 6, March-April 2025 26 www.dosonline.org35. Srour M., Querques G., Semoun O., El Ameen A., Miere A., Sikorav A., Zambrowski O., Souied E.H. Optical coherence tomography angiography characteristics of polypoidal choroidal vasculopathy. Br. J. Ophthalmol. 2016;100:1489–1493. doi: 10.1136/bjophthalmol-2015-307892. 36. Demirel S., Yanik O., Nalci H., Batioglu F., Ozmert E. The use of optical coherence tomography angiography in pachychoroid spectrum diseases: A concurrent comparison with dye angiography. Graefe’s Arch. Clin. Exp. Ophthalmol. 2017;255:2317–2324. doi: 10.1007/s00417-017-3793-8. 37. Cheung Cmg, Yanagi Y, Mohla A, Lee Sy, Mathur R, Chan Cm, Et Al. Characterization And Differentiation Of Polypoidal Choroidal Vasculopathy Using Swept Source Optical Coherence Tomography Angiography. Retina (Philadelphia, Pa). 2017 Aug;37(8):1464–74. 38. Guduru A, Gupta A, Tyagi M, Jalali S, Chhablani J. Optical Coherence Tomography Angiography Characterisation Of Best Disease And Associated Choroidal Neovascularisation. Br J Ophthalmol. 2018;102(4):444-447. 39. Lupidi M, Coscas G, Cagini C, Coscas F. Optical Coherence Tomography Angiography Of A Choroidal Neovascularization In Adult Onset Foveomacular Vitelliform Dystrophy: Pearls And Pitfalls. Invest Ophthalmol Vis Sci. 2015;56(13):7638-7645. 40. Querques G, Zambrowski O, Corvi F, Et Al. Optical Coherence Tomography Angiography In Adultonset Foveomacular Vitelliform Dystrophy. Br J Ophthalmol. 2016;100(12):1724-1730. 41. Bonini Filho Ma, De Carlo Te, Ferrara D, Et Al. Association Of Choroidal Neovascularization And Central Serous Chorioretinopathy With Optical Coherence Tomography Angiography. Jama Ophthalmol. 2015;133(8):899-906. 42. De Carlo Te, Rosenblatt A, Goldstein M, Baumal Cr, Loewenstein A, Duker Js. Vascularization Of Irregular Retinal Pigment Epithelial Detachments In Chronic Central Serous Chorioretinopathy Evaluated With Oct Angiography. Ophthalmic Surg Lasers Imaging Retina. 2016;47(2):128-133. 43. Di, G.; Weihong, Y.; Xiao, Z.; Zhikun, Y.; Xuan, Z.; Yi, Q.; Fangtian, D. A morphological study of the foveal avascular zone in patients with diabetes mellitus using optical coherence tomography angiography. Graefe’s Arch. Clin. Exp. Ophthalmol. 2016, 254,873–879. 44. De Carlo, T.E.; Bonini Filho, M.A.; Baumal, C.R.; Reichel, E.; Rogers, A.; Witkin, A.J.; Duker, J.S.; Waheed, N.K. Evaluation of Preretinal Neovascularization in Proliferative Diabetic Retinopathy Using Optical Coherence Tomography Angiography. Ophthalmic Surg. Lasers Imaging Retin. 2016, 47, 115–119. 45. Al-Khersan, H.; Russell, J.F.; Lazzarini, T.A.; Scott, N.L.; Hinkle, J.W.; Patel, N.A.; Yannuzzi, N.A.; Fowler, B.J.; Hussain, R.M.;Barikian, A.; et al. Comparison Between Graders in Detection of Diabetic Neovascularization With Swept Source Optical Coherence Tomography Angiography and Fluorescein Angiography. Am. J. Ophthalmol. 2021, 224, 292–300. 46. Couturier A., Rey P.A., Erginay A., Lavia C., Bonnin S., Dupas B., Gaudric A., Tadayoni R. Widefield OCT-Angiography and Fluorescein Angiography Assessments of Nonperfusion in Diabetic Retinopathy and Edema Treated with Anti-Vascular Endothelial Growth Factor. Ophthalmology. 2019;126:1685–1694. doi: 10.1016/j.ophtha.2019.06.022. 47. Rispoli M, Savastano Mc, Lumbroso B. Capillary Network Anomalies In Branch Retinal Vein Occlusion On Optical Coherence Tomography Angiography. Retina (Philadelphia, Pa). 2015 Nov;35(11):2332–8. 48. Casselholmde Salles M., Kvanta A., Amren U., Epstein D. Optical Coherence Tomography Angiography in Central Retinal Vein Occlusion: Correlation Between the Foveal Avascular Zone and Visual Acuity. Investig. Ophthalmol. Vis. Sci. 2016;57:OCT242–OCT246. doi: 10.1167/iovs.15-18819. 49. Feucht N., Zapp D., Reznicek L., Lohmann C.P., Maier M., Mayer C.S. Multimodal imaging in acute retinal ischemia: Spectral domain OCT, OCT-angiography and fundus autofluorescence. Int. J. O p h t h a l m o l . 2018;11:1521–1527. doi: 10.18240/ijo.2018.09.15.50. Wintergerst Mwm Et Al (2018) Optical Coherence Tomography Angiography In Intermediate Uveitis. Am J Ophthalmol 194:35–45. 51. Somkijrungroj T Et Al (2017) Assessment Of Vascular Change Using Swept-source Optical Coherence Tomography Angiography: A New Theory Explains Central Visual Loss In Behcet’s Disease. J Ophthalmol 2017:2180723. 52. Mangeon M, Zett C, Amaral C, Novais E, Muccioli C, Andrade G, Et Al. Multimodal Evaluation Of Patients With Acute Posterior Multifocal Placoid Pigment Epitheliopathy And Serpiginous Choroiditis. Ocular Immunology And Inflammation. 2018;26(8):1212–18. 53. Pereira F, Lima Lh, De Azevedo Agb, Zett C, Farah

Tools & Techniques in OphthalmologyDOS Times - Volume 30, Number 6, March-April 2025 27 www.dosonline.orgMe, Belfort R, Jr. Swept-source Oct In Patients With Multiple Evanescent White Dot Syndrome. J Ophthalmic Inflamm Infect. 2018;8(1):16. 54. Toto L., Di Antonio L., Mastropasqua R., Mattei P.A., Carpineto P., Borrelli E., Rispoli M., Lumbroso B., Mastropasqua L. Multimodal Imaging of Macular Telangiectasia Type 2: Focus on Vascular Changes Using Optical Coherence Tomography Angiography. Investig. Ophthalmol. Vis. Sci. 2016;57:OCT268– OCT276. doi: 10.1167/iovs.15-18872. 55. Chidambara L., Gadde S.G., Yadav N.K., Jayadev C., Bhanushali D., Appaji A.M., Akkali M., Khurana A., Shetty R. Characteristics and quantification of vascular changes in macular telangiectasia type 2 on optical coherence tomography angiography. Br. J. Ophthalmol. 2016;100:1482–1488. doi: 10.1136/bjophthalmol2015-307941. 56. Ayachit A.G., Reddy L.U., Joshi S., Ayachit G.S. Epiretinal Neovascularization: A Novel OCT Angiography Finding in Macular Telangiectasia Type 2. Ophthalmol. Retin. 2019;3:516–522. doi: 10.1016/j.oret.2019.01.022. 57. Batioglu F., Yanik O., Demirel S., Ozmert E. Multimodal Imaging Characteristics and Functional Test Findings in a Case of Acute Macular Neuroretinopathy Accompanied by Behcet Disease. Ocul. Immunol. Inflamm. 2020;29:1424–1430. doi: 10.1080/09273948.2020.1751857. 58. Han I.C., Tadarati M., Pacheco K.D., Scott A.W. Evaluation of Macular Vascular Abnormalities Identified by Optical Coherence Tomography Angiography in Sickle Cell Disease. Am. J. Ophthalmol. 2017;177:90–99. doi: 10.1016/j.ajo.2017.02.007. 59. Wang X-n, Zhao Q, Li D-j, Et Al. Quantitative Evaluation Of Primary Retinitis Pigmentosa Patients Using Colour Doppler Flow Imaging And Optical Coherence Tomography Angiography. Acta Ophthalmol (Copenh). 2019;97(7):E993-e997. 60. Mastropasqua R, Senatore A, Di Antonio L, Et Al. Correlation Between Choriocapillaris Density And Retinal Sensitivity In Stargardt Disease. J Clin Med. 2019;8(9). 61. Murro V, Mucciolo Dp, Giorgio D, Et Al. Optical Coherence Tomography Angiography (Oct-a) In Young Choroideremia (Chm) Patients. Ophthalmic Genet. 2019;40(3):201-206. 62. Stanga Pe, Papayannis A, Tsamis E, Et Al. Sweptsource Optical Coherence Tomography Angiography Of Paediatric Macular Diseases. In: Bandello F, Souied Eh, Querques G, Eds. Developments In Ophthalmology. Vol 56. S. Karger Ag; 2016:166173. 63. Rao HL, Pradhan ZS, Suh MH, Moghimi S, Mansouri K, Weinreb RN. Optical Coherence Tomography Angiography in Glaucoma. Journal of Glaucoma. 2020 Feb 12;29(4):312–21. 64. Yarmohammadi A, Zangwill LM, Diniz-Filho A, Suh MH, Manalastas PI, Fatehee N, et al. Optical Coherence Tomography Angiography Vessel Density in Healthy, Glaucoma Suspect, and Glaucoma Eyes. Investigative Opthalmology & Visual Science. 2016 Jul 13;57(9):OCT451. 65. Suh MH, Jung DH, Weinreb RN, Zangwill LM. Optic Disc Microvasculature Dropout in Glaucoma Detected by Swept-Source Optical Coherence Tomography Angiography. American Journal of Ophthalmology. 2022 Apr;236:261–70. 66. In JH, Lee SY, Cho SH, Hong YJ. Peripapillary Vessel Density Reversal after Trabeculectomy in Glaucoma. Journal of Ophthalmology. 2018 Jun 26;2018:1–7. 67. Tan Acs, Tan Gs, Denniston Ak, Keane Pa, Ang M, Milea D, Et Al. An Overview Of The Clinical Applications Of Optical Coherence Tomography Angiography. Eye. 2018 Feb;32(2):262–86. 68. Sharma S, Ang M, Najjar Rp, Sng C, Cheung Cy, Rukmini Av, Et Al. Optical Coherence Tomography Angiography In Acute Non-arteritic Anterior Ischaemic Optic Neuropathy. Br J Ophthalmol. 2017;101(8):1045–51. 69. Pichi, F., Roberts, P. & Neri, P. The broad spectrum of application of optical coherence tomography angiography to the anterior segment of the eye in inflammatory conditions: a review of the literature. J Ophthal Inflamm Infect 9, 18 (2019). https://doi.org/10.1186/s12348-019-0184-9. 70. Alam, M, Thapa, D, Lim, Ji, Cao, D, Yao, X.computeraided Classification Of Sickle Cell Retinopathy Using Quantitative Features In Optical Coherence Tomography Angiography. Biomed Opt Express2017; 8:4206–16. 71. Alam, M, Thapa, D, Lim, Ji, Cao, D, Yao, X.quantitative Characteristics Of Sickle Cell Retinopathy In Optical Coherence Tomography Angiography. Biomed Opt Express2017; 8:1741–53 72. Ye, H, Zheng, C, Lan, X, Zhao, L, Qiao, T, Li, X, Zhang, Y.evaluation Of Retinal Vasculature Before And After Treatment Of Children With Obstructive Sleep

