Jan-Feb 2026 (Vol 31 No 4)

PresidentJoint Secretary Editor DJO Library OfficerVice President Secretary Treasurer Prof. Rajesh SinhaDr. R. P. SinghDr. Ankur SinghDr. Pranita SahayDr. Rajendra PrasadDr. Anu MalikDr. Rakesh GuptaDr. Jatinder SinghBhallaDr. Deepa SharmaDr. Ritin GoyalDr. AlkeshChaudharyProf. Rohit SaxenaDr. Ikeda LalDr. Siddharth MadanDr. Rahul Mayor Dr. Bhupesh SinghProf. M. Vanathi Dr. Prafulla Kumar Maharana Prof. Kirti SinghDOS Office BearersDOS Executive Committee (2024-2026)Executive MemberDOS Representatives to AIOS Ex-Officio MembersFrom the Desk of President DOS 06From the Desk of Secretary, DOS 07From the Editors 08Table ofContentsHistorical Lanes 09-11A Man of Many Originals: From The Realm of History- ‘Albrecht Von Graefe’Tracing the Origins 12-14Evolution of Antiglaucoma Pharmacotherapy: From Empiricism to Targeted TherapyPost Grdauate Essentials 15-42Overview on Macular Hole and Its ManagementUnmasking Atypical Optic Neuritis: A Case of Diagnostic Challenge and Visual Recovery Congenital Lacrimal Fistula: A Rare Case Presentation Unequal Pupils in Clinical Practice: A Systematic Approach to AnisocoriaRetinal Vein Occlusion (RVO) – Current Concepts and UpdatesTherapeutic Molecules 43-47Cenegermin - Drugs in OphthalmologyEmerging Trends & Advances 76-78A “BANG” for Your Buck: Cost-Effective Glaucoma Surgery Meets MSICS Precision on a Budget: Combining MSICS and BANG for Advanced Pseudoexfoliation GlaucomaSmart Scopes & Diagnostics 71-75Beyond the Posterior Pole: How Widefield FFA and OCT-Angiography Are Redefining Retinal Vascular ImagingDialogues and Insights 48-56Mastering Vision: Essential Practical Insights for the Postgraduate OphthalmologistValue-Based Care in Ophthalmology: A Financial Sustainability Framework for IndiaPicture Perspective 57-63Coats Disease Presenting as Leukocoria in a Child: A Case Report and ReviewPyogenic Granuloma of the Lacrimal Caruncle in a Lactating Female: A Case ReportThe Surgeon’s Focus 64-70Digging Deep: Orbital DermoidBilateral Electric Cataract in a Post-Electrical Burn Adolescent with Severe Facial Cicatricial Changes: A Surgical Challenge

PresidentJoint Secretary Editor DJO Library OfficerVice President Secretary Treasurer Prof. Rajesh SinhaDr. R. P. SinghDr. Ankur SinghDr. Pranita SahayDr. Rajendra PrasadDr. Anu MalikDr. Rakesh GuptaDr. Jatinder SinghBhallaDr. Deepa SharmaDr. Ritin GoyalDr. AlkeshChaudharyProf. Rohit SaxenaDr. Ikeda LalDr. Siddharth MadanDr. Rahul Mayor Dr. Bhupesh SinghProf. M. Vanathi Dr. Prafulla Kumar Maharana Prof. Kirti SinghDOS Office BearersDOS Executive Committee (2024-2026)Executive MemberDOS Representatives to AIOS Ex-Officio MembersDOS Times - Volume 31 Number 4, January-February 2026 03

DOS Times - Volume 31 Number 4, January-February 2026 04 DOS Times - Volume 31 Number 4, January-February 2026 05Section InchargesExecutive Editor Managing EditorsThe Editorial BoardDr. Prafulla Kumar MaharanaEditor-in-ChiefDr. Ritu Nagpal Dr. Anu Malik Dr. Neha Chawla GulianiDr. Deepali Singhal Historical Lanes Dr. Vineet Sehgal Therapeutic Molecules Dr. Pranita Sahay Post Graduate Essentials Dr. Sunandini Bose Dr. Esha Aggarwal Dr. Arpan GandhiTracing the Origins From Concept to PracticeResidency Roots Basic Skills and Early SurgeriesDr. Arshi Singh Dr. Nilesh Mohan Dr. Kanika JainDr. Ankur Singh Dr. Nishtha Khurana Dr. Jaya GuptaDr. Siddharth MadanBasic Sciences The Closer View: Through the MicroscopeTransforming Journeys andReal Life ExperiencesDialogues & InsightsExpert Perspectives in Ophthalmology Dr. Nupur GoelBehind the CurtainDr. Gunjan Saluja Surgical Instruments Orchestra of the Operating Room Dialogues & InsightsExpert Perspectives in Ophthalmology Emerging Trends & AdvancesSmart Scopes & Diagnostics The Surgeon’s Focus Picture PerspectiveFounding Stories

DOS Times - Volume 31 Number 4, January-February 2026 04 DOS Times - Volume 31 Number 4, January-February 2026 05Transforming Journeys andReal Life ExperiencesSection 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-OphthalmologyDr. Rebika DhimanDr. Sumit MongaDr. Varshini ShankarStrabisumsDr. Anita GangerDr. Smita KapoorCommunity OphthalmologyOcular OncologyComprehensive OphthalmologyDr. Puneet JainDr. Shaloo BagejaDr. Sima DasDr. Sumit GroverDr. Harinder Singh SethiDr. R.K. DuveshDr. Utsav BansalDr. Suraj SenjamDr. A.K. GroverDr. Anil TanwarDr. Anuj MehtaDr. Ashish KumarDr. Ashok Grover Dr. Col. Ranjit GoenkaDr. Cyrus ShroffDr. D.K. MehtaDr. G K DasDr. Gurbax SinghDr. Jatinder Singh BhallaDr. Jeewan Singh TitiyalDr. Kirti SinghDr. Lalit VermaDr. M. VanathiDr. Mahipal S. SachdevDr. Mahipal SachdevDr. Manavdeep SinghDr. Namrata SharmaAdvisory Board Dr. OmprakashDr. R.B. JainDr. Radhika TandonDr. Rajendra PrasadDr. Rishi MohanDr. S. BhartiDr. Sanjay ChaudhryDr. Sanjay MishraDr. Sarita BeriDr. Sharad LakhotiaDr. Subhash Dadeya Dr. Sudhank BhartiDr. Taru DeewanDr. Uma SridharDr. V P GuptaDr. Vinay GarodiaDr. Virender SangwanDr. KamleshDr. S.K. Khokhar

From The Desk ofPresident, DOSProf. Rajesh Sinha MD, DNB, FIACLE, FRCSCornea, Lens and Refractive Surgery Services, Dr. R. P. Centre for Ophthalmic Sciences, AIIMS, New DelhiDear Esteemed Colleagues and Readers,It is a pleasure to present this issue of DOS Times, which brings together a focused yet diverse collection of contributions reflecting the evolving landscape of contemporary ophthalmology.We begin by honoring the legacy of Albrecht von Graefe, whose pioneering work continues to inspire modern practice. The issue then highlights key advances in retinal imaging, including a comprehensive review of macular hole management and updated perspectives on retinal vein occlusion, alongside the expanding role of widefield angiography and OCT-angiography in vascular imaging.Educational enrichment remains central, with practical insights tailored for postgraduate ophthalmologists that bridge the gap between theory and clinical application. Diagnostic challenges are addressed through structured discussions on leucocoria and orbital dermoid, emphasizing systematic evaluation and surgical considerations.This issue also features a unique case of bilateral electric cataract in a post-burn adolescent, underscoring the importance of individualized surgical planning in complex scenarios. In glaucoma, we present both the evolution of pharmacotherapy toward targeted treatment and an innovative, cost-effective surgical approach combining MSICS with BANG for advanced pseudoexfoliation glaucoma—highlighting the importance of accessible innovation.Finally, the integration of clinical ophthalmology with specialized ocular laboratories is explored, reinforcing the need for stronger diagnostic collaboration in modern practice.I extend my sincere appreciation to all authors and contributors for their valuable scholarly work. I am confident that this issue will educate, stimulate meaningful engagement, and inspire continued progress in the field of ophthalmology.One of the most anticipated highlights of this year’s initiatives is the 76th Annual DOS Conference, to be held from April 24th to 26th, 2026, at the Bharat Mandapam Convention Centre, New Delhi. We extend a warm invitation for you to be part of this premier academic gathering and look forward to your gracious presence, as we engage in enriching discussions, exchange ideas, and work together toward shaping a more progressive and future-ready ophthalmic community.With warm regards,Rajesh Sinha MD, DNB, FIACLE, FRCSProfessor, Dr. R. P. Centre, AIIMS, New DelhiPresident - Delhi Ophthalmological SocietyDOS Times - Volume 31 Number 4, January-February 2026 06

From The Desk ofSecretary, DOSDr. Prafulla Kumar MaharanaAddl. Professor, Dr. R. P. Centre for Ophthalmic Sciences, AIIMS, New DelhiDOS Times - Volume 31 Number 4, January-February 2026 07Dear Esteemed Members,Warm greetings to all.It gives me great pleasure to bring to you this issue of DOS Times. Each issue is a reminder of how active, thoughtful, and academically rich our ophthalmic community continues to be. The effort that goes into creating this journal—from writing and reviewing to compiling—reflects our shared commitment towards learning and growth.In this edition, you will find a wide range of content that touches different aspects of our field. There is a balance of basic understanding, clinical problem-solving, surgical perspectives, and newer developments. The idea is simple—to make the journal useful for everyone, whether you are a postgraduate just starting out, or a practicing ophthalmologist looking to stay updated.What is especially encouraging is the participation from members at all stages of their careers. Young contributors are bringing fresh perspectives and enthusiasm, while experienced clinicians are sharing their valuable insights and real-world experiences. This combination makes learning more meaningful and practical.Ophthalmology today is changing rapidly. New technologies, evolving treatment strategies, and increasing expectations from patients require us to constantly update ourselves. At the same time, the basics—clinical examination, decision-making, and patient communication—remain just as important. Through DOS Times, we aim to support both these aspects: strengthening foundations while keeping pace with change.I would like to encourage all members to actively take part in this academic journey. Whether it is by writing an article, sharing an interesting case, or even giving feedback—every contribution matters. This journal truly belongs to all of us, and it grows stronger with your involvement.I would also like to warmly invite all of you to attend the upcoming Annual Conference of the Delhi Ophthalmological Society. It will be a wonderful opportunity to learn, interact with colleagues, exchange ideas, and reconnect with the larger DOS family. Your presence and participation will make it even more meaningful.Looking forward to meeting many of you there.Warm regards,Dr. Prafulla Kumar MaharanaSecretary, Delhi Ophthalmological Society

DOS Times - Volume 31 Number 4, January-February 2026 08 DOS Times - Volume 31 Number 4, January-February 2026 09From TheEditorsDr. Anu MalikManaging EditorDr. Ritu NagpalExecutive EditorDr. Neha C. GulianiManaging EditorDear Readers,It gives us immense pleasure to present this issue of DOS Times, thoughtfully curated to reflect both the rich legacy and the dynamic evolution of our specialty. This edition brings together a diverse spectrum of topics, ranging from historical insights to cutting-edge therapeutics, and from common clinical scenarios to rare and intriguing conditions.We begin our journey through the Historical Lanes with a tribute to Albrecht von Graefe, whose pioneering contributions laid the very foundation of modern ophthalmology. Glaucoma management remains an ever-evolving field, and this issue features a comprehensive review on the evolution of antiglaucoma pharmacotherapy, highlighting the transition from traditional agents to newer targeted therapies that have significantly improved patient outcomes.The retina section offers valuable updates, including an overview of macular hole and its management, as well as an in-depth discussion on retinal vein occlusion, emphasizing current diagnostic and therapeutic strategies. The inclusion of widefield fluorescein angiography (FFA) underscores the expanding role of advanced imaging in enhancing our clinical acumen.Neuro-ophthalmology continues to challenge and intrigue clinicians. The article on unmasking atypical optic neuritis provides critical insights into recognizing and managing atypical presentations, while anisocoria is revisited with a practical, clinically oriented approach.This issue also highlights rare and interesting conditions such as congenital lacrimal fistula and Coats disease, encouraging clinicians to maintain a high index of suspicion in atypical cases. The discussion on pyogenic granuloma offers practical guidance on diagnosis and management in day-to-day practice.We are also pleased to include a focused piece on cenegermin, a novel therapeutic agent that has opened new avenues in the management of neurotrophic keratitis, reflecting the growing impact of biotechnology in ophthalmology.Surgical advancements are showcased through the article on surgery in bilateral electric cataract and BANG combined with MSICS.For our postgraduate readers, the section on essential practical insights for postgraduate ophthalmologists serves as a concise yet comprehensive guide to bridge the gap between theory and clinical practice.As always, our aim is to provide a balanced blend of knowledge that is academically enriching and clinically relevant. We hope this issue not only enhances your understanding but also stimulates further inquiry and discussion.I extend my sincere gratitude to all the contributors, reviewers, and editorial team members for their dedication and commitment in bringing out this issue.

Historical LanesDOS Times - Volume 31 Number 4, January-February 2026 08 DOS Times - Volume 31 Number 4, January-February 2026 09A Man of Many Originals: From The Realm of History- ‘Albrecht Von Graefe’Introduction‘Von Graefe’: the name evoked awe and mystery (Figure-1). This was in the cusp of early 21st century, when I was a resident in Ophthalmology. It was also the period of rapid innovations in information and technology, with the advent of touch buttons of Nokia as our most prized possession. But alas, the touch screens were still a decade away. Search engines were accessible only through bulky desktop com-puters housed in the college library.Dr. Shruti AnanadAssistant Professor, Dr. Radhakrishnan Government Medical College, Hamirpur, Himachal PradeshShruti Anand | Anurag SharmaDepartment of Ophthalmology, Dr. Radhakrishnan Government Medical College, Hamirpur, Himachal PradeshIt was the time when the knowledge was sought from the books, some of them as old as the college itself. It was one sweltering afternoon in the library, I came across his name. My curiosity grew to know more about the man who had his name as a sign in thyroid disorder, had invented a knife for cataract surgery and whose work in iridectomy reshaped the management of glaucoma. His brilliance spanned systemic ophthalmology, cataract surgery, and glaucoma management alike. His achieve- ments were remarkable given he worked in the nine- tenth century, before modern diagnostics or imaging existed.Drawing Out The Drapes of HistoryA German resident, born in the spring of May 22 in 1828, to an eminent father who was Professor of Ophthalmology in the University of Berlin. He unfortunately lost his father at a tender age of twelve. But this, little more than a decade association with his illustrious father had long term implications. Highly influenced by his father, he also decided to pursue medicine. It is indeed to the benefit of us as the millennial ophthalmologists, as he was responsible for separating Ophthalmology from General surgery and giving us a distinct identity. Hence, he has been rightly bestowed the title of “Father of Modern Ophthalmology.” As his professional journey continued, no aspect of eye was untouched by him.The Man and His Amazing ObservationsLong before eye was categorized into anterior and posterior segments, Van Graefe’s eye for detail made these incredible observations. Some of these laid down the ground work for modern ophthalmology.Some of the observations and discoveries made by him are enumerated as:a) General Ophthalmology: The ophthalmology comFigure 1: Albrecht Von Graefe munity is conscious of a sign named after him –

Historical LanesDOS Times - Volume 31 Number 4, January-February 2026 10 DOS Times - Volume 31 Number 4, January-February 2026 11‘Graefe Sign’ seen in exophthalmic goiter (Basedow disease). An often-asked question of viva voce, in which the subject’s upper lid fails to follow downward movement of the eye ball from looking up to down.b) Glaucoma: The current ophthalmology is indebted to him for classifying the various types of Glaucoma into three categories with which we identify today as: Acute, Chronic and Sub- Acute. He pioneered iridectomy to treat acute glaucoma with elevated pressure.c) Cataract: He pioneered the technique of clear lens extraction which was unquestioned for almost a century.d) Retinal Disorders: He was the second person to describe retinal detachment after Ernst Adolf Coccius.He was the first one to study retina extensively soon after the direct ophthalmoscope was invented by Hermann von Helmholtz. It was him who described choroiditis in detail and also tubercles seen in miliary tuberculosis. He also described in detail the dreaded complication of CRAO and the disease of stress; central serous choroidoretinopathy. If that was not all, the first intra-vitreal manipulations were performed by him. His astute observations also led to the postulation that retinitis pigmentosa was often associated with perceptive deafness in 1858. This fact was posthumously reviewed by Usher.Last but not the least, he also gave early descriptions of optic neuritis and described the embolism of retinal artery.e) Neurophthalmogy: He laid down the foundation of modern neuro-ophthalmology by postulating that the information received by the eyes in the retina was processed in the brain where final image was formed. As early as 1860, he demonstrated that blindness is linked to cerebral disorders and very often from the optic neuritis. He also concluded that brain tumours manifested as papilledema in eye. He described different types of hemianopias and also theorized that unilateral cerebral disease is connected to homonymous hemianopias. Early descriptions of the elusive chronic progressive ophthalmoplegia were provided by him.Diagnostic Tools: The foundations of modern glaucoma investigation were laid by this visionary whose clinical insight transformed ophthalmology forever. He was among the first to recognize that glaucoma was associated with increased intraocular pressure—and more importantly, that this pressure needed to be objectively measured. With relentless experimentation and keen observation, he developed the first practical tonometer, marking a milestone in diagnostic ophthalmology.His contributions did not end there. Through systematic study and meticulous documentation, he described the characteristic visual field defects seen in glaucoma. To evaluate these defects more precisely, he introduced perimetry into clinical practice, revolutionizing visual field assessment.His surgical contributions were equally groundbreaking. Every medical graduate is familiar with the Von Graefe knife (Figure-2)- a precision instrument that trans- formed cataract surgery and refined lens extraction techniques. While ancient pioneers like Sushruta had introduced the couching technique centuries earlier, modern cataract surgery found new precision and safety through von Graefe’s innovations. Another remarkable instrument, the Adson-Graefe forceps (Figure-3)- a 125mm tissue forceps were designed by him.f) Strabismus: He devised a method of measuring the heterophorias by placing two prisms with base up in one eye and base down in the other to dissociate the image. The power of prism that caused the unification of the two images quantified heterophoria.g) Advances in ophthalmology literature: Very initial phase in his career in 1854, he founded the “Archiv für Ophthalmologie,” later which was named in his honour. He also in the year 1857 founded “German Ophthalmological Society.” This extraordinary journal in ophthalmology was the first in the world and exists till date. He also organised the first conference of ophthalmologists where scientific papers were presented and discussed and this in the era of World War II. Figure 2: Von Graefe knife

Historical LanesDOS Times - Volume 31 Number 4, January-February 2026 10 DOS Times - Volume 31 Number 4, January-February 2026 11Figure 3: VVon Graefe fixation forcepsConclusionWhile penning the article, I found myself awed by the scientific temperament of this extraordinary man. Armed only with rudimentary instruments and a zeal to learn and discover, he uncovered the mysteries of mind and its extension: the eye. Today we have various subspecialities of ophthalmology and we take pride in being members of various ophthalmological societies. For this we are grateful to the man who laid the pillars of modern ophthalmology: “Albrecht von Graefe.”References1. Khadamy J (Auoftust 27,2024) Ne Rise of Ophthalmoloofty as Speciality: Albrecht von Graefe’s Pioneerinoft Contributions. Cureus 16(8) e679732. Grzybowski A, Ascaso FJ: Sushruta in 600 B.C. introduction extraocular expulsion of lens material. Acta Ophthalmol. 2014,92:194-7.10.1111/aos.12037.3. Cadooftan M. Albrecht von Graefe. Life in a fast lane.4. Usher CH. On the inheritance of retinitis pioftmentosa, with notes cases. Royal London Ophthalmolooftical Hospital Report.1914;19:122-236.5. Ivanisevic M et al. Int Ophthalmol. 2020 Apr. Albrechtvon Graefe (1828-1870) and his contributions to the development of ophthalmoloofty.6. Obioma- Elemba Jacqueline E, Ubani U.A, Akujobi A. U, Ebisike Philips I. Comparison of Von Graefe and Maddox Rod Techniques in Measurement of Lateral Phoria. International Journal of Health Sciences and Research Volume 14; Issue: 10; October 2024. ISSN: 2249-9571.

DOS Times - Volume 31 Number 4, January-February 2026 12 DOS Times - Volume 31 Number 4, January-February 2026 13Tracing the OriginsDOS Times - Volume 31 Number 4, January-February 2026Evolution of Antiglaucoma Pharmacotherapy: From Empiricism to Targeted TherapyGlaucoma, historically described by the ancient Greeks as glaukos—referring to a bluish-gray discoloration of the eye—has long been associated with irreversible vision loss.[1] While early physicians could recognize visible ocular changes, meaningful understanding of glaucoma’s pathophysiology and targeted treatment strategies evolved slowly over centuries.[2] It was not until the late 19th century that reduction of intraocular pressure (IOP) emerged as the cornerstone of management, marking the beginning of modern antiglaucoma pharmacotherapy.[3]Although surgical interventions such as iridectomy were introduced in the mid-1800s,[4] early pharmacologic approaches to IOP control were largely empirical and derived from botanical sources rather than receptorbased science.[5]Early Pharmacologic Foundations1860s – Calabar BeanClinicians observed that Calabar bean (the source of physostigmine) induced miosis and incidentally lowered IOP.[5]1870s – MioticsPhysostigmine (eserine) and later pilocarpine became the first cholinergic agents deliberately used for glaucoma management.[3] By enhancing aqueous humor outflow through the trabecular meshwork, these agents established the foundation of glaucoma pharmacotherapy.[1]However, their need for frequent dosing and significant side effects limited long-term use.[6]Dr. Poonam SheoranMBBSLady Hardinge Medical College and Hospitals, New DelhiHarshita Garg MBBS | Poonam Sheoran MD | Piyush Kumar R. Ramavat MSDepartment of Ophthalmology, Lady Hardinge Medical College and Hospitals, New DelhiExpansion of Drug Classes in the 20th CenturyAdrenergic AgentsEarly 1900s:Epinephrine was found to reduce IOP by decreasing aqueous production and enhancing outflow.[5]1980s–1990s:Development of selective alpha-2 adrenergic agonists such as apraclonidine and brimonidine improved tolerability and expanded use in both acute and chronic IOP management.[7]Beta-Adrenergic BlockersThe introduction of topical timolol in the 1970s revolutionized glaucoma treatment.[8] By effectively reducing aqueous humor production with fewer systemic effects than oral beta blockers, timolol rapidly became first-line therapy for open-angle glaucoma.[3] Additional agents, including levobunolol and metipranolol, followed.[6]Carbonic Anhydrase Inhibitors (CAIs)1950s: Systemic agents such as acetazolamide effectively lowered IOP but were limited by systemic adverse effects.[9]1990s: Topical formulations (dorzolamide, brinzolamide) offered localized efficacy with improved safety, facilitating widespread adjunctive use.[10]Prostaglandin Analogs: A BreakthroughThe most significant advance in glaucoma pharmacology came with prostaglandin analogs. Following the discovery that PGF2α derivatives enhance uveoscleral outflow,[11]latanoprost was developed and approved by the U.S. FDA

DOS Times - Volume 31 Number 4, January-February 2026 12 DOS Times - Volume 31 Number 4, January-February 2026 13Tracing the OriginsDOS Times - Volume 31 Number 4, January-February 2026in 1996.[12] Subsequent agents—travoprost, bimatoprost, and tafluprost—offered once-daily dosing, robust IOP reduction, and improved adherence, establishing prostaglandins as preferred first-line therapy.[1]Class of Drug Mechanism Concenteration (%)IOP Reduction Side EffectsProstaglandin AnaloguesIncrease uveoscleral flow 25-35 Iris pigmentation, hypertrichosis, Prostaglandin Associated Peri orbitopathy, punctate keratitis1.Latanoprost 0.0052.Bimatoprost 0.033.Travoprost 0.004Non-Selective Beta BlockerDecrease aqueous production20-30 Stinging, local anesthesia, Bradycardia, bronchospasm, hypotension, altered lipid profile if systemic absorption.Timolol 0.25-0.5Selectibe Beta BlockerDecrease aqueous production15-25 Stinging, local anesthesia, pulmonary side effectsBetaxolol 0.25-0.5Selective Alpha 2 Agonistdecrease aqueous production, increase uveoscleral flow20-30 Conjunctival blanching, ocular allergy, drowsinessBrimonidine 0.15Carbonic Anhydrase InhibitorsDecrease aqueous production15-20% (topical CAI),20-30% (systemic CAI)Punctate keratitis, ocular allergy, bitter taste, headache1.Dorzolamide 2 %2.Brinzolamide 1 %Rho Kinase InhibitorsIncrease conventional flow, decrease episcleral venous pressure15 Conjunctival hyperemia, hemorrhage, cornea verticillata1.Netarsudil 0.022.Repasudil 0.4ParasympathomimeticIncrease conventional outflow15-25 Miosis, brow ache, accommodative spasmPilocarpine 2-4 %Advances and Novel Therapeutic TargetsRho Kinase (ROCK) InhibitorsROCK inhibitors represent the first new glaucoma drug class in decades.[13] By relaxing the actin cytoskeleton of the trabecular meshwork, these agents directly enhance conventional aqueous outflow—the primary site of resistance in glaucoma.[14]

DOS Times - Volume 31 Number 4, January-February 2026 14 DOS Times - Volume 31 Number 4, January-February 2026 15Tracing the OriginsDOS Times - Volume 31 Number 4, January-February 2026Nitric Oxide–Donating Prostaglandin AnalogsLatanoprostene Bunod (LBN) combines prostaglandin analog activity with nitric oxide donation, enhancing aqueous outflow through both uveoscleral and trabecular pathways.[15] Clinical trials have demonstrated superior IOP reduction compared with timolol, with a safety profile similar to traditional prostaglandins.[15]Novel Prostaglandin DerivativesOmidenepag Isopropyl (OMDI) is a selective EP2 receptor agonist offering IOP-lowering efficacy comparable to existing prostanoids.[16]Sustained-Release Drug Delivery SystemsPoor adherence to chronic topical therapy remains a major challenge in glaucoma care.[17] Bimatoprost Implant (Durysta) provides months-long drug release, with demonstrated non-inferiority to timolol.[18] Repeated dosing is currently limited due to corneal endothelial safety concerns.Neuroprotective and Adjunctive StrategiesWhile IOP reduction remains the primary therapeutic goal, increasing attention is directed toward neuroprotection.[1] Nicotinamide (Vitamin B3) has shown early promise in improving retinal ganglion cell resilience.[19]References1. Weinreb RN, Aung T, Medeiros FA. The pathophysiology andtreatment of glaucoma. JAMA. 2014;311(18):1901–11.2. Quigley HA. Glaucoma. Lancet. 2011;377(9774):1367–77.3. Ritch R, Shields MB, Krupin T. The Glaucomas. 2nd ed. StLouis: Mosby; 1996.4. von Graefe A. Iridectomy in glaucoma. Arch Ophthalmol. 1857;3:456–555.5. Kaufman PL, Alm A. Adler’s Physiology of the Eye. 10th ed. St Louis: Mosby; 2003.6. Katz LJ, Ritch R. Medical therapy of glaucoma. Ophthalmol Clin North Am. 1997;10(3):405–18.7. Cantor LB. The evolving pharmacotherapeutic profile ofbrimonidine. Surv Ophthalmol. 2000;44 Suppl 1:S25–31.8. Zimmerman TJ, Kaufman HE. Timolol and intraocular pressure. Arch Ophthalmol. 1977;95(4):601–4.9. Becker B. Decrease in intraocular pressure in man by a carbonic anhydrase inhibitor. Am J Ophthalmol. 1954;37:13–15.10. Silver LH. Clinical efficacy and safety of topical carbonicanhydrase inhibitors. Surv Ophthalmol. 1998;42 Suppl 1:S107–13.11. Camras CB, et al. Mechanism of action of prostaglandins in glaucoma. Surv Ophthalmol. 1992;36 Suppl:S27–34.12. Camras CB. Latanoprost treatment for glaucoma. Ophthalmology. 1996;103(11):1916–24.13. Tanihara H, et al. Ripasudil for glaucoma. Ophthalmology. 2015;122(7):1480–8.14. Weinreb RN, et al. Primary open-angle glaucoma. Nat Rev Dis Primers. 2018;4:17067.15. Weinreb RN, et al. Latanoprostene bunod 0.024% in glaucoma. Ophthalmology. 2016;123(5):965–73.16. Aihara M, et al. Omidenepag isopropyl versus latanoprost in primary open-angle glaucoma. Ophthalmology. 2020;127(10):1334–45.17. Olthoff CM, et al. Noncompliance with ocular hypotensivetreatment. Ophthalmology. 2005;112(6):953–61.18. Lewis RA, et al. Bimatoprost sustained-release implant. Ophthalmology. 2020;127(12):1627–41.19. Williams PA, et al. Vitamin B3 modulates mitochondrial vulnerability in glaucoma. Science. 2017;355(6326):756–60.

15Post Graduate EssentialsDOS Times - Volume 31 Number 4, January-February 2026 14 DOS Times - Volume 31 Number 4, January-February 2026 DOS Times - Volume 31 Number 4, January-February 2026Overview on Macular Hole and Its ManagementIntroductionWhen a patient describes that straight lines appear broken or that a loved one’s face has a dark spot in the centre, the clinician must recognise both the visual and psychological distress these symptoms represent. A macular hole is not merely a structural injury of the retina; it affects reading, driving, mobility, selfconfidence, and independence. Historically, macular hole carried a poor prognosis until the 1990s, when OCT imaging and modern vitrectomy transformed the therapeutic landscape. Today, closure rates exceeding 90–95% are common for standard-sized idiopathic macular holes.[1]This review integrates modern classification, diagnostic standards, surgical techniques, and humanised patientcentred care to provide a comprehensive perspective on MH (Figure-1).EpidemiologyGlobal PrevalenceMacular hole is relatively uncommon but clinically significant, particularly in ageing populations. Population-based studies estimate the prevalence of idiopathDr. Sanjeev Kumar Nainiwal MD, DNB, MNAMSSenior Professor Ophthalmology Sawai Man Singh, Medical College & Hospital, Jaipur RajasthanSanjeev Kumar Nainiwal MD, DNB, MNAMS | Dimple Nehra MBBS | Payal Singh MS | Rashmi MBBSVitreo Retinal Services, Department of Ophthalmology, Sawai Man Singh Medical College & Hospital, Jaipur, RajasthanAbstract: Macular hole (MH) is a full-thickness defect of the foveal retina that results in central visual loss, metamorphopsia, and significant impairment of daily functioning. Recent decades have transformed MH management from guarded prognosis to predictable recovery, owing to developments in high-resolution optical coherence tomography (OCT), refined understanding of vitreoretinal interface dynamics, and innovations including inverted internal limiting membrane (ILM) flap and advanced graft techniques. This review provides an integrated understanding of MH epidemiology, etiology, pathogenesis, classification (Gass, IVTS, CLOSE), clinical features, diagnostic modalities, and evidence-based management. Consideration is given to surgical nuances, high-myopia–related challenges, biological scaffolds, intraoperative OCT, and postoperative strategies. A humanised patient-centric approach underlies the discussion, emphasizing shared decision-making and realistic expectation-setting.Keywords: Macular hole, OCT, inverted ILM flap, Gass classification, vitrectomyFigure 1: (A) Fundus photograph shows a full thickness MH in a male (B) OCT photograph shows a full thickness MH of the same patient.ic full-thickness macular hole at approximately 0.2–0.8 per 1,000 adults, with increasing prevalence in older age groups.[2] Women are affected more often than men, reflecting differences in vitreoretinal interface anatomy and vitreous liquefaction. The Blue Mountains Eye Study and other large cohorts confirm greater MH occurrence in individuals over 60 years of age, correlating with the natural progression of posterior vitreous detachment (PVD).[2]Prevalence in IndiaIn India, data from community-based studies suggest a prevalence of 0.17%, with mean age around 67 years.[3] The availability of OCT has improved the detection of early or small holes, and MH is increasingly recognised in routine screenings and cataract surgery evaluations. India also has a significant burden of high myopia and posterior