Tools & Techniques in OphthalmologyDOS Times - Volume 30, Number 6, March-April 2025 28 www.dosonline.orgApneahypopnea Syndrome By Optical Coherence Tomography Angiography. Graefes Arch Clin Exp Ophthalmol2019; 257:543–48. 73. Zahid, S, Dolz-marco, R, Freund, Kb, Balaratnasingam, C, Dansingani, K, Gilani, F, Mehta, N, Young, E, Klifto, Mr, Chae, B, Yannuzzi, La, Young, Ja.fractal Dimensional Analysis of Optical Coherence Tomography Angiography In Eyes With Diabetic Retinopathy. Invest Ophthalmol Vis Sci2016; 57:4940–47. 74. Le, D, Alam, M, Miao, Ba, Lim, Ji, Yao, X.fully Automated Geometric Feature Analysis In Optical Coherence Tomography Angiography For Objective Classification Of Diabetic Retinopathy. Biomed Opt Express2019; 10:2493–503. 75. Son, T, Alam, M, Kim, T-h, Liu, C, Toslak, D, Yao, X.near Infrared Oximetryguided Artery–vein Classification In Optical Coherence Tomography Angiography. Exp Biol Med2019; 244:813–818. 76. Kadomoto S, Uji A, Muraoka Y, Akagi T, Miyata M, Tsujikawa A. A Novel Strategy For Quantification Of Panoramic En Face Optical Coherence Tomography Angiography Scan Field. Graefes Arch Clin Exp Ophthalmol. 2019;257(6):1199-1206. 77. Freund Kb, Gattoussi S, Leong Bcs. Dense B-scan Optical Coherence Tomography Angiography. Am J Ophthalmol. 2018;190:78-88. 78. Guo M, Zhao M, Cheong Amy, Dai H, Lam Akc, Zhou Y. Automatic Quantification Of Superficial Foveal Avascular Zone In Optical Coherence Tomography Angiography Implemented With Deep Learning. Vis Comput Ind Biomed Art. 2019;2(1):21. 79. Kadomoto S, Uji A, Muraoka Y, Akagi T, Tsujikawa A. Enhanced Visualization Of Retinal Microvasculature In Optical Coherence Tomography Angiography Imaging Via Deep Learning. J Clin Med. 2020;9(5). 80. Sawai Y, Miyata M, Uji A, Et Al. Usefulness Of Denoising Process To Depict Myopic Choroidal Neovascularisation Using A Single Optical Coherence Tomography Angiography Image. Sci Rep. 2020;10(1):6172. 81. Lee Cs, Tyring Aj, Wu Y, Et Al. Generating Retinal Flow Maps From Structural Optical Coherence Tomography With Artificial Intelligence. Sci Rep. 2019;9(1):5694.Sonal Praveen Paliwal MBBS, DNB, FVRS Consultant Vitreoretina ServicesSewa Sadan Eye Hospital, BhopalCorresponding Author:

Drugs in OphthalmologyDOS Times - Volume 30, Number 6, March-April 2025 29 www.dosonline.orgFDA Approved Ophthalmic Drugs in 2023Riya Kedia MBBS | Smita Harne MBBS , DNB Department of Ophthalmology, B.J. Government Medical College and Hospital, PuneIn ophthalmology, 2023 proved as a big year with 12 approvals by FDA. There are thousands of drugs in market but there are always more drugs needed to be approved, a key goal is the recognition of new molecular entities that may be of value in the treatment of diseases that qualify as presenting unmet medical needs. Some drugs are approved with different drug delivery method reducing overdosing, adverse effects and exposure to drug and preservatives improving the effectiveness of the drug.This article describes recently FDA approved drugs in ophthalmology (in the year 2023). The year started off with breakthrough approval of first and only drug for Geographic atrophy secondary to age related macular degeneration Apellis Pharmaceuticals’ Syfovre (pegcetacoplan) which is C3 inhibitor and 6 months later second drug for geographical atrophy was approved Iveric Bio received FDA approval for Izervay (avacincaptad pegol intravitreal solution) which is a complement protein C5 inhibitor, both the drugs slows the progression of GA and does not cure it.[1]Regeneron Pharmaceuticals revealed that the FDA approved the use of EYLEA® (aflibercept) Injection to treat preterm infants with retinopathy of prematurity (ROP). Following this first pediatric approval, EYLEA is now indicated to treat five retinal conditions caused by ocular angiogenesis.[2]Regeneron secured FDA approval for Eylea HD (aflibercept 8mg), prolonging dosing intervals for patients dealing with retinal diseases such as wet age-related macular degeneration (AMD), diabetic macular edema (DME), and diabetic retinopathy (DR).[3] It is a higherdose, longer-acting injectable form of aflibercept that only needs to be given once every 2 to 4 months after an initial dosing period. This allows patients to receive less frequent injections for similar visual gains, and anatomic improvements, without an increased risk of side effects.Allergan announced that the FDA approved the use of Vuity (pilocarpine HCl ophthalmic solution) 1.25% twice a day for adults experiencing presbyopia, earlier VUITY was approved for once daily dosing in October 2021.[4] Similarly, lower concentration, near neutral ph and preservative-free Orasis Pharmaceuticals, Qlosi (pilocarpine hydrochloride ophthalmic solution) 0.4% has also been approved for presbyopia.[5] Given Qlosi’s lower concentration, it will be curious to see whether it results in fewer adverse effects than Vuity. Another potential plus: the formulation is preservative-free.[6]With three new therapies recently approved by the FDA, we now have more targeted options for patients than ever.FDA has approved for Novaliq’s VEVYE™ (cyclosporine ophthalmic solution) 0.1% in treating signs and symptoms of dry eye disease. VEVYE™, previously known as CyclASol®. It is an anti-inflammatory drug for dry eye disease. It contains the same active ingredient - an anti-inflammatory called cyclosporine - as Restasis (cyclosporine ophthalmic emulsion) 0.05% and CEQUA (cyclosporine - ophthalmic solution) 0.09%. But VEVYE contains a slightly higher concentration of the drug and uses a different delivery method.[7]Second drug, Miebo a collaboration between Bausch & Lomb and Novaliq, received FDA approval for Miebo (perfluorohexyloctane ophthalmic solution; formerly NOV03) for dry eye disease due to meibomian gland dysfunction with objective of reducing tear evaporation on ocular surface.[8] As the first and currently the only prescription treatment approved directly addressing the pathophysiology of excessive tear evaporation, perfluorohexyloctane ophthalmic solution is a valuable emerging option for the management of DED.[9]Tarsus Pharmaceuticals obtained FDA approval for XDEMVY™ (lotilaner ophthalmic solution) 0.25%, the first and the only treatment against Demodex mites causing Demodex blepharitis to effectively and safely target, paralyze, and kill Demodex mites.[10]Eyenovia got FDA approval of MydCombi, the first ophthalmic spray designed for mydriasis. Mydcombi is a micro-dose ophthalmic spray containing tropicamide 1% and phenylephrine 2.5%, using Optejet dispenser which

Drugs in OphthalmologyDOS Times - Volume 30, Number 6, March-April 2025 30 www.dosonline.orgadministers an easier, more accurate and appropriate dose directly where it is needed in the eye.[11] Ophthalmic solution administered with the Optejet is less than 20% of that delivered using conventional eyedroppers, thus reducing overdosing and exposure to drug and preservatives.[12]Ocuphire Pharma and Viatris jointly announced the FDA approval for Ryzumvi (phentolamine ophthalmic solution) 0.75% a nonselective alpha-I and alpha-2 adrenergic antagonist has now been approved for the treatment of pharmacologically induced mydriasis mydriasis caused by adrenergic agonists (such as phenylephrine) or parasympatholytic agents (like tropicamide).[13]FDA has approved for Genentech’s Vabysmo (faricimabsvoa) 6mg prefilled syring and macular edema following retinal vein occlusion (RVO), first and only bispecific antibody acts by inhibiting VEGF-A and Angiopoietin2.[14] It was already approved for the treatment of wet age-related macular degeneration (nAMD) and diabetic macular edema (DME).The FDA approvals of these top 12 ophthalmic drugs in 2023 signify a transformative era in eyecare, offering diverse and advanced treatment options for various eye conditions.References1. Kang C. Avacincaptad Pegol: First Approval. Drugs [Internet] 2023 [cited 2024 Jul 25];83(15):1447–53. Available from: https://doi.org/10.1007/s40265-023-01948-82. EYLEA® (aflibercept) Injection Approved as the First Pharmacologic Treatment for Preterm Infants with Retinopathy of Prematurity (ROP) by the FDA | Regeneron Pharmaceuticals Inc. [Internet]. [cited 2024 Jul 26];Available from: https://investor.regeneron.com/news-releases/news-release-details/eylearaflibercept-injection-approved-first-pharmacologic/3. Eylea & Eylea HD Eye Injections for Retinal Disorders [Internet]. Drugs.com [cited 2024 Jul 26];Available from: https://www.drugs.com/eylea.html4. Meghpara BB, Lee JK, Rapuano CJ, Mian SI, Ho AC. Pilocarpine 1.25% and the changing landscape of presbyopia treatment. Curr Opin Ophthalmol 2022;33(4):269–74. 5. Orasis Pharmaceuticals Announces FDA Approval of QLOSITM (pilocarpine hydrochloride ophthalmic solution) 0.4% for the Treatment of Presbyopia – Orasis [Internet]. [cited 2024 Jul 26];Available from: https://www.orasis-pharma.com/orasispharmaceuticals-announces-fda-approval-of-qlosipilocarpine-hydrochloride-ophthalmic-solution-0-4-for-the-treatment-of-presbyopia/6. Topical Pilocarpine for Presbyopia [Internet]. American Academy of Ophthalmology2022 [cited 2024 Jul 26];Available from: https://www.aao.org/eyenet/article/topical-pilocarpine-for-presbyopia7. Why Is Dry Eye So Difficult to Treat? [Internet]. American Academy of Ophthalmology2024 [cited 2024 Jul 26];Available from: https://www.aao.org/eye-health/tips-prevention/fix-dry-eye-treatmenteyedrops8. Tauber J, Berdy GJ, Wirta DL, Krösser S, Vittitow JL, Alpern LM, et al. NOV03 for Dry Eye Disease Associated with Meibomian Gland Dysfunction. Ophthalmology [Internet] 2023 [cited 2024 Jul 25];130(5):516–24. Available from: https://linkinghub.elsevier.com/retrieve/pii/S01616420220101689. Bausch + Lomb and Novaliq Announce FDA Approval of MIEBOTM (Perfluorohexyloctane Ophthalmic Solution) for the Treatment of the Signs and Symptoms of Dry Eye Disease [Internet]. Bausch + Lomb Corporation2023 [cited 2024 Jul 26];Available from: https://ir.bausch.com/press-releases/bausch-lomb-and-novaliq-announce-fda-approvalmiebotm-perfluorohexyloctane10. XdemvyTM (Lotilaner Ophthalmic Solution) 0.25% Topical Solution for the Treatment of Demodex Blepharitis - PubMed [Internet]. [cited 2024 Jul 26];Available from: https://pubmed.ncbi.nlm.nih.gov/38494618/11. MydCombiTM - Eyenovia [Internet]. 2024 [cited 2024 Jul 26];Available from: https://eyenovia.com/products/mydcombi/12. Eyenovia announces FDA approval of MydCombi, first ophthalmic spray for mydriasis [Internet]. [cited 2024 Jul 26];Available from: https://www.ophthalmologytimes.com/view/eyenoviaannounces-fda-approval-of-mydcombi-firstophthalmic-spray-for-mydriasis13. Azhar A, Riaz R, Khan A, Kumari V, Habib A, Akilimali A. Ryzumvi: pioneering advances in countering drug-induced mydriasis. Ann Med Surg (Lond) 2024;86(6):3530–4. 14. Vabysmo Approved for Macular Edema Following Retinal Vein Occlusion [Internet]. [cited 2024 Jul 26];Available from: https://www.empr.com/home/

Drugs in OphthalmologyDOS Times - Volume 30, Number 6, March-April 2025 31 www.dosonline.orgnews/vabysmo-approved-for-macular-edemafollowing-retinal-vein-occlusion/Riya Kedia MBBS PG ResidentNursing Girls Hostel, Sassoon Hospital, 411001Corresponding Author:

Ophthalmic ImagingDOS Times - Volume 30, Number 6, March-April 2025 32 www.dosonline.orgUnusual Occurrence of Granular Dystrophy Even in Nonrelated Spouses of the Affected Family MembersAlok Sati MS, DNB, FLVPEI | Mrinalini Singh MS| Sarvadarshi Shukla MS | Sanjay Kumar Mishra MSDepartment of Ophthalmology, Army Hospital (Research & Referral), New DelhiA 07-year-old girl reported with features suggestive of bilateral granular dystrophy. On screening of family members, 9 out of 10 members (except her grandmother) had features of granular dystrophy. The most striking feature in this family tree is the occurrence of corneal granular deposits in spouses of the two sons. With no history of consanguinity, it can be attributed to either an incidental finding or common environmental exposure to family members, thereby making this report an interesting one. Granular dystrophy, being inherited (mutation on chromosome 5q31),[1] is a proven fact, however, the role of environmental influence needs to be investigated. References1. Wilson CM, Ath PJ, Parmar DN, et al. Keratoconus and granular dystrophy. BMJ Case Rep. 2014; 2014: bcr2014205584.Alok Sati MS, DNB, FLVPEI ProfessorDepartment of OphthalmologyArmy Hospital (R&R), New Delhi-01, IndiaCorresponding Author:

Subspecialty - Cornea & External Eye DiseasesDOS Times - Volume 30, Number 6, March-April 2025 33 www.dosonline.orgArborizing Dendrites: The Art of Clinical DiagnosisNishi Prasad MBBS, MS | Prashant Singh MBBS, MS | Ganesh Pillay MBBS, MD, DNB, MNAMS, FICO, MRCSDepartment of Ophthalmology, ASG Eye Hospital, BhopalCase ReportA 53-year old male presented with complaint of pain, photophobia and foreign body sensation in his left eye. The patient was diabetic with poor glycemic control. The best- corrected visual acuity in the left eye was 6/12. On slit-lamp examination, the left eye had multiple arborizing dendritic epithelial keratitis with terminal bulbs (Figure-1). Rest anterior segment and fundus examination was unremarkable. Patient was treated with oral acyclovir for 10 days, topical ganciclovir 0.15%, topical ofloxacin and copious lubricants for 2 weeks. DiscussionHSV epithelial keratitis presents with classical dendritic pattern epithelial keratitis with terminal bulbs. Recurrent activations within the sensory ganglion can result in cornea scarring, necrosis, and decreased corneal sensation which can be vision threatening condition. The diagnosis of HSV is made clinically. Primary HSV epithelial keratitis usually resolves spontaneously, however treatment with antiviral medication shortens the course of the disease and hence reduce the long-term complications of HSV. The mainstay of therapy is antiviral treatment either in the form of oral administration of acyclovir or famciclovir for 10 to 14 days and topical antiviral medications. Topical ganciclovir 0.15% can be utilized. It is usually dosed five times a day until the corneal ulcer heals, and then three times a day for another week. Topical antibiotics, cycloplegic eye drops and lubricants should be added. Topical steroids are contraindicated in the presence of active epithelial lesion. The patient should be closely monitored and if no response to treatment occurs after one week of therapy, the possibility of resistance to antiviral therapy, antiviral toxicity, neurotrophic disease, poor compliance with medication or an alternative diagnosis should be considered. If there is visually significant stromal scarring, a penetrating keratoplasty may be performed once the disease is stable. Depending on the location and size of the scar, a lamellar keratoplasty may also be used to clear the visual axis. Corneal complications ranges from epitheliopathy to neurotrophic corneas. Neurotrophic corneas are corneas Abstract: Herpes simplex virus (HSV) is a very common viral infection that is often asymptomatic but can result in significant eye disease. HSV can cause corneal epithelial, stromal and endothelial manifestations. HSV keratitis is a leading cause of corneal blindness worldwide. Here is a case of a middle aged diabetic male who presented with a classical sign of HSV keratitis who when treated with antiviral therapy was resolved completely.Keywords: Herpes simplex virus, dendritic ulcer, epithelial keratitisFigure 1: The bed of the ulcer stained with fluorescein, shows multiple small dendritic epithelial keratitis with terminal bulbs.