Post Graduate EssentialsDOS Times - Volume 31 Number 4, January-February 2026 16staphyloma, predisposing individuals to more complex MH presentations and macular hole retinal detachment (MHRD).EtiologyMH may arise from multiple influences. 1. Idiopathic (Most Common)Idiopathic MH accounts for >80–90% of cases. It is strongly associated with age-related vitreous liquefaction, perifoveal vitreous adhesion, and Müller cell dysfunction.2. Traumatic Macular HoleSeen commonly in young males following blunt trauma, resulting from contrecoup forces and rapid anteroposterior vitreous traction. Many traumatic MH may spontaneously close in 2–4 months.3. High Myopia with Posterior StaphylomaExcessive axial elongation, scleral thinning, posterior staphyloma, and tangential traction increase MH risk; these cases may associate with retinal detachment (MHRD) and have worse prognosis.4. Other Documented Causes• Cystoid macular edema (CME)• Epiretinal membrane (ERM)• Vitreomacular traction syndrome (VMT)• Rhegmatogenous retinal detachment• Proliferative diabetic retinopathy• Hypertensive retinopathy• Solar retinopathy• Inadvertent laser exposure (including Nd:YAG, industrial)PathogenesisModern pathogenesis combines classical theories (from Gass) with OCT-derived insights (IVTS and Müller cell biomechanics).1. Vitreous Traction TheoryAge-related vitreous syneresis causes partial posterior vitreous detachment. Persistent vitreofoveal adhesion produces anteroposterior and tangential traction, initiating foveal dehiscence.[4]2. Müller Cell Cone HypothesisThe foveal centre relies on the structural “Müller cell cone.” Tangential traction + degenerative stress lead to vertical displacement and separation, producing a fullthickness defect.[5]3. Cystoid Degeneration Theory (Gass)Gass proposed that intraretinal cystoid spaces coalesce over the fovea, breaking through the external limiting membrane and evolving into a MH.[6]4. Combined Traction–Degeneration ModelOCT studies support a multifactorial mechanism:• Traction → foveal deformation• Cystoid spaces → weakening of tissue• ERM → added tangential stress• Müller cell dysfunction → impaired repair 5. High Myopia–Specific MechanismsIncludes posterior staphyloma, scleral thinning, vertical traction, foveoschisis, and schitic lamellar separation.ClassificationMacular hole classification has evolved from early ophthalmoscopic descriptions to precise OCT-based anatomical systems that guide prognosis and surgical planning. The earliest schema, proposed by Gass, remains foundational in understanding disease evolution. In Stage 1A, vitreo-foveal traction leads to loss of the normal foveal depression and appearance of a central yellow spot. Stage 1B reflects a foveal cyst with a yellow ring, representing deepening traction and an impending fullthickness defect. Stage 2 marks the formation of a small full-thickness dehiscence, commonly accompanied by an operculum. Stage 3 is characterised by a fully developed macular hole with the posterior hyaloid still attached.Stage 4 presents with complete posterior vitreous detachment and a full-thickness defect.[6] Although Gass’s system is historically influential, it lacks the anatomical precision that modern imaging provides.OCT revolutionised macular hole assessment and led to

17Post Graduate EssentialsDOS Times - Volume 31 Number 4, January-February 2026the International Vitreomacular Traction Study (IVTS) classification, which remains the most widely used system in current clinical practice. IVTS differentiates vitreomacular adhesion (VMA), in which the vitreous remains attached without deforming the fovea, from vitreomacular traction (VMT), where attachment distorts the inner retina or causes cystic changes. A full-thickness macular hole (FTMH) is defined as complete interruption of all retinal layers from internal limiting membrane (ILM) to retinal pigment epithelium. FTMH is further categorised by minimum linear diameter (MLD) into small (≤250 µm) (in Figure-2a), medium (251–400 µm), and large (>400 µm) (in Figure-2b), reflecting strong prognostic significance in closure rates and selection of surgical technique. IVTS also documents the presence or absence of VMT, which influences spontaneous hole evolution and determines the role of pharmacologic vitreolysis.[7]Advances in surgical techniques, especially those involving ILM manipulation, revealed that holes >400 µm exhibit diverse anatomical behavior not captured fully by IVTS size bands. Modern vitreoretinal surgeons therefore employ a more granular approach, conceptualised in the surgical “CLOSE” framework. Rather than a formal consensus classification, CLOSE offers a pragmatic method that stratifies large macular holes into subgroups (400–550 µm, 550–800 µm, 800–1000 µm, and >1000 µm), integrating OCT-based parameters such as base diameter, hole height, hole form factor, macular hole index, and the configuration of hole edges. These structural biomarkers are strongly correlated with surgical success, need for inverted ILM flap, suitability for free ILM patch or neurosensory retinal graft, and expected visual improvement.[8]Thus, Gass (Table-1), IVTS (Table-2), and CLOSE (Table-3) collectively provide a complementary hierarchy—Gass conceptualises pathogenesis, IVTS standardises diagnosis, and CLOSE optimises surgical decision-making in the era of advanced retinal reconstruction.Stage Description Key Features Clinical SignificanceStage 1A Impending macular hole Loss of foveal depression; central yellow spotEarly vitreofoveal traction; may resolve or progressStage 1B Impending macular hole with foveal cystYellow ring; intraretinal cyst outlining foveal detachmentRepresents deeper tractional failure; risk of progression to FTMHStage 2 Small full-thickness macular hole Small FTMH often <400 µm; operculum may be presentHighest risk of progression; early surgery improves outcomesStage 3 Full-thickness macular hole with attached posterior hyaloidMedium/large FTMH; posterior hyaloid remains attachedVitreous traction contributes to enlargementStage 4 Full-thickness macular hole with complete PVDLarge FTMH with full PVD Vitreous no longer exerts traction; stable configuration but often requires surgeryCategory Definition/Criteria OCT Characteristics Management ImplicationsVitreomacular Adhesion (VMA)Persistent vitreous attachment without retinal distortionNo intraretinal cysts or distortion; normal foveal contourObservation; low risk of progressionVitreomacular Traction (VMT)Vitreous attachment with morphological distortionCystic changes, schisis, foveal deformationConsider ocriplasmin or vitrectomy depending on symptomsFull-Thickness Macular Hole (FTMH)Complete interruption of all retinal layersDefined by MLD measurement Requires size-based subclassificationTable 1: Gass Clinical Classification of Macular Hole.

Post Graduate EssentialsDOS Times - Volume 31 Number 4, January-February 2026 18Category Definition/Criteria OCT Characteristics Management ImplicationsSmall FTMH MLD ≤ 250 µm Narrow vertical gap; less cystic changeMay observe briefly; excellent surgical prognosisMedium FTMHMLD 251–400 µm Moderate defect with surrounding cystsPPV + ILM peeling standardLarge FTMH MLD > 400 µm Wide defect; often flattened edges; cystic cuffPrefer inverted ILM flap for higher closure ratesSize CategoryTypical OCT Features Associated Structural BiomarkersPreferred Surgical Approach400–550 µm Moderate MLD; elevated edges Good hole height; favourable HFF; limited base diameterWide ILM peeling; gas tamponade550–800 µm Large MLD; broad base; cystic cuff Reduced MHI; higher vertical traction componentInverted ILM flap strongly recommended800–1000 µm Very large hole with flat edges Significant base widening; outer retinal disruptionFree ILM flap, ILM insertion, or neurosensory retinal graft>1000 µm (Giant MH)Extremely large FTMH; chronic appearanceOften absent ELM/EZ; staphyloma in myopiaNeurosensory graft, amniotic membrane, or capsule flapTable 2: IVTS OCT-Based Classification of Macular Hole.Figure 2: (A) Small Macular Hole of diameter 230um (B) Large Macular Hole of diameter 472um.Table 3: CLOSE Surgical Classification for Large Macular Holes.Clinical FeaturesPatients with macular hole typically present with gradual but disturbing changes in central vision. Metamorphopsia, micropsia, central blurring, or a central scotoma are common complaints, and many describe difficulty reading fine print or recognising faces. Straight lines may appear wavy, and a dark spot may interfere with fixation. Symptoms often correspond to structural retinal distortion seen on OCT, where early foveal detachment and cystic spaces precede development of full-thickness defects. Visual acuity in early stages may remain relatively preserved, but functional impairment—particularly reading discomfort or reduced contrast sensitivity—can precede measurable acuity loss. Fundus examination in a full-thickness macular hole reveals a round, well-demarcated foveal defect with loss of the foveal reflex; an operculum may be floating anteriorly. In chronic cases, pigment changes may appear at the edges, and the retina may appear thinned. Clinical features should always be

19Post Graduate EssentialsDOS Times - Volume 31 Number 4, January-February 2026correlated with OCT findings to avoid misclassification and ensure accurate prognostication.DiagnosisA comprehensive diagnostic evaluation is essential not only for identifying a macular hole but also for determining prognosis, guiding surgical planning, and counselling the patient. Modern evaluation relies heavily on multimodal imaging, yet classical tests still hold significant clinical relevance. 1. Direct Ophthalmoscopy:Direct ophthalmoscopy remains an accessible first-line method for identifying foveal abnormalities, especially in early stages where subtle loss of foveal contour or a central yellow spot may be appreciated. Although resolution is limited compared to slit-lamp biomicroscopy, ophthalmoscopy allows rapid detection of gross structural changes, operculum, and pigment alterations, serving as an important bedside screening tool.2. Slit-Lamp Fundus Biomicroscopy:Slit-lamp examination with a fundus lens provides high-magnification evaluation of the macula and remains a cornerstone of clinical diagnosis. It allows precise visualisation of the foveal defect, its margins, cystic changes, and operculum. In early impending macular holes, the foveal cyst and yellow ring described by Gass can be detected. Although largely supplanted by OCT for objective staging, slit-lamp biomicroscopy remains invaluable for correlating structural findings with patient symptoms and guiding differential diagnosis.3. Watzke–Allen Test:The Watzke–Allen slit beam test is a functional assessment that helps determine whether a full-thickness defect exists. A thin vertical slit beam is projected across the fovea, and patients with a macular hole typically report a break or narrowing in the line. While not specific, the test provides useful adjunctive information where imaging is unavailable or equivocal, and it reflects functional foveal disruption.4. Laser Aiming Beam Test:This test projects a small, bright laser spot over the fovea. When a full-thickness macular hole is present, the patient may perceive distortion or a missing spot corresponding to the scotoma. It gives functional corroboration of structural defects and aids in distinguishing macular hole from lamellar defects or metamorphopsia due to epiretinal membranes.5. Optical Coherence Tomography (OCT):OCT is the gold standard for diagnosing macular hole and provides quantitative metrics crucial for classification and prognosis. Key parameters include minimum linear diameter (MLD), base diameter (BD), hole height, hole form factor (HFF), macular hole index (MHI), and the integrity of the external limiting membrane (ELM) and ellipsoid zone (EZ). OCT confirms the full-thickness nature of the hole, assesses vitreomacular traction, identifies cystic changes, and evaluates chronicity. The morphology of the outer retinal layers is a strong predictor of postoperative visual recovery.Minimum Linear Diameter (MLD)The minimum linear diameter represents the narrowest point of the macular hole at the mid-retinal level. It is a critical determinant of prognosis, as smaller MLD values correlate with higher rates of anatomical closure and better postoperative visual acuity. Clinically, macular holes less than 400 μm generally have more favorable outcomes because they reflect less tangential traction and better-preserved foveal tissue.Basal Diameter (BD)The basal diameter is measured at the level of the retinal pigment epithelium and reflects the degree of centrifugal, tangential expansion of the hole. A smaller BD is associated with superior functional and anatomical outcomes. Larger basal diameters typically indicate chronicity and more extensive photoreceptor loss, which can limit postoperative visual recovery.Hole Height (HH)Hole height is defined as the maximum perpendicular distance from the RPE to the innermost vitreoretinal interface at the center of the hole. It quantifies the extent of anteroposterior traction. Larger hole heights are associated with worse long-term postoperative visual acuity, likely due to greater retinal stretching and photoreceptor displacement.Hole Form Factor (HFF)The hole form factor is one of the earliest OCT-derived predictive indices.

Post Graduate EssentialsDOS Times - Volume 31 Number 4, January-February 2026 20Figure 3: Hole Forming factor formula.It is calculated using the formula:HFF=(Left arm length(c) + Right arm length(d))/Basal diameter of macular Hole (a)Higher HFF values reflect steeply sloping edges that tend to approximate more readily with gas tamponade. Values above 0.9 have historically been associated with favorable surgical outcomes, as this configuration allows improved centripetal closure.Ellipsoid Zone (EZ) IntegrityThe ellipsoid zone appears on OCT as a distinct hyper-reflective band corresponding to the inner segments of photoreceptors. Disruption or discontinuity of this layer indicates photoreceptor damage and is strongly predictive of limited visual recovery even if anatomical closure is achieved. Preoperative EZ defect length correlates with postoperative macular sensitivity and final best-corrected visual acuity, making it one of the most important functional prognostic markers.Macular Hole Index (MHI)The macular hole index is calculated as: MHI= Macular Hole height(b)/Basal diameter (a) It represents the relative contribution of vertical traction compared with basal expansion. MHI values greater than 0.5 have been associated with improved anatomical closure and better postoperative visual outcomes.Diameter Hole Index (DHI)The diameter hole index is derived as:DHI=Minimum hole diameter(c)/Basal diameter(a)This ratio reflects the extent of tangential traction acting on the fovea. Larger DHI values suggest stronger centrifugal traction and a more unfavorable geometric configuration.Traction Hole Index (THI)The traction hole index is defined as:THI=Hole height(b)/Minimum hole diameter(c)It offers a refined understanding of the balance between anteroposterior and tangential forces. Higher THI values indicate dominant anteroposterior traction, which typically responds well to vitrectomy. A THI greater than 1.4, especially when accompanied by an MLD less than 310 μm, predicts high closure rates and strong postoperative visual outcomes.Postoperative OCT Closure PatternsPostoperative OCT helps categorize structural restoration following surgery. Type 1 closure shows a restored, smooth foveal contour without a residual neurosensory defect and is associated with the best visual prognosis. Type 2 closure exhibits persistent central tissue loss despite anatomical approximation. Imai’s classification further refines these into U-type (normal foveal contour), V-type (steep contour), and W-type (persistent central defect) patterns. These closure types correlate with preoperative indices such as EZ integrity, chronicity, and baseline hole dimensions, thereby aiding postoperative prognostic evaluation.Figure 4: Macular Hole Index (MHI)

21Post Graduate EssentialsDOS Times - Volume 31 Number 4, January-February 20266. Fundus Fluorescein Angiography (FFA):Although not routinely required, FFA may be used to exclude differential diagnoses such as choroidal neovascular membrane, central serous chorioretinopathy, or macular ischemia. A macular hole typically demonstrates a window defect without leakage, helping differentiate it from inflammatory or neovascular processes.7. Amsler Grid Testing:This simple, patient-oriented test provides qualitative assessment of metamorphopsia and central scotoma severity. Patients with macular holes often report missing central squares or distortion, complementing OCT findings and serving as a monitoring tool for symptom progression.8. Microperimetry:Microperimetry assesses central retinal sensitivity and fixation stability, offering insights into functional outcomes beyond visual acuity. It is particularly useful in postoperative evaluation, where it correlates with the restoration of outer retinal layers and functional integration.9. Additional Imaging (as indicated):Ultra-widefield imaging or swept-source OCT may be employed in high myopia to assess posterior staphyloma and macular architecture. These modalities contribute to identifying risk factors for macular hole retinal detachment and tailoring surgical strategy.Management Management of macular hole has evolved dramatically over the past three decades, transitioning from a once hopeless condition to one with highly predictable anatomical and functional recovery. The choice of management is determined by hole size, chronicity, vitreomacular interface configuration, patient symptoms, and OCT biomarkers. Current strategies range from careful observation in selected early stages to advanced reconstructive vitreoretinal procedures for large and refractory macular holes. Each stage of management is guided by the underlying pathophysiology, as described by Gass and subsequently refined by OCT-based classifications. The aim of treatment is to relieve traction, approximate the retinal edges, promote glial bridging, and restore the outer retinal architecture, thereby maximising visual outcomes.1. Observation and Non-Surgical Management:Observation remains appropriate for Stage 1 Gass lesions and for small full-thickness macular holes ≤250 μm, particularly when symptoms are minimal or when OCT indicates stable morphology. Spontaneous closure, although uncommon, has been reported in approximately 3–11% of small holes, especially when acute and associated with relief of vitreofoveal traction. Patients should be monitored with OCT every 4–6 weeks. Pharmacologic vitreolysis with ocriplasmin, as evaluated in the MIVI-TRUST trials, is indicated only in eyes with symptomatic vitreomacular traction and small macular holes ≤250 μm. Although the drug can induce vitreous separation and hole closure, its effectiveness is limited, with closure rates of around 40%, and the risk of dyschromatopsia and photopsia mandates careful patient selection. Overall, non-surgical management plays a limited role in modern practice but remains relevant in early or minimally symptomatic cases.2. Standard Pars Plana Vitrectomy with ILM Peeling:Pars plana vitrectomy (PPV) with internal limiting membrane (ILM) peeling remains the standard approach for most small and medium macular holes. The procedure involves induction of posterior vitreous detachment (if not already present), removal of the cortical vitreous, and staining of the ILM using Brilliant Blue G or indocyanine green to facilitate a circumferential peel of approximately 2–3 disc diameters around the fovea. ILM peeling relieves tangential traction, reduces the risk of reopening, and promotes glial migration across the defect. Closure rates for small and medium holes routinely exceed 90–95%, and anatomical success translates into meaningful functional gains, particularly when the ELM and ellipsoid zone are intact preoperatively. Early RCTs and comparative studies (e.g., Kelly & Wendel’s pilot study[1] and subsequent series ) established vitrectomy as a transformative therapy for macular hole, and its effectiveness remains consistent across subgroups stratified by IVTS classification.[7]3. Inverted ILM Flap Technique for Large Holes:The inverted ILM flap technique, introduced by Michalewska et al., represents a major advancement in managing large macular holes, especially those >400 μm. Instead of removing the ILM entirely, a remnant is preserved, inverted, and draped over or into the macular hole. This flap acts as a biological scaffold supporting Müller cell proliferation and enhancing gliotic sealing.

Post Graduate EssentialsDOS Times - Volume 31 Number 4, January-February 2026 22Multiple meta-analyses have demonstrated superior closure rates (95–98%) and better early visual recovery with the inverted flap technique compared to ILM peeling alone in large holes.[9] Structural restoration of the ELM and ellipsoid zone occurs more completely with the flap technique, correlating with superior long-term visual outcomes. Variants such as temporal flaps, hemi-flaps, viscoelastic-stabilised flaps, and fovea-sparing flaps have been developed to individualise treatment and reduce surgical trauma.4. Free ILM Grafts, Neurosensory Retinal Grafts, and Other Advanced Techniques:For very large (≥700–1000 μm) or refractory macular holes, more extensive reconstructive techniques may be required. Free ILM patch grafts, first used for persistent macular holes when ILM around the fovea has already been peeled, provide an alternative scaffold and achieve closure when conventional flaps are not feasible. Neurosensory retinal grafts, described by Morizane et al., involve transplanting a small piece of peripheral retina into the macular defect to promote tissue integration and closure. Amniotic membrane plugs and lens capsule flaps offer additional options in eyes with limited residual ILM or severely thinned macula, with promising anatomical results reported in small series. These approaches are generally reserved for complex, chronic, or giant macular holes and often require postoperative silicone oil tamponade to stabilise the graft.5. Management of Macular Hole in High Myopia:Macular hole surgery in high myopia presents unique challenges due to posterior staphyloma, retinal thinning, and reduced Müller cell support. High myopia is associated with poorer healing capacity and increased risk of macular hole–related retinal detachment (MHRD). In such eyes, fovea-sparing ILM peeling, longer-acting gas tamponades, or silicone oil may be used. Inverted ILM flap techniques have demonstrated high anatomical success, with closure rates above 90% in some prospective series, including those with associated retinal detachment. Swept-source OCT aids surgical planning by visualising the contour of the staphyloma and guiding flap positioning.6. Gas and Silicone Oil Tamponade:Internal tamponade remains central to macular hole surgery. Sulfur hexafluoride (SF6) and perfluoropropane (C3F8) are the most commonly used gases. SF6 provides moderate duration and is preferred for small to medium holes, whereas C3F8 offers longer tamponade suitable for large holes but may require prolonged postoperative positioning. Silicone oil is useful in patients unable to posture, in high myopia with retinal detachment, and in complex cases requiring graft stabilisation. Several studies suggest that face-down positioning may be shortened or omitted for holes <400 µm, without compromising outcomes.7. Intraoperative OCT and Technological Advances:The emergence of intraoperative OCT (iOCT) enables real-time verification of ILM peeling completeness, flap placement, and foveal configuration, improving precision and reducing unnecessary manipulation. Ehlers et al. demonstrated that iOCT alters surgical decision-making in a substantial proportion of macular hole surgeries.[10]Small-gauge vitrectomy (25G and 27G) further reduces surgical trauma, enhances postoperative comfort, and maintains comparable closure rates to larger-gauge systems. Brilliant Blue G has become the dye of choice due to its superior safety profile and selective ILM staining.8. Postoperative Care and Reopening Prevention:Proper postoperative follow-up ensures timely detection of complications such as persistent macular hole, reopening, cystoid macular edema, and epiretinal membrane formation. Reopening, reported in 5–10% of cases, is associated with incomplete ILM peel, persistent traction, or new epiretinal membrane formation. OCT monitoring allows assessment of outer retinal restoration and correlation with functional recovery. Microperimetry is increasingly used to evaluate fixation stability and central retinal sensitivity during postoperative rehabilitation.Complications Complications following macular hole surgery can occur intraoperatively or postoperatively, although modern surgical refinements have significantly reduced their incidence. Intraoperative complications include iatrogenic retinal breaks, vitreous hemorrhage, and accidental lens touch in phakic eyes, particularly during induction of posterior vitreous detachment, where adhesion is firm or visualization is suboptimal. Use of small-gauge vitrectomy systems and intraoperative OCT has helped minimise these risks by improving tissue visualization and reducing

23Post Graduate EssentialsDOS Times - Volume 31 Number 4, January-February 2026mechanical trauma. Postoperative complications remain more common and include cataract progression, which affects the majority of phakic patients, and transient elevation of intraocular pressure due to gas expansion or retained viscoelastic. Macular hole reopening is a well-recognised complication and occurs in approximately 5–10% of cases, typically triggered by the formation of an epiretinal membrane, incomplete ILM peel, new vitreomacular traction, or trauma. Cystoid macular edema and disruption of the outer retinal layers may delay visual recovery, whereas persistent subfoveal fluid may be seen even in anatomically closed holes. In high myopia, complications such as macular hole retinal detachment are more frequent due to staphyloma-induced mechanical instability, necessitating careful follow-up and sometimes silicone oil tamponade. Despite these potential complications, most are manageable with timely clinical intervention and do not prevent overall anatomical success.Prognosis The prognosis for macular hole has improved dramatically since the advent of modern surgical techniques, with closure rates regularly exceeding 90% for small and medium holes and 95–98% for large holes treated with inverted ILM flap approaches.[9] Visual prognosis is closely linked to preoperative morphological features on OCT, particularly the integrity of the external limiting membrane (ELM) and ellipsoid zone (EZ). The restoration of these outer retinal layers is a powerful predictor of postoperative visual acuity, and their integrity correlates with improved microperimetric sensitivity and fixation stability. Duration of symptoms is another critical determinant, as long-standing holes often exhibit greater photoreceptor loss and reduced responsiveness to surgical repair. Larger macular holes (>500–700 µm), those associated with persistent vitreomacular traction, and holes in highly myopic eyes carry a guarded prognosis due to chronic tractional changes, foveoschisis, and structural thinning. Reopening of the macular hole, although uncommon, may negatively impact long-term visual recovery and is more likely in eyes with incomplete ILM peeling or postoperative ERM formation. Nevertheless, even in such scenarios, secondary interventions such as free ILM graft or retinal autotransplantation have shown promising anatomical and functional outcomes. Overall, with appropriate classification-based surgical planning and OCT-guided postoperative monitoring, prognosis for both anatomical closure and meaningful visual improvement remains highly favourable.ConclusionMacular hole, once considered a visually devastating condition, is now one of the most successfully treated entities in vitreoretinal surgery thanks to advances in imaging, refined classification systems, and sophisticated surgical techniques. The integration of Gass’s clinical staging, the OCT-based IVTS classification, and the surgically oriented CLOSE framework allows clinicians to approach each patient with a personalised strategy that reflects the structural and biomechanical context of the disease. Modern techniques, particularly the inverted ILM flap and its variants, have dramatically improved success rates for large and complex holes, while reconstructive approaches such as ILM free grafts and neurosensory retinal transplants offer hope for refractory and giant macular holes. Technological enhancements, including small-gauge vitrectomy and intraoperative OCT, continue to elevate surgical precision and safety. As management becomes increasingly anatomy-driven and patient-centred, emphasis on counselling, realistic expectation-setting, and postoperative rehabilitation is essential. The future of macular hole care will likely incorporate biological scaffolds, regenerative therapies, and artificial intelligence–assisted prognostication, further enhancing outcomes. Ultimately, contemporary macular hole treatment exemplifies how scientific innovation, surgical skill, and humanised patient care converge to restore not only anatomical alignment but also functional vision and quality of life.References1. Kelly NE, Wendel RT. Vitreous surgery for idiopathic macular holes: results of a pilot study. Arch Ophthalmol. 1991;109(5):654–659.2. Mitchell P, Smith W, Chey T, Wang JJ, Chang A. Prevalence of macular diseases in the Blue Mountains Eye Study. Ophthalmology. 1997;104(10):1742–1749.3. Prema R, George R, Sulochana KN, Hemamalini A, Vijaya L. Prevalence of macular hole in South India. Indian J Ophthalmol. 2008;56(6):437–442.4. Sebag J. Vitreous and macular hole formation. Surv Ophthalmol. 2003;48(2):215–234.5. Bringmann A, Reichenbach A, Wiedemann P. Role of Müller cells in the pathogenesis of macular holes. Prog Retin Eye Res. 2006;25(4):397–424.

Post Graduate EssentialsDOS Times - Volume 31 Number 4, January-February 2026 246. Gass JD. Idiopathic senile macular hole: its early stages and pathogenesis. Arch Ophthalmol. 1988;106(5):629–639.7. Duker JS, Kaiser PK, Binder S, de Smet MD, Gaudric A, Reichel E, Sadda SR, Sebag J, Sharma S, Stalmans P, Wolff B,Tadayoni R. The International Vitreomacular Traction StudyGroup classification of vitreomacular adhesion, traction, andmacular hole. Ophthalmology. 2013;120(12):2611–2619.8. Steel DHW, Rushton H, Riley R, Fletcher E, Charles S. TheCLOSE study: macular hole closure, lens outcomes, and safety evaluation. Eye. 2021;35:1–10.9. Shen Y, Chen X, Xu J, Zhang J, Zheng Q, Li W. Internal limiting membrane flap versus conventional ILM peeling for macularhole: a meta-analysis. PLoS One. 2020;15(11):e0239035.10. Ehlers JP, Tao YK, Farsiu S, Maldonado R, Izatt JA, Toth CA. Integration of intraoperative OCT in macular hole surgery. Ophthalmology. 2014;121(3):1783–1791.

25Post Graduate EssentialsDOS Times - Volume 31 Number 4, January-February 2026Retinal Vein Occlusion (RVO) – Current Concepts and UpdatesIntroductionRetinal vein occlusion (RVO) is the second most common retinal vascular disorder following diabetic retinopathy. It occurs due to obstruction of venous outflow from the retina, leading to vascular congestion, haemorrhage, edema, and ischemia. RVO affects both males and females equally and is particularly common in the elderly, though younger individuals may also be affected in the presence of systemic or hematologic risk factors.[1-3]Classification of Retinal Vein Occlusion1. Based on anatomical location of the occlusion (Figure-1):Dr. Afsana MSSenior Resident, Department of Ophthalmology, Lady Hardinge Medical CollegeAfsana[1] MS | Kaveri Birla[1] MBBS | Neha C Guliani[1] DNB | Rahul Bhatia[2] MS1. Department of Ophthalmology, Lady Hardinge Medical College2. Dr. Agarwal Eye Hospital, DelhiAbstract: Retinal vein occlusion (RVO) is the second most common retinal vascular disorder after diabetic retinopathy and a major cause of visual impairment. It results from obstruction of retinal venous outflow, leading to haemorrhage, macular edema, and retinal ischemia. RVO is classified anatomically into branch (BRVO), central (CRVO), and hemi-retinal (HRVO) types, and functionally into ischemic and non-ischemic variants based on capillary perfusion status. Advances in multimodal imaging—including optical coherence tomography (OCT), OCT angiography (OCTA), fundus fluorescein angiography, and ultra-widefield angiography—have enhanced early detection, quantification of ischemia, and risk stratification for neovascular complications. Management has evolved from laser photocoagulation to intravitreal pharmacotherapy, with anti-vascular endothelial growth factor (anti-VEGF) agents now established as first-line treatment for macular edema. Corticosteroids remain useful in selected cases. Emerging longer-acting biologics promise reduced treatment burden. This review highlights contemporary concepts in diagnosis, imaging, and management of RVO, emphasizing evolving therapeutic strategies that continue to improve visual outcomes.Figure 1: Classification of RVO.Table 1: Classification of RVO Based on Perfusion Status. Table 2: Risk Factors for Retinal Vein Occlusion.2. Based on retinal perfusion status (Table-1):Non-ischemic RVO can convert into ischemic RVO in 12–30% of cases during follow-up. Regular monitoring is essential.[4]Risk Factors for Retinal Vein Occlusion (Table-2)Type Non-Ischemic IschemicCRVO <10-disc diameters (DD) of non-perfusion>10 DDBRVO <5 DD of non-perfusion >5 DDGeneral Ocular SystemicAge >50 years Glaucoma HypertensionCigarette Smoking Elevated IOP Decreases ocular perfusion pressureOrbital neoplasmEndocrine orbitopathyDiabetes Mellitus Dyslipidemia, Renal DiseaseDrug therapy: oral contraceptive pills, diuretics, hypotensive drugs

Post Graduate EssentialsDOS Times - Volume 31 Number 4, January-February 2026 26Figure 2: Sectoral flame shaped haemorrhages along superotemporal arcade with hard exudates – Major BRVOIn Young Patients (<50 years) or Bilateral Involvement: Consider evaluating for:• Hypercoagulable states(e.g., Protein C/S deficiency, Factor V Leiden, Prothrombin gene mutation)• Hyperhomocysteinemia• Autoimmune diseases(e.g., antiphospholipid syndrome, Systemic Lupus Erythematosus)• Inflammatory conditions(e.g. Tuberculosis, sarcoidosis, Behçet’s disease, vasculitis)Clinical FeaturesBRVOTypes:• Major BRVO (Figure-2)• Macular BRVO (Figure-3)• Peripheral BRVOFeatures:• Sectoral retinal involvement• Flame-shaped intraretinal haemorrhages• Venous tortuosity• Cotton-wool spots• Macular edemaFigure 3: Macular BRVO.Figure 4: Flame shaped haemorrhages involving all 4 quadrant. CRVO (Figure-4)Features:• Involvement of all four quadrants• Extensive haemorrhages• Dilated and tortuous veins• Optic disc edemaDifferentiating non-ischemic vs Ischemic CRVO (Table-3)Parameter Nonischaemic CRVOIschemic CRVOIncidence ~80% ~20%

27Post Graduate EssentialsDOS Times - Volume 31 Number 4, January-February 2026Parameter Nonischaemic CRVOIschemic CRVOAge Young adults & past middle ageUsually, past middle ageSymptoms (Vision) VA usually > 6/60 Marked, sudden deterioration, often < 6/60 (esp. on waking)Pupil Normal RAPD present > 0.7 log unitsSite of Occlusion Further back in retro-laminar regionAt/near retrolaminar regionEarly Stages Mild to moderate dilatation of branches of central retinal veinMarked tortuosity & engorgement of veinRetinal HemorrhagesMild to moderate, mainly peripheralExtensive, involving periphery + posterior poleCotton-wool Spots Rare CommonOptic Disc Hyperemic, may be edematousMarked disc edemaMacula Normal or may show edemaGross hemorrhages & edemaFFA < 10-disc areas of capillary nonperfusion> 10-disc areas of capillary nonperfusionERG Minimal or no changeMarked reduction of b-wave amplitude (<60%)Table 3: Clinical Features of Non-Ischemic vs Ischemic CRVO.HRVO (Figure-5)Figure 5: Flame shaped haemorrhages involving superior hemiretina. Figure 7: Intraretinal fluid and subretinal fluid in case of CRVO.• Involves either superior or inferior hemiretinaLate Findings (Figure-6)• Hard exudates• Microaneurysms• Optociliary (retinochoroidal) shunts • Vascular sclerosis and sheathing• Vitreous hemorrhage• Tractional retinal detachment• Ocular neovascularizationMultimodal Imaging in RVO1. Optical Coherence Tomography (OCT) Figure-7• Key modality to assess macular edema and subretinal fluid• Hyperreflectivity of inner retinal layers indicate ischemia.Figure 6: Sclerosed vessels along inferior retina with hard exudates.