Subspecialty - Cornea & External Eye DiseasesDOS Times - Volume 30, Number 6, March-April 2025 34 www.dosonline.orgwith decreased sensation due to corneal nerve changes after infection, can cause a wide array of issues ranging from severe dry eyes to corneal perforation from a nonhealing neurotrophic ulcer. Prognosis of HSV epithelial keratitis is usually good, however varies depending on the severity and recurrences of the disease.Depending on the location and size of the scar, a lamellar keratoplasty may also be used to clear the visual axis. Neurotrophic corneas are corneas with decreased sensation due to corneal nerve changes after infection, can cause a wide array of issues ranging from severe dry eyes to corneal perforation from a non-healing neurotrophic ulcer. It is usually dosed five times a day until the corneal ulcer heals, and then three times a day for another week. Corneal complication ranges from epitheliopathy to neurotrophic corneas.Nishi Prasad MBBS, MS Fellowship Phaco-Refractive SurgeryASG Eye Hospital, BhopalCorresponding Author:

Subspecialty - Cornea & External Eye DiseasesDOS Times - Volume 30, Number 6, March-April 2025 35 www.dosonline.orgFirecracker-Associated Ocular InjuriesSidrah Imran MBBS, MS | Arushi Saini MBBS, MS | Om Prakash MBBS, MS | Prabhash Shekhar Mishra MBBS, MSDepartment of Ophthalmology, Lady Hardinge Medical College, DelhiIntroductionFirecrackers have a fascinating history that dates back over a thousand years to ancient China. Firecrackers became deeply rooted in Indian culture, especially associated with Diwali, the Hindu festival of lights. Diwali celebrates the victory of light over darkness, and fireworks were seen as a symbolic representation of dispelling evil and bringing prosperity. The tradition of bursting firecrackers during Diwali grew significantly over time and became a nationwide custom.Firecracker injuries typically include burns, eye injuries, hand and finger trauma, hearing damage, and respiratory problems from inhaling smoke and toxic chemicals. The hands, face, and eyes are particularly vulnerable. Severe cases can lead to permanent disability or disfigurement. Firework injuries are responsible for about 2% of all reported ocular injuries[1], these are a significant cause of vision impairment worldwide, particularly in countries where fireworks are widely used during cultural festivals and celebrations. The visual consequences of these injuries can range from minor irritations to permanent blindness. This review summarizes the current literature on the types, causes, mechanisms, and management of ocular injuries associated with firecrackers.Epidemiology and DemographicsStudies have shown that firecracker-related ocular injuries are common in certain parts of Asia, particularly in India and China, where fireworks play an integral role in cultural celebrations like Diwali and the Lunar New Year. Research also indicates that young males and children are disproportionately affected due to their higher likelihood of handling fireworks unsupervised. In a large epidemiological study in India[2], found that males below the age of 15 accounted for almost 60% of firecracker-related ocular injuries.Risk FactorsSeveral risk factors have been identified in literature. Risk factors for ocular trauma include lack of protective eyewear, lack of parental supervision, close distance to fireworks, use of illegal or modified fireworks, and improper handling are significant contributors.[3] Festive periods often see spikes in firecracker-related injuries, with crowded and poorly monitored areas posing additional risks. Notably, studies highlight that injuries frequently occur among bystanders who are not actively handling the firecrackers but are in close proximity.[4]Mechanisms of InjuryThe mechanism of injury varies depending on the type and handling of the firecracker. Injuries frequently occur from either blast trauma or contact with chemical agents present in the explosive materials. Blast trauma can induce high-velocity particles to penetrate the eye, causing both mechanical and thermal damage. Additionally, the caustic materials in fireworks can result in alkaline or acidic burns.[5]Types of InjuriesThe spectrum of ocular injuries due to fireworks ranges from minor, self-limiting conditions to severe, visionthreatening injuries. Common types of injuries include[6]:Superficial Eye Injuries: These include corneal abrasions, corneal burns and conjunctival lacerations, which are often caused by direct contact with debris or sparks. These injuries, while generally mild, can lead to secondary infections if untreated.Closed Globe Injuries: These involve injuries where the eye wall remains intact but may suffer internal damage. Hyphaema, traumatic cataracts, and vitreous haemorrhage are common manifestations which can occur due to the shock-wave from an explosion. Closed globe injuries are often associated with blunt trauma from misfired fireworks.Open Globe Injuries: This category includes rupture of the eyeball, which are severe and carry a poor prognosis for vision recovery. Open globe injuries often require

Subspecialty - Cornea & External Eye DiseasesDOS Times - Volume 30, Number 6, March-April 2025 36 www.dosonline.orgmultiple surgeries and may lead to irreversible vision loss, and carry a high risk of complications, including endophthalmitis (intraocular infection) and retinal detachment.Thermal Burns: Firecrackers release high temperatures, which can lead to thermal burns on the eyelids and conjunctiva. These burns are often associated with pain, swelling, and scarring.Chemical Injuries: Chemicals in fireworks, such as sulphur, magnesium, and nitrates, may cause severe chemical burns when they come into direct contact with ocular tissues. Limbal ischemia resulting from chemical injuries can lead to non-healing corneal epithelial defects. These injuries require immediate intervention to prevent long-term damage to the ocular surface.Clinical Presentation and EvaluationPatients typically complain of foreign body sensation, ocular pain, decreased vision, redness, tearing, and photophobia. Clinical examination should include a detained history with complete ocular examination. In patients with globe injuries, calculation of the Ocular Trauma Score with prognostication based on presentation may be useful. Likewise in patients with Open Globe injuries, the Retinal Detachment-Open Globe injury index is also useful for prediction of posterior segment complications. BETT classification can also be used for prognostication. A CT scan (Thin cut (1-mm sections) axial, coronal, and parasagittal views) of the face and orbits should be strongly considered in the case of projectile injuries to exclude intraocular or infraorbital foreign bodies.[5] Chemical injuries of the ocular surface should be graded according to the Dua’s classification which leads to better management and prognostication based on the degree of severity of injury. Both, limbal and conjunctival involvement should be taken into account.Management and PreventionThe management of firecracker-induced ocular injuries generally involves a multi-step approach, focusing on immediate care, medical management, and, in some cases, surgical intervention. Immediate treatment often involves copious irrigation for chemical injuries, debridement for superficial injuries, and protective eye shields for more severe trauma. Systemic antibiotics should be administered in addition to tetanus prophylaxis. Surgical intervention may be necessary for open globe injuries, traumatic cataracts, and retinal repair. Globe exploration should be performed in suspected globe rupture or penetrating trauma, with possible early vitrectomy if intraocular foreign bodies or retinal detachment is suspected.[8] Ocular surface grafting using amniotic membrane is helpful in restoring the ocular surface. Prevention strategies recommended by the World Health Organization include public awareness campaigns, stricter regulation of firecracker sales, and protective eyewear. Countries using restrictive fireworks legislation showed 87% less ocular trauma (P < 0.005).[9] There was a drastic decrease in the number of firecracker injuries during Diwali in the COVID-19 period (2020) as there was a nationwide ban on sale of firecrackers, thus laying the emphasis on strict legislative policies. Media, in the form of television, mobile, or newspaper, can also be used for public education.[10] The spectrum of ocular trauma due to firecracker use in Diwali is protean due to the banning of firecrackers and different legislations in place each year. It is essential to be able to segregate and triage the different clinical presentations of the same spectrum for efficient management, which has to be done on a case-to-case customized basis, entailing a multidisciplinary approach for optimum rehabilitation in certain cases.Clinical Outcomes and PrognosisThe prognosis for firecracker-related ocular injuries depends largely on the type and severity of the injury. Closed globe injuries generally have a favourable prognosis when promptly treated, whereas open globe injuries have poorer outcomes leading to vision loss. Visual acuity is often diminished in patients with penetrating injuries, and Figure 1: Limbal and scleral perforation with iris prolapse with lid burns and loss of eyelashes.

Subspecialty - Cornea & External Eye DiseasesDOS Times - Volume 30, Number 6, March-April 2025 37 www.dosonline.orgcomplications such as endophthalmitis and retinal detachment may arise in severe cases. Long-term outcomes may include chronic pain, visual field loss, corneal scarring with irregular astigmatism, cataract or angle-recession glaucoma, exposure keratopathy, phthisis bulbi, and blind disfigured eyes and sometimes enucleation of the eye in severe cases. Visual acuity may range from 20/20 to no light perception, and in a study looking at 18 globe ruptures from firework injuries, 10 (59%) of eyes were no light perception at last follow-up.[11]ConclusionFirecracker-associated ocular injuries continue to be a preventable yet significant cause of visual impairment. Research underscores the need for public awareness, proper regulation, and preventive measures to mitigate these injuries. Future research may benefit from more extensive population studies and improved data collection, which could provide a more comprehensive understanding of the causes and best practices for managing these injuries.References1. Arya SK, Malhotra S, Dhir SP, Sood S. Ocular fireworks injuries. Clinical features and visual outcome. Indian J Ophthalmol. 2001 Sep;49(3):189–90. 2. Menon GR, Singh L, Sharma P, Yadav P, Sharma S, Kalaskar S, et al. National Burden Estimates of healthy life lost in India, 2017: an analysis using direct mortality data and indirect disability data. Lancet Glob Health. 2019 Dec;7(12):e1675–84. 3. Academy Resource Newsroom and Media / News Releases View Topics Reports of Eye Injuries From Fireworks Have Doubled. 2019. 4. Parija S, Chakraborty K, Ravikumar SR. Firework related ocular injuries in Eastern India - A clinicoepidemiological analysis. Indian J Ophthalmol. 2021 Dec;69(12):3538–44. 5. Gupta D, Bhatia C, Vignesh S, Sarabahi S. Firecracker Powder: A Unique Source of Burn Injuries. Eplasty. 2023;23:e61. 6. Kurien NA, Peter J, Jacob P. Spectrum of Ocular Injuries and Visual Outcome Following Firework Injury to the Eye. J Emerg Trauma Shock. 2020;13(1):39–44. 7. Wisse RPL, Bijlsma WR, Stilma JS. Ocular firework trauma: A systematic review on incidence, severity, outcome and prevention. Vol. 94, British Journal of Ophthalmology. 2010. p. 1586–91. 8. Wisse RPL, Bijlsma WR, Stilma JS. Ocular firework trauma: A systematic review on incidence, severity, outcome and prevention. Vol. 94, British Journal of Ophthalmology. 2010. p. 1586–91. 9. See LC, Lo SK. Epidemiology of Fireworks Injuries: The National Electronic Injury Surveillance System, 1980-1989. Ann Emerg Med. 1994 Jul;24(1):46–50. 10. Mat Johar F, Halim AS, Wan Sulaiman WA, Muhamad H. Prevention of firecracker injuries via the digital platform: A Malaysian experience. Burns. 2021 Nov 1;47(7):1683–7. 11. Chang IT, Prendes MA, Tarbet KJ, Amadi AJ, Chang SH, Shaftel SS. Ocular injuries from fireworks: the 11-year experience of a US level I trauma center. Eye. 2016 Oct 10;30(10):1324–30. Dr. Sidrah Imran MBBS, MS ResidentLady Hardinge Medical College,Delhi-110001Corresponding Author:Figure 2: Conjunctival congestion with corneal abrasion.