Post Graduate EssentialsDOS Times - Volume 31 Number 4, January-February 2026 282. Optical Coherence Tomography Angiography (OCTA) Figure-8:• Enables assessment of superficial (SCP) and deep capillary plexus (DCP)• Evaluates:• Capillary non-perfusion• Neovascularization• Collateral formation• Foveal Avascular Zone (FAZ) enlargement in both SCP and DCP3. Choroidal Imaging:• Choroidal Vascularity Index (CVI):Ratio of luminal to stromal area; increased CVI observed in non-occluded hemiretina of BRVO.Not routinely used in clinical practice4. Fundus Fluorescein Angiography (FFA):• Crucial for:• Defining ischemic status• Detecting capillary non-perfusion (Figure-9), neovascularization• Delayed venous filling is a classic findingIschemia Definitions via FFA• CRVO: >10 DD of non-perfusion• BRVO: >5 DD of non-perfusion*Capillary nonperfusion >10 disc-areas at the posterior pole of eyes with CRVO would suggest a high risk of neovascularisation.[5-7]5. Ultra-Wide Field Fluorescein Angiography (UWFA):figure 2. Ultra-widefield angiography demonstrating peripheral ischemia in BRVO.Ultra-widefield angiography has revolutionized the assessment of capillary nonperfusion• Detects peripheral ischemia more effectively• Ischemic Index:% of retina with non-perfusion / total retinal area45% correlates with increased risk of neovascularization*Total area of nonperfusion >75 disc-areas on ultrawidefield angiography have been correlated to ocular NV.*In BRVO, ischemic areas can range from 5 to 35 DD and are associated with increased risk of neovascularization elsewhere (NVE) over 2 years.• Leakage Index:Figure 8: 8*8 montage image of a non-ischemic CRVO patient. Figure 9: FFA showing areas of capillary non-perfusion in ischemic CRVO.

29Post Graduate EssentialsDOS Times - Volume 31 Number 4, January-February 2026Leakage area / total retinal area• Correlates with severity of cystoid macular edema (CME)ManagementMultidisciplinary approach is needed for optimal treatment.A. Systemic Management• Address modifiable systemic risk factors:• Blood pressure controlLandmark StudiesThe Branch Vein Occlusion Study (BVOS) study It was a landmark clinical trial conducted to evaluate the effectiveness of grid laser photocoagulation for macular edema secondary to branch retinal vein occlusion (BRVO).• Glycaemic control in diabetics• Lipid profile management• Smoking cessation• Renal function monitoring• In younger patients, work-up for thrombophilia or autoimmune conditions is essential.[8-9]B. Ophthalmological ManagementTreatment options include Anti VEGF, intravitreal steroids, laser photocoagulation and pars plana vitrectomy. (Figure-10)Figure 10: Treatment timeline.Table 4: Major Anti-VEGF Trials in BRVO.Conclusion: Retinal photocoagulation is considered the gold standard treatment for retinal neovascularisation causing vitreous haemorrhage. Trial for anti VEGF – indicated for BRVO/CRVO with macular edema (Table-4)Trial Name Study Design Key Findings Conclusion BRAVO (2010) Ranibizumab (0.3 mg & 0.5 mg) vs. ShamSignificant visual improvement in ranibizumab groupsApproved as first-line treatmentHORIZON (2014) Long-term BRAVO followupSome patients needed continued injectionsNeed for individualized treatmentRETAIN (2018) 4-Year Follow-up of BRAVO patients~50% of patients still required injectionsBRVO has a chronic componentVIBRANT STUDY (2016) Compared intravitreal aflibercept versus grid laserIntravitreal aflibercept is effective as compared to laserLess need of rescue therapy in intravitreal aflibercept group

Post Graduate EssentialsDOS Times - Volume 31 Number 4, January-February 2026 30Clinical Trial for CRVO (Table-6)The Central Vein Occlusion Study (CVOS) was a multicenter prospective study conducted in the early 1990s to better understand the natural history, complications, Trial Name Study Design Key Findings SCORE IVTA vs Laser No superiority over laser; higher cataract & IOP riskGENEVA Ozurdex vs Sham ≥15-letter gain at 90 daysTable 5: Intravitreal Steroid Trials.and treatment outcomes of Central Retinal Vein Occlusion. The CVOS also evaluated the effectiveness of grid laser photocoagulation for macular edema associated with CRVO. Although grid laser reduced angiographic macular edema, it did not produce a statistically significant improvement in visual acuity compared with simple observation. In addition, the study demonstrated that prophylactic or early panretinal photocoagulation (PRP) does not prevent the development of iris or angle neovascularization. Therefore, PRP is not recommended as a preventive treatment. Instead, the study recommended careful monitoring and performing PRP only after the development of at least two clock hours of iris neovascularization or any angle neovascularization.Clinical Trial on Brolucizumab (Table-7)Clinical Trials on Faricimab (Table-8)Trial Name Study Design Key Findings Conclusion CRUISE Ranibizumab (0.3 mg & 0.5 mg) vs. ShamSignificant visual improvement in ranibizumab groupsApproved as first-line treatmentCOPERNICUS & GALILEO Intravitreal aflibercept versus sham Better visual outcome in aflibercept treated groupNeed for individualized treatmentLEAVO Compared ranibizumab, aflibercept and bevacizumabRanibizumab was non inferior to aflibercept Aflibercept group required fewer injections Trial Name Study Design Key Findings Conclusion KITE & KESTREL (2022) Brolucizumab vs. Aflibercept Similar visual gains, fewer injectionsPromising option for BRVO higher inflammationKINGFISHER (2023) Brolucizumab 6 mg vs. Aflibercept 2 mgComparable efficacy, longer dosing intervalsReduced treatment burdenTrial Name Study Design Key Findings Conclusion BALATON (2023) Faricimab vs. Aflibercept in BRVOSimilar VA gains, better durabilityFaricimab extends treatment intervalsCOMINO (2023) Faricimab vs. Aflibercept in CRVOComparable VA improvement, better fluid controlFaricimab Reduced treatment burdenTable 6: Major Anti-VEGF Trials in CRVO.Table 7: Trials on Brolucizumab.Table 8: Trials on Faricimab.ConclusionOver the past three decades, the diagnosis and treatment of retinal vein occlusions have evolved significantly. Modern multimodal imaging has deepened our understanding of retinal vascular dynamics. Anti-VEGF therapy Trial for Intravitreal Steroids (Table-5)

31Post Graduate EssentialsDOS Times - Volume 31 Number 4, January-February 2026has transformed visual prognosis. Emerging longer-acting agents promise reduced treatment burden.As our therapeutic arsenal expands, so does our responsibility—to diagnose early, stratify risk accurately, and tailor therapy to each patient’s systemic and ocular profile.References1. Scott IU, Campochiaro PA, Newman NJ, Biousse V. Retinal vascular occlusions.The Lancet. 2020 Dec 12;396(10266):1927-40.2. Rogers S, McIntosh RL, Cheung N, Lim L, Wang JJ, Mitchell P, Kowalski JW, Nguyen H, Wong TY, International Eye Disease Consortium. The prevalence of retinal vein occlusion: pooleddata from population studies from the United States, Europe, Asia, and Australia. Ophthalmology. 2010 Feb 1;117(2):313-9.3. Mitchell P, Smith W, Chang A. Prevalence and associations of retinal vein occlusion in Australia: the Blue Mountains Eye Study. Archives of ophthalmology. 1996 Oct 1;114(10):1243-7.4. Frangieh GT, Green WR, Barraquer-Somers E, Finkelstein D. Histopathologic study of nine branch retinal vein occlusions. Archives of Ophthalmology. 1982 Jul 1;100(7):1132-40.5. Ehlers JP, Fekrat S. Retinal vein occlusion: beyond the acute event. Survey of ophthalmology. 2011 Jul 1;56(4):281-99.6. Ponto KA, Scharrer I, Binder H, Korb C, Rosner AK, Ehlers TO, Rieser N, Grübel NC, Rossmann H, Wild PS, Feltgen N. Hypertension and multiple cardiovascular risk factors increase the risk for retinal vein occlusions: results from the Gutenberg Retinal Vein Occlusion Study. Journal of hypertension. 2019 Jul 1;37(7):1372-83.7. Rath EZ, Frank RN, Shin DH, Kim C. Risk factors for retinal vein occlusions: a case-control study. Ophthalmology. 1992 Apr 1;99(4):509-14.8. Hayreh SS, Zimmerman B, McCarthy MJ, Podhajsky P. Systemic diseases associated with various types of retinal vein occlusion. American journal of ophthalmology. 2001 Jan 1;131(1):61-77.9. Central Vein Occlusion Study Group. Natural history and clinical management of central retinal vein occlusion. Arch Ophthalmol. 1997; 115:486-91.

Post Graduate EssentialsDOS Times - Volume 31 Number 4, January-February 2026 32Unmasking Atypical Optic Neuritis: A Case of Diagnostic Challenge and Visual Recovery IntroductionOptic neuritis is the inflammation of the optic nerve and is conventionally known to present unilaterally in young females with sudden diminution of vision associated with painful ocular movements. Most cases of typical optic neuritis present with a normal optic disc or a hyperaemic disc with oedema, with or without macular star at times. But in the absence of all such findings and the sudden onset of vision loss, atypical optic neuropathy remains an important differential. To our rescue, neuroimaging and serum markers play a major role in differentiating various entities of atypical optic neuritis. Atypical features of optic neuritis (ON)—including prominent optic disc oedema, bilateral involvement, and a poor response to standard treatments—are often associated with autoantibodies against aquaporin-4 (AQP4) and myelin oligodendrocyte glycoprotein (MOG).Specifically, neuromyelitis optica spectrum disorder (NMOSD)-related ON typically presents with bilateral involvement , severe visual acuity loss, limited response to acute-phase therapies, and poor recovery outcomes.[1][2] MRI of the Dr. Mohit Sharma MSFellow, Department of Pediatric Ophthalmology Strabismus and Neuro Ophthalmology, Dr Shroff’s Charity EyeHospital, New DelhiMohit Sharma MS | Soveeta Rath DNB, FICO | Shailja Tibrewal MS | Suma Ganesh MS, DNBDepartment(s) and institution(s)-Department of Pediatric Ophthalmology, Strabismus and Neuro-ophthalmology, Dr. Shroff’s Charity Eye Hospital, New DelhiAbstract: Typical optic neuritis (ON) presents with acute, unilateral visual loss, commonly associated with demyelinating diseases such as multiple sclerosis. However, even when the presentation is atypical, clinical diagnosis of optic neuritis should maintain a high level of suspicion and be guided by characteristic clinical features, serum markers and appropriate investigations. However, atypical presentations with negative serum marker are less commonly reported, posing diagnostic and therapeutic challenges. We report the case of a young female who presented with unilateral visual loss characterized by atypical features, including severe initial vision loss to perception of light (PL). Comprehensive investigations, including serologic testing for Myelin Oligodendrocyte Glycoprotein (MOG-IgG) and Aquaporin-4 (AQP4) antibodies, returned negative. MRI of the orbits showed a long segment of optic nerve enhancement without brain lesions. Despite the absence of specific biomarkers, the patient demonstrated significant visual recovery following extended intravenous methyl prednisolone, achieving a best corrected visual acuity of 6/18 over several weeks.optic nerves usually shows extensive lesions with long segments, and chiasmal involvement is reported in up to two-thirds of NMOSD patients.[3] Conversely, MOGantibody-associated disease (MOGAD)-related ON may also present with a profound drop in visual acuity, but is generally more responsive to corticosteroid treatment but with increased chance of recurrence. Notably, optic disc oedema is found in approximately 80% of MOGADON cases, sometimes accompanied by peripapillary haemorrhages. In rare double seronegative cases without conclusive serological evidence, strong clinical and radiological indicators become crucial. This guides clinicians to exclude functional (non-organic) pathology and justify the initiation of timely treatment. We report such a case of diagnostic dilemma that was promptly managed, resulting in the restoration of vision.Case ReportA 25-year-old female presented with a one-month history of diminished vision in the left eye, accompanied by pain on eye movement and headaches. She had no prior similar episodes, no trauma, no systemic illness, and no previous neurological symptoms. On clinical examination, her right eye visual acuity was 6/6, while the left eye had perception of light with inaccurate projection of rays and grade 3 RAPD. Fundus examination was normal in both eyes with no optic disc oedema. (Figure-1). Investigations showed that Optical Coherence Tomog-

33Post Graduate EssentialsDOS Times - Volume 31 Number 4, January-February 2026raphy (OCT) revealed a normal retinal nerve fibre layer (RNFL) but a reduced ganglion cell complex (GCC) in the left eye (Figur-2). Visual fields were normal in the right eye, and left eye fields could not be reliably performed. Contrast-enhanced MRI of the brain and orbits demonstrated left optic nerve T2 hyperintense signals with enhancement involving long segments of the optic nerves and mild thickening of the optic nerves (Figure-3). Laboratory evaluation showed negative anti-AQP4 (NMO) antibodies and negative anti-MOG antibodies. An infectious work-up was negative for tuberculosis, syphilis, HIV, and Lyme disease. Given the bilateral involvement of the optic nerves, a normal fundus appearance, the absence of systemic autoimmune disease, and negative AQP4 and MOG antibodies, the diagnosis of double seronegative atypical optic neuritis was made. The patient was treated with intravenous methylprednisolone (IVMP) at a dose of 1 g/day for five days. Following the treatment course, her visual acuity in the left eye improved significantly to 6/18. She was discharged on a tapering course of oral corticosteroids. At 3 months follow up, she has stable vision with no further recurrence and other neurological complaints.Figure 1: Shows normal fundus (no disc oedema) of both eyes.

Post Graduate EssentialsDOS Times - Volume 31 Number 4, January-February 2026 34Figure 2: Shows OCT images of macular ganglion cell complex which is normal in Right Eye and with complete loss in Left Eye.Figure 3: Shows T2 weighted hyperintense left optic nerve as compare to right, second coronal section showing left optic nerve enhancement and the sagittal section showing left optic nerve enhancement till chiasma. DiscussionEvaluation of optic nerve function is essential in all patients presenting with unexplained vision loss. This should include assessment of pupils, testing of colour vision and contrast sensitivity, as well as a thorough examination of the optic disc and macula. In this case, the patient presented with profound visual loss (perception of light positive, PL+) in the left eye and a grade 3 RAPD—an important clinical indicator suggestive of optic neuropathy. The next critical step in such presentations is contrast-enhanced Magnetic Resonance Imaging (MRI) of the brain and orbits. Imaging findings were consistent with atypical optic neuritis. However, serological testing for known causes of atypical neuritis, including aquaporin-4 (AQP4-IgG) and myelin oligodendrocyte glycoprotein (MOG-IgG) antibodies, returned negative. The patient showed partial visual recovery to 6/18 following intravenous methylprednisolone therapy. This clinical course, including the absence of both AQP4 and MOG antibodies, imaging positive findings and the observed recovery, favours an atypical presentation. Thus we categorise this case as a double seronegative optic neuritis. In such cases, further investigation into rarer causes of atypical optic neuritis is warranted.[4] However other possible etiologies like sarcoid, tuberculosis, other autoimmune disorder were also negative in our case. The optimal management strategy for seronegative atypical optic neuritis remains uncertain, particularly whether these cases should be treated identically to their seropositive counterparts. A large cohort study[5] demonstrated that while seropositive and seronegative patients differed in clinical presentation—seropositive patients more frequently exhibited profound visual acuity loss (≤0.1) and had a higher prevalence of motor symptoms—the overall relapse rates and long-term outcomes (complete, partial, or no remission) were comparable between the two groups. This suggests that, even in the absence of serological confirmation, patients with supportive clinical and radiological findings may benefit from early initiation of high-dose intravenous corticosteroids, particularly during acute attacks, after ruling out infectious, parainfectious, and other secondary causes. In our case, no infectious ethology was identified, and the patient was promptly initiated on intravenous methylprednisolone, followed by a tapering course of oral steroids, which led to substantial visual improvement. A similar case has been reported in a 35-year-old female with double seronegative optic neuritis, but a normal MRI, and positive RAPD.[6] However, unlike our patient, she did not respond to intravenous methylprednisolone and ultimately required plasma exchange, which resulted in dramatic visual recovery. This highlights the potential role of plasma exchange as a second-line therapy in steroid-unresponsive seronegative optic neuritis. ConclusionIn the absence of positive antibody markers, the diagnostic process must rely heavily on clinical signs such as a relative afferent pupillary defect (RAPD), and radiological findings. In our case, long-segment optic nerve enhancement on MRI, coupled with RAPD, prompted early initiation of immunosuppressive therapy, resulting in significant visual improvement. This case reinforces the principle that detailed clinical evaluation and targeted imaging remain central to the diagnostic and therapeutic approach in seronegative atypical ON.References1. Masuda H, Mori M, Uzawa A, Muto M, Uchida T, Ohtani R, et al. Recovery from optic neuritis attack in neuromyelitis optica spectrum disorder and multiple sclerosis. J Neurol Sci. 2016;367:375–9.2. Srikajon J, Siritho S, Ngamsombat C, Prayoonwiwat N, Chirapapaisan N. Differences in clinical features between

35Post Graduate EssentialsDOS Times - Volume 31 Number 4, January-February 2026optic neuritis in neuromyelitis optica spectrum disorders and in multiple sclerosis. Mult Scler J Exp Transl Clin. 2018;4:2055217318791196.3. Moheb N, Chen JJ. The neuro-ophthalmologicalmanifestations of NMOSD and MOGAD—A comprehensive review. Eye. 2023;37:2391–8.4. Greco G, Colombo E, Gastaldi M, Ahmad L, Tavazzi E, Bergamaschi R, et al. Beyond Myelin Oligodendrocyte Glycoprotein and Aquaporin-4 Antibodies: Alternative Causes of Optic Neuritis. Int J Mol Sci. 2023;24(21):15986.5. Jarius S, Ruprecht K, Wildemann B, et al. Contrasting disease patterns in seropositive and seronegative neuromyelitis optica: a multicentre study of 175 patients. J Neuroinflammation.2012;9:14.6. Mason MC, Marotta DA, Kesserwani H. Steroid-resistant double-seronegative optic neuritis responds favorably to plasma exchange. Cureus. 2021;13(5):e15260.

Post Graduate EssentialsDOS Times - Volume 31 Number 4, January-February 2026 36Congenital Lacrimal Fistula: A Rare Case PresentationIntroductionCongenital lacrimal fistula is a rare developmental anomaly of the lacrimal drainage system characterized by the presence of an abnormal epithelial-lined tract that connects the skin surface to the lacrimal sac or canalicular system. Although considered uncommon, with an estimated incidence of approximately 1 in 2,000 live births, the actual prevalence may be higher due to underreporting of asymptomatic cases.[2] These fistulas are typically identified as small openings located inferonasal to the medial canthus, most often in proximity to the lower punctum.The embryogenesis of the lacrimal drainage system plays a crucial role in understanding this anomaly. The system originates from a solid cord of surface ectoderm that becomes buried between the lateral nasal and maxillary processes. This epithelial cord subsequently canalizes to form the canaliculi, lacrimal sac, and nasolacrimal duct. Congenital lacrimal fistulas are believed to arise due to aberrant budding or incomplete separation of this epithelial cord during embryonic development, resulting in the formation of a supernumerary tract.[3,5] This tract may maintain a direct communication with the lacrimal sac or canalicular system, thereby predisposing patients to symptoms depending on the patency of the nasolacrimal duct.Clinically, congenital lacrimal fistulas may remain asymptomatic throughout life, particularly when the nasolacrimal drainage system is patent. However, symptoms develop when there is associated nasolacrimal duct (NLD) obstruction or recurrent infections. Common presenting features include epiphora, mucous or mucopurulent disDr. Divyansh Singla MBBSJunior Resident, Department of Ophthalmology, SGT Medical CollegeDivyansh Singla MBBS | J. P. Chugh B.D | Tulika Gupta MBBS, MS | Bhawna P. Khurana MS, FICO, FRCS | Sonakshi Sehrawat MSDepartment of Ophthalmology, SGT Medical College, Gurgaon, Haryana, Indiacharge, recurrent conjunctivitis, and local skin maceration.[4,8] In rare cases, patients may present later in adulthood, often due to progressive obstruction or increased awareness of cosmetic concerns.The importance of early recognition lies in the fact that this condition is readily treatable. Surgical management, tailored according to the presence or absence of associated obstruction, yields excellent anatomical and functional outcomes.[5] This report describes a case of congenital lacrimal fistula presenting in adulthood, highlighting the clinical features, diagnostic workup, and successful surgical management.Case ReportA 25-year-old female presented with complaints of intermittent watering from her right eye since birth. The epiphora was occasionally associated with mucopurulent discharge, particularly during episodes of upper respiratory tract infections. The patient reported that the symptoms were initially mild but had gradually increased in frequency and severity over the past few years, prompting her to seek medical attention.There was no history of trauma, previous ocular surgery, or acute inflammatory episodes involving the eye. The patient denied symptoms such as pain, redness, photophobia, blurred vision, or eyelid swelling. There was no history suggestive of sinus disease or nasal obstruction.Her systemic history was unremarkable, and there was no known family history of similar complaints or congenital anomalies. The absence of precipitating factors and the lifelong nature of symptoms strongly suggested a congenital etiology.Clinical FindingsOn examination, the patient was comfortable, and visual acuity was within normal limits in both eyes. External

37Post Graduate EssentialsDOS Times - Volume 31 Number 4, January-February 2026ocular examination revealed a small, pinpoint opening measuring approximately 1 mm in diameter, located inferomedial to the lower punctum on the right side.Closer inspection showed that the opening was epithelialized, with mild surrounding skin maceration, likely due to chronic discharge. On applying gentle pressure over the lacrimal sac area, mucopurulent material regurgitated through both the fistulous opening and the opposite punctum. This finding suggested a communication between the fistula and the lacrimal drainage system, along with distal obstruction.Slit-lamp examination of the anterior segment was unremarkable, with no signs of conjunctival congestion or corneal involvement. The tear meniscus height was increased on the affected side, consistent with impaired tear drainage.These clinical features are characteristic of congenital lacrimal fistula associated with nasolacrimal duct obstruction.[2,8]InvestigationsA comprehensive evaluation of the lacrimal drainage system was undertaken to confirm the diagnosis and guide management.Lacrimal Syringing and Probing: Syringing revealed regurgitation of fluid through the fistulous opening and the opposite punctum, indicating obstruction distal to the lacrimal sac. Probing helped delineate the anatomical pathway and confirmed communication of the fistulous tract with the lacrimal system.Fluorescein Dye Disappearance Test (FDDT): The test showed delayed clearance of dye (Grade +3), indicating impaired tear drainage and supporting the diagnosis of nasolacrimal duct obstruction.Dacryocystography (DCG): Imaging confirmed the presence of nasolacrimal duct obstruction and clearly demonstrated the fistulous tract communicating with the lacrimal sac. DCG remains a valuable diagnostic tool in delineating anatomical abnormalities in the lacrimal system.[4,5]Nasal Endoscopy: Endoscopic examination of the nasal cavity revealed no abnormalities such as septal deviation, turbinate hypertrophy, or masses that could contribute to obstruction. This step is essential to rule out secondary causes and to plan surgical intervention.Together, these findings established the diagnosis of congenital lacrimal fistula with associated nasolacrimal duct obstruction.ManagementThe management strategy was guided by the presence of symptoms and confirmed obstruction. While asymptomatic fistulas with a patent drainage system may be managed conservatively, symptomatic cases—particularly those associated with obstruction—require surgical correction.[5,7]In this case, the patient underwent external dacryocystorhinostomy (DCR) combined with fistulectomy under local anesthesia.The surgical procedure involved: A standard external DCR approach to create a direct anastomosis between the lacrimal sac and nasal mucosa, bypassing the obstructed nasolacrimal ductIdentification and careful dissection of the fistulous tractComplete excision of the tract to prevent recurrenceLayered closure of the wound with attention to cosmetic outcomeExternal DCR remains the gold standard due to its high success rate and direct visualization of the lacrimal sac and surrounding structures.[5,7] Although endoscopic DCR is an alternative, external DCR is often preferred in cases requiring simultaneous fistulectomy.Outcome and Follow-UpThe postoperative course was uneventful. The patient was managed with topical and systemic antibiotics along with nasal decongestants.Sutures were removed at 1 week Lacrimal syringing demonstrated a patent drainage pathway. The patient reported complete resolution of epiphora and discharge.The surgical site healed well with minimal scarring.At follow-up visits up to 3 months, there was no recurrence of symptoms or evidence of restenosis. The outcome observed in this case is consistent with previously reported high success rates of combined DCR and fistulectomy.[2,5]DiscussionCongenital lacrimal fistula is a rare entity first described by William Mackenzie in 1854.[1] The condition typically presents as a small cutaneous opening located inferona-

Post Graduate EssentialsDOS Times - Volume 31 Number 4, January-February 2026 38sal to the medial canthus and may be unilateral or, less commonly, bilateral.The pathogenesis is attributed to abnormal budding of the epithelial lacrimal cord during embryogenesis, leading to the formation of an accessory tract.[3,5] Histologically, the fistulous tract is lined by stratified squamous epithelium, similar to the normal lacrimal drainage system.The clinical presentation varies widely. Many patients remain asymptomatic, especially when the nasolacrimal duct is patent. However, when obstruction is present, symptoms such as epiphora, discharge, and recurrent infections become prominent.[2,8] The presence of mucopurulent discharge and regurgitation from both puncta and the fistula is highly suggestive of associated obstruction.Differential diagnoses include acquired lacrimal fistula secondary to trauma, infection, or prior surgery. However, the absence of such history and the presence of lifelong symptoms support a congenital origin.Management strategies depend on the functional status of the lacrimal drainage system:Asymptomatic cases: Observation without interventionSymptomatic without obstruction: Simple fistulectomy may suffice Symptomatic with obstruction: Combined DCR and fistulectomy is recommendedExternal DCR has consistently demonstrated high success rates exceeding 90%, making it the preferred approach in such cases.[5,7] Endoscopic techniques offer advantages such as absence of external scar but may be technically demanding and less suitable when fistulectomy is required.Learning Points• Congenital lacrimal fistulas are rare and may remain undiagnosed until adulthood[2]• Lifelong epiphora with a peri-punctal cutaneous opening is a key diagnostic clue• Associated nasolacrimal duct obstruction significantly influences clinical presentation and management• Comprehensive lacrimal system evaluation, including imaging, is essential for diagnosis[4,5]• External DCR combined with fistulectomy provides excellent functional and cosmetic outcomes[5,7]ConclusionCongenital lacrimal fistula is an uncommon but clinically significant cause of lifelong epiphora. A high index of suspicion, thorough clinical examination, and appropriate imaging are essential for accurate diagnosis. In symptomatic patients, particularly those with nasolacrimal duct obstruction, surgical intervention in the form of external dacryocystorhinostomy combined with fistulectomy offers excellent anatomical and functional outcomes. Early diagnosis and appropriate management ensure a favorable prognosis with minimal risk of recurrenceDeclarationThe authors declare no financial or proprietary interests in the materials or methods used in this study.References1. Mackenzie W. A Practical Treatise on the Diseases of the Eye. London: Longman; 1854.2 Welham RAN, Bergin DJ. Congenital lacrimal fistulas. ArchOphthalmol. 1985;103(4):545–548.3. Jones LT. The lacrimal system. In: Duane’s ClinicalOphthalmology. Philadelphia: Lippincott Williams & Wilkins; 1994.4. Woog JJ. Obstruction of the lacrimal drainage system. Curr Opin Ophthalmol. 1998;9(5):35–43.5. Ali MJ. Principles and Practice of Lacrimal Surgery. New Delhi: Springer; 2018.6. Linberg JV, McCormick SA. Primary acquired nasolacrimal duct obstruction. Ophthalmology. 1986;93(8):1055–1063.7. Hurwitz JJ. The Lacrimal System.Philadelphia: Lippincott-Raven; 1996.Paul TO, Shepherd R. Congenital lacrimal fistula. J PediatrOphthalmol Strabismus. 1994;31(6):363–367.

39Post Graduate EssentialsDOS Times - Volume 31 Number 4, January-February 2026Unequal Pupils in Clinical Practice: A Systematic Approach to AnisocoriaIntroductionThe pupil is a window into the autonomic nervous system. Its size at any given moment reflects the dynamic balance between parasympathetic (constrictor) and sympathetic (dilator) innervation. When this balance is disrupted unilaterally, the result is anisocoria — a difference in the diameter of the two pupils. Clinically significant anisocoria is generally defined as a pupillary asymmetry greater than 0.4 mm, though physiological anisocoria (present in up to 20–30% of the healthy population) can account for differences up to 1 mm.[1,2]For the clinician, the challenge lies not in detecting anisocoria — which is visible to the naked eye — but in systematically determining which pupil is abnormal, why it is abnormal, and whether urgent intervention is required. The stakes are considerable: a dilated, poorly reactive pupil from third nerve compression by a posterior communicating artery (PComA) aneurysm demands emergency neurosurgical intervention, while a small pupil from Horner syndrome may herald an internal carotid artery dissection requiring immediate anticoagulation.[3]Neuroanatomical Basis of Pupillary ControlThe iris has two muscle groups: the sphincter pupillae (constricts the pupil) and the dilator pupillae (dilates the pupil), each under different autonomic control.1. The Parasympathetic (Constrictor) PathwayPupillary constriction is mediated by the parasympathetDr. Sonali Gupta MSAssistant Professor, Department of Ophthalmology, Lady Hardinge Medical CollegeKaveri Birla MBBS | Poonam MD | Sonali Gupta MS, FRCOphth, FRCSDepartment of Ophthalmology, Lady Hardinge Medical Collegeic division of the autonomic nervous system. The pathway begins in the Edinger-Westphal nucleus (pretectal area, midbrain), travels with the oculomotor nerve (CN III) along its inferior division, synapses in the ciliary ganglion (located posteriorly in the orbit), and reaches the iris sphincter via the short ciliary nerves. Critically, the parasympathetic fibers travel on the outer surface of CN III, rendering them vulnerable to extrinsic compression (e.g., by an aneurysm or herniation) before the motor fibers within the nerve core are affected.[4]2. The Sympathetic (Dilator) PathwayPupillary dilation follows a three-neuron arc. The first-order (central) neuron originates in the hypothalamus and descends through the lateral tegmentum of the brainstem to the ciliospinal centre of Budge (C8–T2). The second-order (preganglionic) neuron exits the spinal cord, loops around the apex of the lung and subclavian artery, and ascends to the superior cervical ganglion along the carotid sheath. The third-order (postganglionic) neuron travels along the internal carotid artery into the cavernous sinus, then along the ophthalmic division of CN V (V1), and ultimately innervates the iris dilator and Müller’s muscle. Interruption at any level produces Horner syndrome: miosis, partial ptosis, and anhidrosis[5]Case Presentation: The Large PupilCase VignetteA 30-year-old female school teacher presented to the ophthalmology outpatient clinic with a 3-week history of noticing that her right pupil appeared larger than the left, first observed in the mirror under bright light. She reported mild difficulty reading fine print at close range over the same period and occasional photophobia in the right eye in bright sunlight. She denied headache, diplopia, eyelid drooping, periorbital pain, or any recent trauma. Systemic review was notable for a viral upper