Subspecialty - Cornea & External Eye DiseasesDOS Times - Volume 30, Number 6, March-April 2025 38 www.dosonline.orgCase Report - Intrastromal Voriconazole for Post Phacoemulsification Incision Site Fungal KeratitisGunjan Verma Shah MS, DNBGunjan Eye Hospital, 306, Copper Leaf, Bhuyangdev Char Rasta, Ahmedabad, GujaratAbstract: 60-year-old diabetic female, underwent uneventful right eye phacoemulsification surgery with intraocular lens implantation. She had good post op recovery of best corrected visual acuity, 6/6. After 6 weeks, she presented with complaints of foreign body sensation and watering in operated eye. She had stromal keratitis with endothelial exudates, intrastromal voriconazole (50 microgram/0.1ml) was given at the junction of clear cornea and infiltrates, using a 30G needle in five quadrants to form a barrage around the circumference of the lesion. Post operatively, patient continued to receive topical antifungal therapy. On follow up examinations, reduction in size and density of exudates were noted. Intrastromal voriconazole maybe considered as an effective mode of therapy in deep fungal keratitis.[1,3]Keywords: fungal keratitis, voriconazole, post phacoemulsification keratitisCase ReportA 60-year-old diabetic female patient had undergone uneventful right eye phacoemulsification surgery with intraocular Lens implantation. She had good post op recovery attaining BCVA of 6/6. After 6 weeks post operatively, she presented with complaints of foreign body sensation, watering and photophobia to the operating surgeon in the same eye. Frequency of antibiotic steroids were increased (moxifloxacin and prednisolone acetate eyedrops). After one-week corneal stromal exudates were noted and corneal surgeon reference was advised for further management.On presentation, visual acuity was 6/12. Patient had lid edema and blepharospasm. On Slit Lamp Examination, feathery satellite stromal lesion noted at superior 12 o’ clock position. Endothelial exudates were present with surrounding corneal stromal edema however fluorescein stain was negative.(Figure-1) Left eye amblyopic with Pseudophakia. BCVA OF 6/75.Intraocular pressure right eye 18mmHg, Left eye 16mmHg. With Non-Contact Tonometer.Patient was not sure about trauma.On systemic evaluation she had deranged blood sugar level. Random Blood Sugar levels of 320mg/dl was noted. Urgent physician reference was done for glycemic control.Patient was started on Voriconazole eyedrops 1% every hour, Natamycin eyedrops 5% every hour, atropine eyedrops 1% three times per day. Steroid eyedrops were discontinued.Figure 1: Day 1-tunnel exudates, edema and endothelial exudates.

Subspecialty - Cornea & External Eye DiseasesDOS Times - Volume 30, Number 6, March-April 2025 39 www.dosonline.orgShe seemed to be doing well for 3 days after that increased pain and exudates marginally increased (Figure-3) with drop in visual acuity 6/60. Possibility of rebound inflammation after stopping steroid eyedrops cannot be ruled out.Patient was taken for Endothelial scrapping and Anterior chamber tap with intrastromal voriconazole (Figure-4) After physician fitness clearance. Detailed written consent was taken. Need for further surgical intervention was explained.Microbiology examination of Endothelial scrapping was KOH (potassium hydroxide) wet mount Positive and fungal growth was noted on Sabouraud Dextrose agar. Intrastromal voriconazole (50 microgram/0.1ml) was given at the junction of clear cornea and infiltrates, using a 30G needle in five quadrants to form a barrage around the circumference of the lesion.[3] Procedure was done in Operation theatre under aseptic precautions under topical anesthesia.Post operatively, patient was continued on Natamycin eyedrops 5% every one hourly, Fortified Voriconazole eyedrops 1% every two hourly and atropine eyedrops three times per day. Topical voriconazole seems to be a useful adjunct to natamycin in fungal keratitis not responding to topical natamycin.[2]After the intervention, faster reduction in size and density of corneal infiltrate and Endothelial exudates was documented and complete recovery within 3 months was observed (Figure-4-9). In the initial few months, superficial corneal vascularization was noted, which aided in healing. On subsequent follow up vascularization reduced. Best Corrected Visual Acuity on last follow up (18 months) was 6/12. (Figure-10).Figure 2: Day 3-Exudates retracting.Figure 3: Day 5-deep stromal cellularity increased marginally.Figure 4: Day 10-exudates increased, deep stromal edema streak hypopyon.Figure 5: Post op day 1 image, inflammatory membrane, streak hypopyon.Thorough counselling done. Further need for surgical intervention in the form of Anterior chamber tap and endothelial scrapping and intrastromal voriconazole was explained to the patient, after control of blood sugar levels.

Subspecialty - Cornea & External Eye DiseasesDOS Times - Volume 30, Number 6, March-April 2025 40 www.dosonline.orgFigure 8: 3 Months clinical image.Figure 9: 6 Months clinical image.Figure 10: 18 Months clinical image, showing complete recovery with nebular corneal opacity.DiscussionFungal Tunnel keratitis is medical emergency which needs prompt management. It poses a great challenge in diagnosis and management. Delay in diagnosis or neglecting the symptoms may lead to fulminant infection with vision threatening complications such as Corneal perforation, Endophthalmitis causing vision loss.[7] It may present with a variety of clinical presentations. Indiscriminate use of antimicrobials leading to the emergence of resistant or refractory microorganisms has further worsened the prognosis.[6]Immunocompromised patients are at great risk, and post operative steroid usage may mask the symptoms and delay in diagnosis. A high index of suspicion is required for timely management.Deep mycotic keratitis is not amenable to topical antimicrobial therapy because none of the present-day antiFigure 6: One month, healing corneal lesion, decreased cellularity.Figure 7: 2 Months clinical image.

Subspecialty - Cornea & External Eye DiseasesDOS Times - Volume 30, Number 6, March-April 2025 41 www.dosonline.orgfungal agents can optimally penetrate the deeper layers of cornea, which leads to delayed healing and further spread of infection. Targeted delivery of voriconazole in the form of intrastromal injection by forming a barrage around the ulcer acts as a depot and aids in healing.[3]Meticulous clinical examination and detailed microbiology work up is necessary for optimal results.Patient education about importance of immediate consultation in case they experience any symptoms like redness, itching, drop in vision or photophobia in post operative period. Timely diagnosis and proper intervention are crucial.References1. Evalaution of Intrastromal Injection of Voriconazole as a therapeutic Adjunctive for the management of Deep Recalcitrant Fungal Keratitis. Gaurav Prakash, Namrata Sharma, Manik Goel, Jeewan S. Titiyal, Rasik B. Vajpayee. American Journal of Ophthalmology, Volume 146 Issue 1 ,July 2008, Page 56-59.2. Comparative evaluation of topical versus intrastromal voriconazole as an adjunct to natamycin in recalcitrant fungal keratitis. Namrata Sharma 1, Jacob Chacko, Thirumurthy Velpandian, Jeewan S Titiyal, Rajesh Sinha, Gita Satpathy, Radhika Tandon, Rasik B Vajpayee.Ophthalmology 2013 APR ;120(4):677-81.3. Evaluation of intrastromal voriconazole injection in recalcitrant deep fungal keratitis: case series. Namrata Sharma 1, Prakashchand Agarwal, Rajesh Sinha, Jeewan S Titiyal, Thirumurthy Velpandian, Rasik B Vajpayee. Br J Ophthalmol 2011 Dec;95(12):1735-7. doi: 10.1136/bjo.2010.192815. Epub 2011 Mar 31.4. Management of tunnel fungal infection with Voriconazole. Vishal Jhanji, Namrata Sharma, Rashmin Mannan, Jeevan S Titiyal, Rasik B Vajpayee. J Catarct Refract Surg. 2007 May ;33(5):915-7.Gunjan Verma Shah MS, DNB Gunjan Eye Hospital, 306, Copper Leaf, Bhuyangdev Char Rasta, Ahmedabad, GujaratCorresponding Author:5. Fungal Keratitis: Clinical Features, Risk Factors, Treatment, and Outcomes. Sarah Atta, Chandrashan Perera, Regis P Kowalski, Vishal Jhanji.J Fungi (Basel). 2022 Sep 15;8(9):962. doi: 10.3390/jof8090962.6. Update on diagnosis and management of refractory corneal infections. Shweta Agarwal, Tanveer A Khan, Murugesan Vanathi, Bhaskar Srinivasan, Geetha Iyer, Radhika Tandon.Indian J Ophthalmol. 2022 May;70(5):1475-1490. doi: 10.4103/ijo.IJO_2273_21.7. Castano G., Elnahry A.G., Mada P.K. Fungal Keratitis. StatPearls; Treasure Island, FL, USA: 2022.