Post Graduate EssentialsDOS Times - Volume 31 Number 4, January-February 2026 40respiratory tract infection approximately 6 weeks prior, which had resolved fully. She was otherwise healthy, on no medications, and had no prior ocular history. Blood pressure was 112/70 mmHg, and general examination was entirely unremarkable.Figure 1:Colour photograph demonstrating anisocoria with the right pupil being 6.5 mm diameter and the left 3.0 mm diameter — an asymmetry of 3.5 mm Consent taken from the patient) Figure 2: Colour photograph demonstrating pharmacological confirmation with 0.125% pilocarpine which shows that the right (mydriatic) pupil constricted briskly to 3.0 mm while size of left pupil remained unchanged. (Consent taken from the patient) Examination FindingsBest-corrected visual acuity was 6/6 in the left eye and 6/7.5 in the right, with near vision reduced to N10 at 33 cm in the right eye (N5 in the left), consistent with accommodative paresis. Colour vision was full bilaterally. There was no proptosis, no ptosis, and no lid retraction. The anterior segment and fundus were normal in both eyes.Pupillary examination under bright illumination revealed the right pupil right pupil being 6.5 mm diameter and the left 3.0 mm diameter — an asymmetry of 3.5 mm, greater in light (Figure1). Under dim illumination, the asymmetry reduced to approximately 1.5 mm (right 6.5 mm, left 5.0 mm). The right pupil demonstrated a markedly sluggish, tonic light reflex — extremely slow constriction to a sustained light stimulus, followed by characteristically slow tonic re-dilation when the light was removed. The near reflex was better preserved than the light reflex in the right eye, a phenomenon termed light-near dissociation.[6] No relative afferent pupillary defect was present. Pharmacological TestingPharmacological Confirmation — Adie’s Tonic PupilDilute 0.125% pilocarpine drops were instilled in both eyes. After 30 minutes, the right (mydriatic) pupil constricted briskly to 3.0 mm, while the left (normal) pupil showed no significant change, remaining at 3.0 mm (Figure 2). This striking constriction of the larger pupil in reInvestigations and DiagnosisThe constellation of findings — unilateral mydriasis with tonic light reflex, light-near dissociation, segmental iris sphincter palsy on slit-lamp, accommodative paresis, intact extraocular movements, absence of ptosis or pain, and a preceding viral illness in a young woman — established the diagnosis of right Adie’s tonic pupil on clinical and pharmacological grounds.[7]A Systematic Approach to AnisocoriaStep 1 — Is the Anisocoria Real and Acquired?Before embarking on an investigation pathway, the clinician must first determine whether anisocoria is truly present and whether it is new. Physiological anisocoria is present in approximately 20–30% of the population and generally does not exceed 1 mm.[1,2] Crucially, the degree of asymmetry in physiological anisocoria is equal in both light and dark conditions. The patient’s old photographs should be examined under magnification to document prior pupil size, as this simple step can prevent unnecessary investigation.Step 2 — Which Pupil Is Abnormal?The single most important clinical manoeuvre is observing pupillary behaviour in bright light versus dim light. The sympathetic system dilates the pupil; the parasympathetic system constricts it.(Table-1)sponse to a sub-threshold cholinomimetic concentration confirmed Adie’s tonic pupil. The response reflects denervation supersensitivity: degeneration of postganglionic parasympathetic fibres to the iris sphincter causes upregulation of muscarinic receptors, which then respond to concentrations of pilocarpine entirely ineffective on a healthy, normally innervated pupil.[7,8]

41Post Graduate EssentialsDOS Times - Volume 31 Number 4, January-February 2026Step 3 — Look for Associated SignsThe isolated pupil never tells the complete story. Concurrent clinical features often immediately localise the lesion and determine urgency.• Ptosis + miosis + ± anhidrosis → Horner syndrome; urgently image the sympathetic chain from hypothalamus to orbit.• Ptosis + mydriasis + ophthalmoplegia → Compressive CN III palsy; treat as aneurysm until proven otherwise.• Mydriasis + intact extraocular movements + no ptosis Condition Anisocoria Greater In Abnormal Pupil Key MechanismHorner Syndrome Darkness (dim light) Small (miotic) Sympathetic failure — dilator paresisPhysiological Equal in both / slightly more in darkNeither (both normal) Normal variantCN III Palsy (compressive) Light (bright) Large (mydriatic) Parasympathetic failure — sphincter paresisAdie's Tonic Pupil Light (bright) Large (mydriatic) Post-ganglionic parasympathetic denervationPharmacological mydriasis Light (bright) Large (mydriatic) Anticholinergic blockade of sphincterPharmacological miosis Darkness Small (miotic) Cholinergic/sympatholytic agentTable 1: Differential diagnosis of anisocoria by lighting condition, abnormal pupil, and underlying mechanism.→ Adie’s tonic pupil or pharmacological mydriasis.• Miosis + pain + redness + high IOP → Acute angleclosure glaucoma (fixed mid-dilated pupil is classic).• Bilateral miosis with systemic signs → Opioid toxicity, organophosphate poisoning, or pontine haemorrhage.• Argyll Robertson pupils (bilateral, irregular, miotic, with light-near dissociation) → Neurosyphilis.Step 4 — Pharmacological ConfirmationFigure 3: A flowchart for the clinical evaluation of anisocoria (Image Credit: American Academy of Ophthalmology- Neuro-ophthalmology)

DOS Times - Volume 31 Number 4, January-February 2026 42 DOS Times - Volume 31 Number 4, January-February 2026 43Post Graduate EssentialsDOS Times - Volume 31 Number 4, January-February 2026Pharmacological testing (Figure3) provides objective confirmation of the clinical impression. The two most important tests in current practice are:Apraclonidine (0.5%): Used to confirm Horner syndrome. Reversal of anisocoria (miotic pupil becomes larger) constitutes a positive test, reflecting denervation supersensitivity of alpha-1 receptors on the iris dilator. It is contraindicated in children due to risk of systemic bradycardia and hypotension.[9]Dilute Pilocarpine (0.1%): Used to confirm Adie’s tonic pupil. The denervated sphincter is supersensitive to cholinomimetics; a concentration of pilocarpine that would not affect a normal pupil causes brisk constriction of the Adie’s pupil. Step 5 — NeuroimagingImaging modality selection depends on the clinical context. In patients with Horner syndrome, MRI with MR angiography (MRA) of brain, neck and thorax is the initial investigation of choice. It is essential to organise it immediately especially if associated with ipsilateral neck pain or headache, to assess the carotid artery, given its sensitivity for mural haematoma and vessel wall imaging.10 In acute CN III palsy with pupil involvement, CT angiography of the circle of Willis should be performed emergently (within 1 hour of suspicion), as its speed and sensitivity for aneurysm rival catheter angiography in most centres.11 For central Horner syndrome, MRI of the brain and entire cervical spine is required. In children with Horner’s, extensive workup should be performed for neuroblastoma so imaging of abdomen should also be ordered.ConclusionAnisocoria is never merely an observation — it is a clinical gateway to the autonomic nervous system. A rigorous application of clinical principles: light-versus-dark pupillometry, assessment of associated signs, judicious pharmacological testing, and targeted imaging can help to reach a timely diagnosis. A systematic, unhurried, and anatomically informed approach ensures that no pupil — large or small — is allowed to mislead.References1. Loewenfeld IE. The Pupil: Anatomy, Physiology, and ClinicalApplications. Ames: Iowa State University Press; 1993.2. Wilhelm H. Disorders of the pupil. Handb Clin Neurol. 2011;102:427–466.3. Thompson HS, Pilley SF. Unequal pupils: a flow chart forsorting out the anisocorias. Surv Ophthalmol. 1976;21(1):45–48.4. Kardon R. Anatomy and physiology of the autonomic nervous system. In: Miller NR, Newman NJ, eds. Walsh and Hoyt’s Clinical Neuro-Ophthalmology. 6th ed. Philadelphia: Lippincott Williams & Wilkins; 2005.5. Reede DL, Garcon E, Smoker WR, Kardon R. Horner’s syndrome: clinical and radiographic evaluation. Neuroimaging Clin N Am. 2008;18(2):369–385.6. Loewenfeld IE,Thompson HS.The tonic pupil: a re-evaluation.Am J Ophthalmol. 1967;63(1):46–87.7. Jacobson DM, Vierkant RA. Comparison of cholinergic supersensitivity in third nerve palsy and Adie’s syndrome. J Neuroophthalmol. 1998;18(3):171–175.8. Leavitt JA, Wayman LL, Hodge DO, Brubaker RF. Pupillary response to four concentrations of pilocarpine in normal subjects: application to testing for Adie tonic pupil. Am J Ophthalmol. 2002;133(3):333–336.9. Koc F, Kavuncu S, Kansu T, Acaroglu G, Firat E.The sensitivityand specificity of 0.5% apraclonidine in the diagnosis ofoculosympathetic paresis. Br J Ophthalmol. 2005;89(11):1442–1444.10. Romero JM, Ackerman RH, Dault NA, Lev MH. Non invasive evaluation of carotid artery stenosis: indications, strategies, and accuracy. Neuroimaging Clin N Am. 2005 May;15(2):351–365.11. Okahara M, Kiyosue H, Yamashita M, et al. Diagnostic accuracy of MR angiography for cerebral aneurysms in correlation with 3D-DSA. Stroke. 2002;33(7):1803–1808.

DOS Times - Volume 31 Number 4, January-February 2026 42 DOS Times - Volume 31 Number 4, January-February 2026 43Therapeutic MoleculesDOS Times - Volume 31 Number 4, January-February 2026Cenegermin - Drugs in OphthalmologyIntroductionCenegermin is a recombinant human nerve growth factor formulated as a 0.002% (20 mcg/mL) sterile ophthalmic solution, indicated for the treatment of moderate to severe neurotrophic keratitis (NK). It holds the dual distinction of being the first drug approved by the European Medicines Agency (EMA) for NK (2017) and the first approved by the US Food and Drug Administration (FDA) for this condition (2018).[1,2] It is also the first topical biologic ever approved in ophthalmology.[3]Unlike prior supportive therapies, Cenegermin directly targets the neurobiological root cause— representing a paradigm shift in the management of this rare, visionthreatening disease.[4]Neurotrophic Keratitis (NK)Neurotrophic keratitis is a rare degenerative corneal disease resulting from impaired trigeminal innervation, leading to reduction or total loss of corneal sensation, spontaneous epithelial breakdown, and non-healing corneal ulcers.[5] Its estimated prevalence is less than 5 cases per 10,000 persons.[6]Herpetic aetiology (HSV and HZV) is the most common cause, followed by diabetes mellitus (12.4%), prior ocular surgery (10.4%), and CNS pathology (9.0%).[7] Other recognised causes include chemical burns, neurosurgical procedures for trigeminal neuralgia or acoustic neuroma, multiple sclerosis, and topical medication toxicity from preserved glaucoma drops or long-term topical anaesthetics.[5,8]The cornea is the most densely innervated tissue in the human body, supplied by the ophthalmic branch of the Dr. Kaveri Birla MBBSDepartment of Ophthalmology, Lady Hardinge Medical CollegeKaveri Birla MBBS | Harshvardhan Chilkoti MS | Om Prakash MS | Fiza Khan MBBS | Vaibhav ShingolkarMBBS Department of Ophthalmology, Lady Hardinge Medical CollegeFigure 1: Neurotrophic keratitis (central epithelial defect with fluorescein staining)(Courtesy - Bu JB et al Neurotrophic keratopathy: Clinical presentation and effects of cenegermin)[13]trigeminal nerve (V1).[5] Corneal nerves maintain ocular surface homeostasis by releasing epitheliotrophic neuromediators — substance P, calcitonin gene-related peptide, and NGF itself — while corneal epithelial cells reciprocally release neurotrophic factors that support nerve survival.[9] When trigeminal innervation is disrupted, this trophic axis collapses: NGF levels at the ocular surface fall, epithelial renewal slows, tear secretion diminishes, and the blink reflex is impaired, producing

DOS Times - Volume 31 Number 4, January-February 2026 44 DOS Times - Volume 31 Number 4, January-February 2026 45Therapeutic MoleculesDOS Times - Volume 31 Number 4, January-February 2026a vicious cycle of progressive ulceration and impaired healing that can culminate in corneal perforation.[5,6]A diagnostic paradox is that patients typically do not experience pain despite on-going tissue destruction, as reduced corneal sensation eliminates the warning signal that would prompt early presentation.[6] Diagnosis relies Figure 2: NK is staged by the Mackie Classification: Impaired cornea sensitivity and lack of trophic support trigger nonspecific epithelial irregularity and tear film changes (A, B). Stage 1- mild (C, D) is characterized by corneal punctate keratopathy due to focal epithelial damage and loss of tight junctions. It is associated with mild stromal edema with or without corneal neovascularization. Stage 2 – moderate (E, F) is distinguished by the presence of central persistent epithelial defect, surrounded by edematous, cloudy, and poorly adherent epithelium. Stage 3- severe (G, H) is characterized by stromal ulceration and thinning that may progress to melting and perforation (arrows).[8,10]on Cochet-Bonnet aesthesiometry (a reading of ≤4 cm indicating impaired sensitivity), slit-lamp examination with fluorescein staining, and increasingly, in-vivo confocal microscopy (IVCM) to visualise sub-basal nerve plexus density.[9,10]

DOS Times - Volume 31 Number 4, January-February 2026 44 DOS Times - Volume 31 Number 4, January-February 2026 45Therapeutic MoleculesDOS Times - Volume 31 Number 4, January-February 2026Current Treatment OptionsTraditional management has been supportive and does not address the underlying NGF deficiency. Preservative-free artificial tears, bandage and scleral contact lenses, punctal occlusion, and cessation of toxic topical medications form the conservative first line.[8] Autologous serum eye drops provide endogenous growth factors but are non-standardised and logistically demanding.[11] Amniotic membrane transplantation (AMT) promotes epithelial healing with reported rates of 65–80%, but without restoring nerve function.[6] Surgical options include tarsorrhaphy and corneal neurotization.[8] The fundamental limitation of all these modalities is their failure to restore the NGF-mediated trophic axis, which is the core pathogenic defect in NK.Mechanism of ActionNGF is a 13 kDa neurotrophin first characterised by Nobel laureate Rita Levi-Montalcini in the 1950s.[9] The human cornea both produces NGF endogenously and expresses high-affinity NGF receptors, and NGF is essential for epithelial cell proliferation, sensory nerve survival, stem cell maintenance, and reflex tear secretion.[11]Cenegermin is an Escherichia coli-derived recombinant human NGF.[3] It modulates cell survival and apoptotic pathways.[9] By supplementing depleted endogenous NGF, cenegermin restores the trophic axis, enabling epithelial renewal, stimulating sub-basal nerve plexus regeneration, and interrupting the cycle of innervation loss and surface failure.[4]Pharmacokinetics and PharmacodynamicsCenegermin is administered as one drop of the 20 mcg/mL solution in the affected eye(s), six times daily at twohour intervals for eight consecutive weeks.[1] Clinical effects on epithelial healing appear as early as week 4 of treatment.[10] Long-term confocal microscopy studies have documented progressive sub-basal nerve plexus regeneration continuing beyond the 8-week treatment course, indicating that cenegermin initiates a self-sustaining neuroregenerative process. Corticosteroid-containing drops and preservatives such as benzalkonium chloride may impair corneal healing and should not be co-administered.[1,3]Indications1. Moderate to Severe NK — Stage 2 and Stage 3 Figure 3: Shows a vial of Cenegermin (Oxervate®)(CourtesyDompé U.S. Inc. OXERVATE)Figure 4: Corneal confocal microscopy images showing a reduction in the sub-basal nerve plexus (white lines) in moderate/severe neurotrophic keratitis eyes (a, c) compared with contralateral unaffected eyes (b, d) (Courtesy- Zhang Z et al)[12](Primary Approved Indication): This is the core FDA and EMA-approved indication for adults with persistent epithelial defects or stromal ulceration with documented decreased corneal sensitivity.[1,2]2. Stage 1 NK (Emerging Evidence): The Phase IV DEFENDO trial (2024) prospectively evaluated cenegermin in 37 adults with Stage 1 NK,

DOS Times - Volume 31 Number 4, January-February 2026 46 DOS Times - Volume 31 Number 4, January-February 2026 47Therapeutic MoleculesDOS Times - Volume 31 Number 4, January-February 2026demonstrating complete corneal epithelial healing in a 24-week follow-up.[10]3. Post-Herpetic NK: Herpetic keratitis is the leading cause of NK globally, and the pivotal trials enrolled patients across all aetiologies with consistent outcomes.[7] Real-world series confirm cenegermin’s utility in this subgroup.4. Diabetic Neurotrophic Keratopathy (Investigational): Corneal neuropathy is a well-recognised complication of diabetes. Cenegermin has shown improvements in corneal nerve regeneration and epithelial healing on confocal microscopy in diabetic NK, though larger controlled trials are needed.[11]5. NK Associated with Limbal Stem Cell Deficiency (Investigational): An observational study enrolled six eyes of five patients with co-existing LSCD and NK who had failed prior treatment; cenegermin effectively reduced abnormal epithelial area, improved visual acuity, and restored corneal sensation.[11]Advantages1. Disease-Modifying Mechanism: Cenegermin is the only approved drug that directly replaces the deficient trophic factor at the core of NK pathogenesis, offering potential for durable disease modification rather than temporary surface stabilisation.[4]2. High Healing Rates Across Stages: Pivotal trials consistently achieved complete corneal healing in 65–74% of Stage 2/3 NK patients.[10]3. Neurobiological Restoration: Improvement in corneal sensitivity was demonstrated in Stage 1 patients in the DEFENDO trial,[10] with confocal microscopy studies confirming progressive nerve plexus regeneration beyond the treatment period.4. Non-Invasive: A topical drop avoids anaesthesia, surgery, and hospitalisation required by alternatives such as tarsorrhaphy, AMT, or corneal neurotization — none of which address the underlying trophic deficit.5. Durable Healing: Approximately 80% of patients remain healed at 6 months post-treatment, with longterm data supporting maintained corneal integrity over 48 months in the majority of treated cases.[9]Disadvantages1. Common Adverse Effects: Eye pain during or after instillation is the most frequent adverse event, reported in the pivotal trials and in the DEFENDO study.[3,10] Other adverse effects include ocular hyperaemia, increased lacrimation, foreign body sensation, photophobia, and eyelid irritation.[1]2. Acute Calcific Band Keratopathy (ACBK): A serious post-marketing adverse effect is the rapid development of corneal calcium deposition in Bowman’s layer and superficial stroma. A multicenter case series identified 5 patients from 3 institutions who developed ACBK within weeks of starting cenegermin; histopathological examination in one case confirmed calcification extending to 90% stromal depth.[10]3. Demanding Dosing and Storage: Six instillations daily at strict 2-hour intervals for 8 weeks using single-use pipettes, combined with a cold-chain requirement (2–8°C refrigeration), represents a significant compliance and logistical burden.[1]ConclusionCenegermin represents a landmark advancement in corneal therapeutics — the first treatment to correct the NGF deficiency that underlies neurotrophic keratitis rather than managing its surface consequences. The REPARO and NGF0214 trials established healing rates of 70–74% in Stage 2/3 NK, and the DEFENDO trial extended its utility to Stage 1 disease with even higher efficacy and demonstrable corneal sensitivity restoration. Long-term data confirm durable outcomes with low recurrence over follow-up of up to 48 months. The emergence of post-marketing safety signals — particularly acute calcific band keratopathy — underscores the importance of regular slit-lamp monitoring throughout therapy. The drug’s principal real-world limitations remain its prohibitive cost, refrigerated storage, demanding dosing schedule, and absence of approval in countries including India, where NK remains a significant unmet need. For patients with active Stage 2 or 3 NK in regions where it is accessible, cenegermin now represents the standard of care and has meaningfully reduced reliance on surgical intervention.

DOS Times - Volume 31 Number 4, January-February 2026 46 DOS Times - Volume 31 Number 4, January-February 2026 47Therapeutic MoleculesDOS Times - Volume 31 Number 4, January-February 2026References1. US Food and Drug Administration. Oxervate (cenegerminmfgr) Prescribing Information. Dompé US Inc.; 2018. Available from: www.fda.gov/medwatch2. European Medicines Agency. Oxervate – EPAR Summary for the Public. EMA; 2017. Available from: www.ema.europa.eu3. Sheha H, Tighe S, Hashem O, Hayashida Y. Update on cenegermin eye drops in the treatment of neurotrophic keratitis. Clin Ophthalmol. 2019;13:1973–1980.4. Deeks ED, Lamb YN. Cenegermin: A review in neurotrophic keratitis. Drugs. 2020;80(5):489–494.5. Versura P, Giannaccare G, Pellegrini M, Sebastiani S, Campos EC. Neurotrophic keratitis: current challenges and future prospects. Eye Brain. 2018;10:37–45.6. StatPearls. Neurotrophic Keratitis. [Updated 2025 Mar 27]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing.7. Choi CJ, Liu L, Qian Y, Herrinton LJ. Neurotrophic keratopathy: Clinical presentation and outcomes in 354 eyes in a community-based population. Eur J Ophthalmol. 2024.8. Vera-Duarte GR, Jimenez-Collado D, Kahuam-López N, et al. Neurotrophic keratopathy: General features and new therapies. Surv Ophthalmol. 2024;69(5):789–804.9. Mastropasqua L, Massaro-Giordano G, Nubile M, Sacchetti M. Understanding the pathogenesis of neurotrophic keratitis: the role of corneal nerves. J Cell Physiol. 2017;232(4):717–724.10. Hamrah P, Massaro-Giordano M, Schanzlin D, et al. Phase IV multicenter, prospective, open-label clinical trial of cenegermin (rhNGF) for stage 1 neurotrophic keratopathy (DEFENDO). Ophthalmol Ther. 2024;13(2):553–570.11. Sacchetti M, Komaiha C, Bruscolini A, et al. Long-term clinical outcome and satisfaction survey in patients with neurotrophic keratopathy after treatment with cenegermin or amniotic membrane transplantation. Graefes Arch Clin Exp Ophthalmol. 2022;260:917–925.12. Zhang Z, Lu S, Jiang Y, Sun S. Assessing the corneal subbasal nerve plexus by in vivo confocal microscopy in patients with blepharoptosis. Ann Med. 2022 Dec;54(1):227-234. doi: 10.1080/07853890.2021.2024246. PMID: 35014936; PMCID: PMC8757600.13. Bu JB, Gericke A, Pfeiffer N, Wasielica-Poslednik J.Neurotrophic keratopathy: Clinical presentation and effectsof cenegermin. Am J Ophthalmol Case Rep. 2022 Mar 16;26:101488. doi: 10.1016/j.ajoc.2022.101488. PMID: 35330588; PMCID: PMC8938625.

Dialogues and InsightsDOS Times - Volume 31 Number 4, January-February 2026 48Mastering Vision: Essential Practical Insights for the Postgraduate OphthalmologistIntroductionOphthalmology is a highly technical and surgically intensive specialty, requiring postgraduate trainees to demonstrate not only clinical expertise but also surgical precision, ethical judgment, and strong communication skills. The shift from traditional apprenticeship models to competency-based education (CBE) emphasizes measurable outcomes, continual feedback, and structured mentorship.[1] Global authorities such as the International Council of Ophthalmology (ICO) and European Board of Ophthalmology (EBO) advocate for standardized curricula incorporating simulation, reflective practice, and workplace-based assessments like Mini Clinical Evaluation Exercise (Mini-CEX) and Direct Observation of Procedural Skills(DOPS).[2,3]Dr. Niraj Kumar Yadav MS, FIOPS, FAICO, FICM, FID, NDEPAssistant Professor, Department of Ophthalmology, Dr KNS Memorial Institute of Medical Sciences, Barabanki, IndiaNiraj Kumar Yadav MS, FIOPS, FAICO, FICM, FID, NDEPOphthalmic Plastic & Aesthetic Surgeon, Assistant Professor, Department of Ophthalmology, Dr KNS Memorial Institute of Medical Sciences, Barabanki, IndiaAbstract: Background: The evolving landscape of ophthalmic education demands a shift from traditional apprenticeship models to structured, competency-based training. As postgraduate ophthalmologists face increasing clinical, surgical, and technological complexity, it is essential to redefine the core educational framework to produce safe, ethical, and globally competent practitioners.Objective: This article presents a comprehensive and practical overview of the essential components required in modern postgraduate ophthalmology training, aligning with global standards and future healthcare needs.Content: The discussion spans key domains including clinical examination proficiency, stepwise surgical training, simulation and wet lab integration, and formalized mentorship. Non-clinical competencies such as leadership, ethics, communication, and digital literacy are emphasized as integral to holistic development. Additionally, the role of AI, virtual simulation, and international exposure in enhancing training quality and equity are explored. Curriculum alignment with global benchmarks like those from the ICO and EBO is also addressed, alongside recommendations for scalable and context-specific implementation strategies.Conclusion: Modern ophthalmology training must evolve to be competency-driven, technologically integrated, and globally harmonized. Through structured mentorship, simulation, and alignment with international curricula, postgraduate education can produce ophthalmologists who are not only surgically skilled but also ethically grounded and system-aware.Keywords: Postgraduate Ophthalmology, Competency-Based Education, Surgical Training, Mentorship, Global Curriculum, Simulation, AI IntegrationYet, significant disparities in training access and mentorship persist in low-resource settings.[4] This article presents a practical overview of the key competencies and evolving frameworks in postgraduate ophthalmology, designed to equip future ophthalmologists with the skills and insight needed for global, ethical, and competent practice.Core Competencies in Postgraduate OphthalmologyCore competencies in ophthalmology encompass clinical skills, surgical expertise, and professional behaviour, each vital for producing competent and confident specialists. Clinical competency involves accurate slit-lamp examination, fundoscopy, and intraocular pressure measurement, essential for diagnosing conditions like glaucoma and diabetic retinopathy.[3] Surgical training follows a stepwise progression, from extracapsular or small incision cataract surgery (SICS) to phacoemulsification and advanced procedures, enhancing microsurgical precision while minimizing complications.[5] Equally critical

49Dialogues and InsightsDOS Times - Volume 31 Number 4, January-February 2026are non-technical skills such as communication, ethics, and professionalism, which support patient-centered care and team collaboration. These are increasingly assessed through structured evaluations and multisource feedback.[6] Together, these domains define the modern ophthalmologist as both a skilled surgeon and a holistic, ethical practitioner.Simulation and Wet Lab TrainingIn the era of patient safety and precision microsurgery, simulation-based training has emerged as an indispensable component of postgraduate ophthalmology education. Unlike traditional “see one, do one” models, simulation provides a risk-free, repeatable, and structured environment for skill acquisition, significantly reducing surgical complications during real patient encounters. Simulation-based training is a vital part of modern ophthalmology education, offering a safe, structured, and repeatable environment that reduces surgical risks. Wet labs using animal eyes or synthetic models help residents develop early proficiency in tissue handling and cataract techniques.[7] Virtual reality simulators like EyeSi provide real-time feedback and complication tracking, with evidence showing improved performance and fewer surgical errors among simulation-trained residents.[8] Scalable and cost-effective, simulation is especially impactful in low-resource settings, and its integration, supported by mentorship and structured feedback, is now considered an international training standard.[2]Mentorship and Feedback CultureEffective mentorship and structured feedback are critical components of postgraduate ophthalmology training, supporting not only technical skill development but also emotional resilience, ethical maturity, and professional growth.[9] Structured mentor–trainee relationships enable personalized feedback, early identification of learning gaps, and improved surgical confidence, especially in under-resourced settings.[10] Incorporating Mini-CEX, DOPS, and 360-degree feedback enhances objective evaluation. Feedback is most effective when timely, constructive, and behavior-focused.[6] Institutions are encouraged to formalize mentorship systems by training mentors, allocating protected time, and recognizing mentorship as a core educational responsibility.[11] Globally, mentorship remains vital to producing skilled, ethical, and confident ophthalmologists.Competency-Based Education (CBE)Competency-Based Education (CBE) marks a shift from time-based training to outcome-focused learning, emphasizing real-world demonstration of skills, behaviours, and knowledge.[1] Ophthalmology’s procedural nature aligns well with CBE, which assesses domains like surgical proficiency, communication, and professionalism through tools such as Mini-CEX, DOPS, and multisource feedback.[3] CBE enhances transparency, supports early remediation, and allows tailored progression, ensuring readiness for independent practice.[12] Models like Canada’s Competence by Design (CBD) and those in India and the EU guide global implementation.[4] Digital portfolios and e-assessment tools support reflective learning and progress tracking, though successful adoption requires institutional buy-in, trained faculty, and a supportive culture.[11]Global Standards and Curriculum AlignmentAligning ophthalmology training with global standards ensures consistent, high-quality care worldwide. Organizations like the ICO and EBO have developed competency-based curricula that emphasize core clinical skills, ethics, and progressive surgical training.[2,4] The ICO curriculum outlines proficiency levels across domains, enabling international benchmarking.[13] Yet, disparities persist in LMICs due to limited resources and surgical exposure.[7] Collaborative efforts, like twinning programs and remote mentorship, are helping bridge these gaps by promoting shared training models and cross-border accreditation.[10] Global alignment also expands access to fellowships and telemedicine, preparing ophthalmologists for international practice. The future depends on adaptable, evidence-based curricula that ensure a uniform standard of competence, regardless of geography.Leadership, Ethics & Non-Clinical TrainingBeyond surgical skill, today’s ophthalmologists must excel in leadership, ethics, and non-clinical competencies to navigate complex healthcare systems.[11] Training in leadership prepares clinicians to manage teams, coordinate multidisciplinary care, and advocate for public eye health. Institutions like the Royal College of Ophthalmologists and ICO now embed leadership and qual-

Dialogues and InsightsDOS Times - Volume 31 Number 4, January-February 2026 50ity improvement into postgraduate curricula.[14] Ethics education, covering consent, autonomy, and complication management, enhances professional behaviour and empathy when taught through bioethics modules and reflective learning.[6] Yet, gaps remain in areas like financial literacy and medico-legal awareness, especially in LMICs.[2] Structured non-clinical modules and mentorship in leadership roles can ensure ophthalmologists are not only clinically skilled but also system-ready and ethically grounded.Innovation & Robotic/AI IntegrationThe future of ophthalmology is being reshaped by technological innovation, particularly through robot-assisted surgery, artificial intelligence (AI), machine learning, and digital education platforms. These innovations are transforming how postgraduate ophthalmologists learn, diagnose, and operate. Robotic surgical systems, though still emerging in ophthalmology, are showing promise in improving precision in retinal microsurgery and complex anterior segment procedures. Structured training curricula for robotic surgery, including virtual simulation, supervised practice, and competency milestones, are being developed to safely integrate this technology into training pipelines.[15] Early exposure to such systems can prepare residents for future-forward surgical practice. Meanwhile, AI-powered diagnostic tools are increasingly used in detecting retinal pathologies such as diabetic retinopathy, age-related macular degeneration, and glaucoma. Incorporating AI into training helps residents develop data literacy, understand algorithmic decision-making, and collaborate with emerging diagnostic platforms.[16] Equally impactful are innovations in digital learning platforms, including flipped classrooms, virtual grand rounds, and adaptive e-learning systems, which support personalized and asynchronous learning for trainees across diverse settings.[3] These tools bridge access gaps, especially in low-resource programs. As these technologies evolve, educational governance must ensure ethical integration, data privacy awareness, and equitable access. Ophthalmology training programs that embed innovation into their core curricula are poised to produce future-ready clinicians capable of leveraging technology for improved patient outcomes.Global Outreach and International ExposureIncorporating global outreach and international exposure into postgraduate ophthalmology training cultivates clinical versatility, cultural competence, and leadership in global health. As preventable blindness remains disproportionately high in low- and middle-income countries (LMICs), global training programs provide young ophthalmologists with the opportunity to address health inequities while expanding their clinical and surgical repertoire10. International rotations and partnerships expose trainees to a broader spectrum of pathologies, advanced cataract, late-stage glaucoma, and infectious eye diseases less commonly seen in high-income countries. These settings often require resource-conscious decision-making, adaptability, and cross-cultural communication, sharpening skills essential for leadership in any healthcare system.[4] Programs such as distance surgical mentorship, simulation-based outreach, and academic twinning have shown measurable success in building bilateral capacity. For instance, remote surgical training initiatives have improved cataract surgical competency and confidence among trainees in underserved regions while strengthening mentorship bonds with international faculty.]7,9] Global exposure also nurtures professionalism, ethical reflection, and advocacy, reinforcing ophthalmology’s role in universal eye health. With structured supervision, ethical planning, and clear educational objectives, global health programs are no longer optional electives, they are becoming integral to comprehensive ophthalmic education.Figure 1: Conceptual framework of modern postgraduate ophthalmology training.Recommendations & Future DirectionsTo meet the demands of advancing ophthalmic care and global health challenges, postgraduate training must become more standardized, adaptable, and learner-fo-