Subspecialty - Cornea & External Eye DiseasesDOS Times - Volume 30, Number 6, March-April 2025 42 www.dosonline.orgRole of Dyslipidaemia and Effect of Lipid Lowering Drugs on Meibomian Gland Disease - A Prospective StudyPrachi Singh[1] DOMS, DNB | Abid Shamshad[2] MS | Lokendra Tyagi[3] MS1. Assistant Professor, ASMC, Pilibhit, Uttar Pradesh2. Consultant Ophthalmologist at Dr. Abids Clinic, Jaipur, Rajasthan3. Senior Consultant, Sahai Hospital and Research Center, Jaipur, RajasthanKeywords: Dyslipidemia, meibomian gland dysfunction, meibomian gland diseaseIntroductionThe term “meibomian gland dysfunction” (MGD) was introduced by Korb and Henriquez in 1980. The terminology “meibomian gland disease” was introduced by Bron et al.[1] as a broad term to indicate any disease affecting the meibomian glands. MGD is a chronic diffuse abnormality of meibomian glands commonly characterized by terminal duct obstruction and changes in the glandular secretion, which may result in alteration of the tear film, symptoms of dry eye, clinically apparent inflammation, and ocular surface disease.[1-2] MGD is one of the most common ophthalmic problems with a very wide prevalence rate (3.5%–77.6%),[3-5] based on geographic location. The knowledge of the aetiology of MGD is limited, and an effective treatment is lacking. A number of ophthalmic conditions, systemic diseases, and therapies have been identified as risk factors for the development of MGD which includs: aging,[6,7] androgen deficiency,[8-10] benign prostatic hyperplasia,[11] discoid lupus erythromatosis,[12] menopause,[13] Parkinson,[14] and dyslipidemia.[15]Dyslipidemia is defined as a disorder of lipid metabolism that manifests as an elevation of total cholesterol, low density lipoprotein (LDL), and triglyceride levels and a decrease in high-density lipoprotein (HDL) levels in the blood. Normal meibomian lipid melting point is 30 to 34°C and that of cholesterol is 46°C, an increased concentration of cholesterol in meibomian lipid would increase the melting point of the meibomian lipid and theoretically increase viscosity, in turn lead to plugging of the meibomian glands.[16,17] Eye care providers may be the first to detect systemic diseases such as cerebrovascular disease because of the presence of Meibomian gland dysfunction. The primary purpose of this study was to determine association between dyslipidaemia and MGD and to assess the extent of improvement in symptoms of MGD on correction of dyslipidaemia. Materials and MethodsAim: To determine association between dyslipidaemia and meibomian gland dysfunction (MGD). To identify factors (age, gender) that play role in this association. To study the outcome of MGD treatment in dyslipidemic and in normal patient.The study was done on eligible patients presented to outpatient department. Total of 90 patients were included in this study. Patients were enrolled from March 2019 till the desired sample size was attained and follow up period of 3 months was completed by October 2019 for all the patients. Inclusion criteria: All OPD patients with MGD, age >40 years, newly diagnosed Dyslipidemic patients. Exclusion criteria-Previous history of hypercholesterolemia, Inflammatory or allergic ocular surface diseases, history of ocular surgery, Lacrimal drainage system dysfunction, Chronic treatment with lipid-lowering drugs, or other systemic drugs affecting tearing, use of topical ophthalmic medications (including corticosteroids) 4 weeks before the study. Diabetes,

Subspecialty - Cornea & External Eye DiseasesDOS Times - Volume 30, Number 6, March-April 2025 43 www.dosonline.orghypertension, thyroid, Pregnancy, Primary or secondary Sjogren syndrome.A primary screening, assessment and detail clinical examination was conducted on OPD patients. Patients fulfilling the criteria mentioned above were enrolled in the study, after explaining the details of the study and obtaining a valid consent for the same. Tear film break up time (TBUT), Schirmer’s-I test (without anaesthesia), Ocular Surface Disease Index (OSDI) scoring done. The clinical diagnosis of MGD was based on descriptions of glandular obstruction and meibum quality. The evaluation for gland obstruction was obtained by firm digital pressure over the central third of the upper and lower eyelid, while observing the ease of excretion under slit lamp biomicroscope. The grade assigned for meibomian gland obstruction was based on the system offered by other authors as follows: 0 (no obstruction, meibum easily expressed), 1 (mild obstruction, meibum expressible with mild pressure), 2 (moderate obstruction, meibum expressible with moderate pressure), and 3 (complete obstruction, no glands expressible, even with hard pressure). The quality of gland secretion was observed via slit lamp biomicroscope exam and graded as follows: 0 (clear fluid), 1 (cloudy fluid), 2 (cloudy particulate fluid), 3 (toothpaste-like). Fasting blood sample was collected and sent to biochemistry for serum Lipid Profile on first visit to the hospital, followed at 3 months (90 days). All patients with deranged lipid profile were referred to physician for treatment of dyslipidaemia.Statistical Analysis: The statistical analysis was performed by STATA 11.2 (College Staiton TX USA). Shaprio wilk test was used to find the normality. Students independent sample t-test or Mann Whintey test was used and results expressed as mean and standard deviation. Chi Square test was used to find the association between the gender with groups and these expressed as frequency and percentage.ResultsResults for 90 patients (45 in each group) group A (MGD with normal lipid levels) and group B (MGD with dyslipidaemia) completed the study and all datas were obtained for 15th day, 30th day and 90th day of follow up visits. Mean of Patient’s age in group A mean 59.33 ± 9.32yrs and group B is 63.11 ± 10.21yrs. No significant difference between the age of two groups (Table-1). Group A had 38% males and 62% females shows a higher prevalence of MGD in females as compared to males. group B had 78% males and 22% females, suggests number of males outnumber females with MGD & deranged lipid profile. In group A most of the patients had grade 2 and grade 3 MGD. On follow-up visits on day 90th most of the patients were in grade 0 or grade 1 MGD at the end of study. In group B most patients were of grade 2, grade 3 and 4 MGD. On follow up visits it was observed that most of them achieved grade 0 but few still had grade 1, 2 and 3 (Table-2). Better outcome of treatment of MGD in group A was noted as compared to group B. Mean TBUT (secs) in group A was 6.39 ± 2.16 on day 0 which improved to 11.0 ± 1.38 at 90th day. In group B mean TBUT (secs) was 4.28 ± 2.18 at day 0 which improved to 10.43 ± 1.71 at day 90. Significant difference in mean TBUT values between the two groups is noted at 90th day (P value is 0.015). Mean Schirmer’s-I in group A was 8.47 ± 3.32mm at day0 which improved to 12.80 ± 2.93mm at 90th day. In group B mean Schirmer’s -I was 7.78 ± 3.03mm at day 0 which improved to 12.88 ± 2.82mm at 90th day. No significant difference noted between the Schirmer‘s -I value among both the groups. More symptomatic improvement in patients of group A as compared to group B at follow-up (90th day) which was significant (P value 0.032) (Table-4).Mean value of Total Cholesterol, Triglycerides, LDL and HDL in group A were 156.96 ± 30.30mg%, 105.67 ± 25.05mg%, 88.84 ± 12.13mg%, 65.29 ± 12.21mg% at diagnosis (all within normal limits). In group B mean value of triglycerides at the time of diagnosis was 224.91 ± 55.13mg% and at day 90 (after treatment) it was 160.69 ± 47.91mg% (Table-5). Hence shows a significant association between TG and MGD (p<0.001). Mean value of total cholesterol at the time of diagnosis was 301 ± 62.28mg% and at day 90(after treatment) it was 197.27 ± 41.39mg% and the difference between both the groups was statistically significant (p value <0.001) (Table-6), mean value of LDL at day 0 was 156.58 ± 38.23mg% and at day 90 it was 108.96 ± 28.42mg% with treatment for hypercholesterolemia (Table-7), Hence shows a significant association between LDL and MGD (p<0.001). In group B mean value of HDL at the time of diagnosis was 45.51 ± 8.32mg% and at day 90 it was 48.42 ± 6.89mg% with treatment for hypercholesterolemia (Table-8). Hence shows a significant association between HDL and MGD (p<0.001).

Subspecialty - Cornea & External Eye DiseasesDOS Times - Volume 30, Number 6, March-April 2025 44 www.dosonline.org Group A Group B P-ValueMean ± SD Mean ± SDAge (in years) 59.33 ± 9.32 63.11 ± 10.21 0.070Range 42 – 79 (years) 44 – 86 (years) Day 90 P-Value0 1 2 3 TotalDay1Group AGrade 1 35 0 0 0 35<0.001Grade 2 47 0 0 0 47Grade 3 2 6 0 0 8Grade 4 0 0 0 0 0Group BGrade 1 15 0 0 0 15<0.001Grade 2 38 4 0 0 42Grade 3 13 12 2 2 29Grade 4 0 4 0 0 4 Group A (90 Eyes) Group B (90 Eyes) Total P-ValueDay 1Grade 1 35 (39%) 15 (17%) 50 <0.001Grade 2 47 (52%) 42 (47%) 89 Grade 3 8 (9%) 29 (32%) 37 Grade 4 0 4 (4%) 4 Day 2Grade 0 84 (93%) 66 (73%) 150 0.003Grade 1 6 (7%) 20 (22%) 26 Grade 2 0 2 (2%) 2 Grade 3 0 2 (2%) 2 Table 1: Distribution of Study Population according to age in Years.Table 2: Distribution of patients (number of eyes) according to the grade of MGD at Day 1 and Day 90.Table 3: Improvement in Grades of MGD at 90 days.

Subspecialty - Cornea & External Eye DiseasesDOS Times - Volume 30, Number 6, March-April 2025 45 www.dosonline.org Group A Group BMean ± SD Mean ± SD P-ValueBefore 23.29 ± 7.79 32.78 ± 8.91 <0.001 15 Days 21.80 ± 7.63 29.06 ± 8.01 <0.001 30 Days 20.02 ± 7.32 24.33 ± 6.25 0.004 90 Days 17.51 ± 6.58 20.30 ± 5.51 0.032 Table 4: Mean OSDI Scoring.Table 5: Mean value of triglyceride (mg%) according to grade of MGD.Table 6: Mean Total cholesterol (mg%) in patients.Table 8: Mean value of HDL (mg%) according to grade of MGD.Table 7: Distribution of the patients according to total LDL (mg%) values. Time Grade I Grade II Grade III Grade IV Mean ± SD Mean ± SD Mean ± SD Mean ± SD Group A Baseline 105.63 ± 29.09 102.44 ± 23.10 126.0 ± 8.12 ---- Group B Baseline 196.43 ± 27.26 208.73 ± 35.07 265 ± 72.59 222.0 ± 31.11 Group B 90 Days 134.29 ± 12.04 147.64 ± 31.76 192.07 ± 31.76 177.0 ± 14.14 Cholesterol Time Grade I Grade II Grade III Grade IV Mean ± SD Mean ± SD Mean ± SD Mean ± SD Group A Baseline 152.31 ± 31.30 159.20 ± 31.98 161.50 ± 14.20 Group B Baseline 252.0 ± 26.65 276.95 ± 36.56 358.07 ± 68.19 337.50 ± 10.61 Group B 90 Days 175.29 ± 23.61 183.41 ± 20.71 223.21 ± 55.80 245.00 ± 31.11 HDL Time Grade I Grade II Grade III Grade IV Mean ± SD Mean ± SD Mean ± SD Mean ± SD Group A Baseline 64.62 ± 12.97 66.16 ± 12.68 62.50 ± 6.35 -- Group B Baseline 48.43 ± 5.32 43.50 ± 8.14 38.86 ± 8.60 36.50 ± 0.71 Group B 90 Days 52.43 ± 4.19 49.36 ± 5.85 45.93 ± 8.52 41.50 ± 2.12 Range Group A Group B Total P-Value≤130 mg% Normal 45 (100%) 10 (22%) 55<0.001 >130 mg% Abnormal 0 35 (78%) 35Total Total 45 45 90DiscussionMeibomian glands are important structures that secrete lipid into the tear film, which prevents excessive evaporation of the tear film by forming a thin oily layer on the tear film.[1] Meibomian gland dysfunction is characterized by terminal duct obstruction and/or

Subspecialty - Cornea & External Eye DiseasesDOS Times - Volume 30, Number 6, March-April 2025 46 www.dosonline.orgqualitative/quantitative changes in glandular secretion. The quantity of Meibomian gland secretions may increase (high-delivery type) or decrease (due to old atrophy), inciting an inflammatory response and increased tear film evaporation.[7-8] Recent research suggests that increased cholesterol in meibum may play a vital role in the pathology of MGD. Many studies were conducted in the past to find association between MGD and dyslipidemia. Dyslipidemia represents an abnormal value in one or more components of the lipid profiles. Low levels of HDL, high levels of LDL, and high levels of TC, have been shown to be independent risk factors for vascular diseases. A strong association between increasing age and severity of MGD is in accordance with a study by Villani et al.[18] which evaluated agerelated changes of the meibomian gland using in vivo laser scanning confocal microscopy. The mean TBUT in group A and group B improved with the treatment at 90th day, significant difference was found between two groups. The mean Schirmer‘s-I in group A and group B improved with the treatment at 90th day, no significant difference between both the groups. The prevalence of dyslipidemia in the general population according to the data available from the National Health and Nutrition Examination Survey. The prevalence of TC >200mg/dL is 45.1% and TG>240mg/dL is 15.7%, LDL >130mg/dL is 32.8%, HDL 150mg/dL is 33.1%. The number of MGD patients with TC >200mg/dL and <200mg% in our study were 45 (100%) and 45 (100%), respectively. This study indicates a strong association between hypercholesterolemia (levels >200mg/dL) and increasing severity of stage of MGD. This is in accordance with the findings obtained by the studies conducted by Dao et al.[15] and Bukhari et al.[5]This study also shows a definite association between increased LDL (>130mg/dL) with increasing severity of stage of MGD (P value <0.001). This observation is also consistent with the findings of other studies.This study also indicates a fairly definite association between decreased HDL (levels <40mg/dL) and increasing severity of stage of MGD. This observation is in accordance with the study conducted by Brahm P Guliani et al. TG levels were found to be associated with increasing severity of MGD. All other studies concluded increased TGs in moderate and severe MGD cases but could not reach statistical significance. Meibomian gland secretions contain TGs in addition to cholesterol, which is known to constitute 1–2% of the normal meibomian glands secretions, and the increase in serum TGs might have a role in increasing the meibum melting point and increasing its viscosity.Group A and group B (started on treatment with lipid lowering drugs) patients were assessed for Improvement in MGD as well as lipid profile on day 1 and day 90th. To conclude there was a better outcome of treatment of MGD in group A as compared to group B who needed prolonged treatment to be cured. It suggests a definite association between dyslipidemia and MGD.This study has found that patients with higher stages of MGD had serum TGs >150mg/dL, TC >200mg/dL, an LDL >130mg/dL, and serum HDL <40mg/dL, and there exists an association between increasing stage of MGD and increasing values of all the lipid profile component. A larger prospective study is required to show that abnormal serum cholesterol levels can cause MGD. Secondly, the etiology of MGD is unknown and may be multifactorial. Thirdly, the sample size was small, obviating the need for larger studies. Fourthly, all the participants in our study were Indians, limiting the generalizability of this study. MGD may be a possible marker of yet undiagnosed hypercholesterolemia, regardless the type of cholesterol involved.ConclusionAn association has been noted between the females and MGD as seen in group A. whereas in group B more no. of males were more than females suggesting the high prevalence of hypercholesterolemia in male patients. An association exists between increasing severity of MGD and increasing levels of derangement of lipid profile. The patients with MGD were diagnosed with hypercholesterolemia for the first time and lipid lowering drugs were started, severity of MGD decreased and ocular condition of patient improved, but duration to get cured completely was prolonged in dyslipidaemia patients. Additional benefit of this study was preventing patient from other systemic diseases due to Dyslipidaemia.References1. Bron AJ, Benjamin L, Snibson GR. Meibomian gland disease.Classification and grading of lid changes. Eye (Lond) 1991;5 (pt 4):395–411.2. Jacob J M, Pillai S S, Goudinho S J. The association of meibomian gland dysfunction with dyslipidemia-A case-control study.World Journal of Pharmaceutical Research 2016;5 (3).3. Nelson JD, Shimazaki J, Benitez-del-Castillo JM, et al. The international workshop on meibomian

Subspecialty - Cornea & External Eye DiseasesDOS Times - Volume 30, Number 6, March-April 2025 47 www.dosonline.orggland dysfunction: report of the definition and classification subcommittee. Invest Ophthalmol Vis Sci 2011;52:1930–7.4. Hom MM, Martinson JR, Knapp LL, et al. Prevalence of meibomian gland dysfunction. Optom Vis Sci 1990;67:710–2.5. Bukhari A. Prevalence of punctal stenosis among ophthalmology patients. Middle East Afr J Ophthalmol 2009;16:85–7.6. Schein OD, Muñoz B, Tielsch JM, et al. Prevalence of dry eye among the elderly. Am J Ophthalmol 1997;124:723–8.7. Den S, Shimizu K, Ikeda T, et al. Association between meibomian gland change and aging, sex, or tear function. Cornea 2006;25:651–5.8. Sullivan BD, Evans JE, Dana MR, et al. Influence of aging on the polar and neutral lipid profiles in human meibomian gland secretions. Arch Ophthalmol 2006;124:1286–92.9. Sullivan DA, Sullivan BD, Evans JE, et al. Androgen deficiency,meibomian gland dysfunction, and evaporative dry eye. Ann N Y Acad Sci 2002;966:211–22.10. Krenzer KL, Dana MR, Ullman MD, et al. Effect of androgen deficiency on the human meibomian gland and ocular surface. J Clin Endocrinol Metab 2000;85:4874–82.11. Schaumberg DA, Dana R, Buring JE, et al. Prevalence of dry eye disease among US men: estimates from the Physicians’ Health Studies. Arch Ophthalmol 2009;127:763–8.12. Ena P, Pinna A, Carta F. Discoid lupus erythematosus of the eyelids associated with staphylococcal blepharitis and meibomian gland dysfunction. Clin Exp Dermatol 2006;31:77–9.13. Mathers WD, Stovall D, Lane JA, et al. Menopause and tear function:the influence of prolactin and sex hormones on human tear production. Cornea 1998;17:353–8.14. Tamer C, Melek IM, Duman T, et al. Tear film tests in Parkinson’s disease patients. Ophthalmology 2005;112:1795.15. Dao AH, Spindle JD, Harp BA, et al. Association of dyslipidemia in moderate to severe meibomian gland dysfunction. Am J Ophthalmol 2010;150:371.e1–5.e1.16. Butovich IA, Millar TJ, Ham BM. Understanding and analyzing meibomian lipids—a review. Curr Eye Res 2008;33:405–20.17. Driver PJ, Lemp MA. Meibomian gland dysfunction. Surv Ophthalmol 1996;40:343–67.18. Villani E, Canton V, Magnani F, Viola F, Nucci P, Ratiglia R. The aging meibomian gland: An in vivo confocal study. Investig Ophthalmol Vis Sci 2013;54:4735-40.Prachi Singh DOMS, DNB Assistant Professor,ASMC, Pilibhit, Uttar Pradesh Corresponding Author:

Subspecialty - StrabismusDOS Times - Volume 30, Number 6, March-April 2025 48 www.dosonline.orgOverview of Visual Assessment in ChildrenSanjeev Kumar Nainiwal MD, DNB, MNAMS | Neha Kharwas MBBS | Sunil K Gurjar MBBS | Manisha Jhajharia MBBSDepartment of Ophthalmology, Sawai Man Singh Medical College & Hospital, Jaipur (Rajasthan), IndiaVision plays a crucial role in a child’s development, affecting not only their ability to see clearly but also their cognitive and motor skills. Children rely heavily on their vision to explore the world around them, engage with peers, and learn in school.Undiagnosed or untreated vision problems can lead to difficulties in reading, writing, or even socializing, which can affect a child’s academic and personal growth. Visual impairment can also lead to secondary effects like low self-esteem or behavioural problems, which can further hinder a child’s development.Early and regular visual assessments allow healthcare providers to detect such conditions early and recommend timely interventions, including corrective eyewear, vision therapy, or surgical procedures. This can prevent longterm complications and ensure that children reach their full potentialAssessment of visual acuity in children is not an easy clinical task. It is actually an art which requires patience and friendliness on part of the examiner. Visual acuity testing in children varies greatly with their age and mental status.Visual Assessment in Children: Tailored Approaches by AgeOver the last four decades several methods have been developed for quantitative as well as qualitative assessments of visual acuity in infants and young children. Infants and children upto the age of 2.5 to 3 years as well as older children with delayed milestones and other disorders are generally not able to accomplish subjective visual acuity tests. In these situations visual acuity is evaluated by using objective methods which are being discussed here.Visual Assessment in Infants (0-12 Months)In the first year of life, visual development progresses rapidly, and early detection of visual impairments can prevent long-term issues. Infants are nonverbal and cannot communicate what they see like an adult. Visual acuity in a newborn and infant up to 3 months of age can be deter-mined by the tests given below:Observation: A considerable degree of information can be gained from simple observation of the child, which should be started from the moment the child is brought into the ex-amination room, while taking the history from the parents throughout the rest of the examination. Assessment of vision begins with observing whether the child shows any interest in the surroundings or remains apathetic to the environment. Any recognition of or response to the surroundings should be considered as a positive indicator of the presence of vision. It is important to remember that the child should be examined in an environment that is comfortable for the child as well as the parents. Ideally, every effort should be made to provide the child with as pleasant and favourable environment as possible. This improves the quality of information obtained from the examination and greatly enhances the child’s level of cooperation on sub sequent visits. Any sour movements should be avoided during the examination because the response of a blind child to auditory stimuli may mislead the examiner and parents to conclude that some degree of visual function is present.1. Blink Reflex Test: Blink reflex is present since birth. When bright light is shown, a normal infant should respond by blinking.2. Pupillary Light Reflex Test: The test is best performed in a semi-darkened room. In the semi dark room, the pupil comes to a state of semi dilatation that reacts briskly. It should include size and shape in both, ambient light as well as darkened room conditions to evaluate the status of the pupillary sphincters and dilator muscles. In addition, the swinging light test should also be employed to test for a relative afferent pupil defect (RAPD). Presence of the light reflexes can be considered as a normal anterior Arc of vision, which indicates integrity of the retina, optic nerve and pupillomotor fibers. Absence of vision despite a normal pupillary reaction represents cortical blindness.

Subspecialty - StrabismusDOS Times - Volume 30, Number 6, March-April 2025 49 www.dosonline.orgVisualization in very young children sometimes requires a magnifying glass, as their pupils are smaller than those of the older children and the light responses are of small amplitude. 3. Vestibulo-Ocular Reflex (VOR) Test: The VOR is generally tested by turning the newborn’s head on his/her long axis and observing that the eyes deviate opposite to the direction of head rotation.4. Eye Popping Test: Eye-popping reflex indicates the baby’s ability to detect changes in the room illumination. When the room lights are suddenly dimmed, the baby’s upper eyelids should pop open wide for a moment. This behaviour is documented as ‘positive eye popping’.5. Optokinetic Nystagmus (OKN) Test: It is an objective method of visual assessment in infants. The optokinetic response is an involuntary sawtooth movement of the eye that occurs in response to moving stimuli such as a rotating drum, or drifting bars on a computer screen.[1] The normal response consists of repeated smooth pursuit movements (slow phase) in the direction of the movement of the stripes followed by saccades (fast phase) in the opposite direction for refixation. The presence of vision is judged on the basis of this specific smooth pursuit saccade response only. Presence of OKN that suggests that vision is present at the cortical level, which indicates intactness of the associated tracts between the visual cortex and the motor centres. Optokinetic nystagmus acuity is at least 6/12 in the newborn and improves fairly rapidly during the first few months of life. Since it has been reported that optokinetic response can be elicited in the presence of cortical blindness. This test must be interpreted cautiously since subcortical mechanisms may be involved. Other example of such test which is based on the same principle (Pendular eye movements but not optokinetic nystagmus) is Catford drum test which was devised by Catford and Oliver.OKNOVIS: This Objective test was devised at Dr. Rajendra Prasad Centre for Ophthalmic Sciences. AIIMS, New Delhi in collaboration with Bio Medical Engineering Department of I.I.T. Delhi. The test is based on the principle of arresting an elicited OKN by introducing optotypes of different sizes. The test instrument consists of a portable hand-held drum moving at 12rpm at 60cms in front of child with colored pictures to elicit an optokinetic nystagmus. Optotypes of different sizes are then introduced to arrest the OKN. Although, this test lacks full optotype standardization, but it has the advantage of being a quick objective test.6. Visually Evoked Responses (VER): VERs are visually evoked electrophysiological signals extracted from the electroencephalographic activity in the visual cortex recorded from the overlying scalp.[2] VER is the only clinically objective technique available to assess the functional state of the visual system beyond the retinal ganglion cells. (Table-1) Age (Months) Optokinetic Nystagmus Preferential Looking Test Visually Evoked Response1 6/120 6/120 6/1202 6/60 6/60 6/606 6/30 6/30 6/6-6/12Age (months at which 6/6 is achieved 20-30 24-36 6-12Table 1: Estimated visual acuity at different ages.Assessment of Visual Acuity from 3 to 6 Months1. Fixation behaviour test: By this age babies should begin to focus on faces or objects placed in front of them. If the child habitually fixates with one eye, it indicates poor vision in the non-fixating eye.2. Central, steady, maintained (CSM) method:It evaluates three key aspects of fixation:1. Central - Is the infant able to fixate on a target using the centre of the macula (as opposed to eccentric fixation)2. Steady Is the fixation steady, or does the eye wander or exhibit nystagmus3. Maintained - Does the infant sustain fixation on the target when one eye is covered (indicating equal vision in both eyes)

Subspecialty - StrabismusDOS Times - Volume 30, Number 6, March-April 2025 50 www.dosonline.orgProcedure:A bright object or light is presented to the infant to elicit fixation.Each eye is tested separately by covering the other eye (monocular testing).The observer checks whether fixation is central, steady, and maintained.Interpretation:CSM: 6/9 to 6/6,Central steady not maintained (CSNM): 6/36 to 6/60 andUnsteady central fixation: <6/60.3. Brückner’s red reflex test: Brückner’s reflex is helpful in children uncooperative to the cover test when an assessment is being carried out for small angle strabismus. The examiner should stay far enough to illuminate both pupils by the same direct ophthalmoscope beam. The examination should be carried out in dim illumination and the child’s attention to be fixed at a distance. Assess the red reflex both before and after dilatation to see how much of the pupillary space is obscured. An overall whitening of the red reflex across the entire pupil of one eye indicates strabismus or anisometropic amblyopia.4. Menace reflex test: Menace reflex, i.e. reflex closure of the eyes on the approach of an object is usually present after the age of 5 months, if vision is normal.5. Cover test: By 3-6 months, infants have ad-equate refixation reflex to permit cover test. In patients with strabismus, one eye is deviated. If the straight eye is covered, the other eye will make a movement to line up the visual target. If a patient is exotropic, the eye will make an inward movement. If an eye is esotropic, it will make an outward movement.Assessment of Visual Acuity from 6 to 12 MonthsIn addition to the above-mentioned tests, the tests described below are more useful in this age group:Preferential looking test: This test is based on the observation presented with two adjacent stimulus, one of which is striped and the other is homogeneous, the infant will tend to look at the striped pattern for a greater portion of the time. Preferential looking test is of based on the principle that a child will look at a patterned in preference to a blank when they are presented simultaneously in the immediate visual field. The child will continue to show this preference as long as it is able to differentiate between the patterned and blank area.The infant is exposed to a pair of stimuli consisting of a field of black and white stamps of a specific spatial frequency and an identical gray homogenous field of equal luminance. An observer watches the infant’s eyes through a central peep and scores the number of times the infant fixates on each stimulus as well as the duration of fixation on each stimulus. The 2 common examples of this test are Teller acuity cards, which consist of black stripes of varying thickness, and Cardiff acuity cards consisting of shapes with variable out lines. Those with a bold out line are seen more easily than those with thin outlines, and an assessment of visual acuity is made accordingly.1. Teller Acuity Cards Test: Teller acuity card (TAC) is a modification based on preferential looking testing, which is designed for a simpler and rapid vision testing. The TAC test can be used as a relatively reliable method for estimating visual acuity in preliterate children.[3]The total set of teller acuity cards consists of seventeen cards of 25.5 X 51cms. Fifteen of these cards contain 12.5 X 12.5cms patches of square-wave gratings (i.e. vertical black and white stripes). The grating range in spatial frequency, which is actually a measure of stripe width, is 38 to 0.32 cycles/cm in approximately half octave steps. A cycle consists of one black and one white stripe. The 16th card, also called as “Low vision card contains a 25.5 X 23cm patch of 0.25 cycle\\cm grating, covering most of the card to one side of peephole. The 17th card is a black gray card with no gratings. A label on the back of each card indicates the grating size on that particular test card.The acuity should be assessed both binocularly and monocularly. During examination, the child should be held in front of gray screen at specified distance (i.e. 38cms for children of 0-6 months of age, 55cms for children of 6 months to 3 years of age and 84cms for children older than 3 years).For children who do not respond to any of the acuity cards presented behind the screen are tested at a near distance (19 or 9.5cms) without the screen. If they still do not respond, they should be tested with “Low vision card.” Since this card is not a part of original series of 15 cards, conversion of cycles/cm to Snellen equivalent is not recommended and only LV seen or LV not seen should be recorded in such cases. Visual acuity determined with this method (TAC) range from approximately 6/240 in the newborn to 6/60 at