The retina is the thin, delicate, light-sensitive tissue that lines the inner surface of the back of the eye. Think of it as the sensor in a digital camera — without it, no image can be formed, no matter how perfect the lens in front of it may be. Measuring roughly 0.5 mm in thickness and spanning about 72% of the inner surface of the eye, the retina contains more than 125 million photoreceptor cells that convert light into electrical signals the brain can interpret.

There are two types of photoreceptor cells in the retina. Rods — numbering approximately 120 million — are scattered across the peripheral retina and are responsible for low-light, night, and peripheral vision. Cones — numbering around 6–7 million — are densely concentrated in the central retina, particularly the macula, and are responsible for sharp, detailed, colour vision.

The macula, located at the very centre of the retina, is the most vital area for detailed central vision — the vision needed for reading, driving, recognising faces, and fine precision work. Within the macula, the fovea — a tiny pit approximately 0.35 mm in diameter — contains the highest concentration of cones and is the point of our sharpest, most acute vision.

The retina receives its blood supply from two sources: the retinal circulation (supplying the inner layers) and the choroid, a rich vascular layer beneath the retina supplying the outer photoreceptor layers. Diseases of either system can profoundly damage vision. Because the retina has no pain receptors, many serious retinal conditions — including diabetic retinopathy, macular degeneration, and early retinal detachment — cause no pain, making regular eye examinations essential for early detection. At Suraj Eye Institute, our dedicated vitreoretinal team uses state-of-the-art technology to detect, diagnose, and treat the full range of retinal diseases.

Diabetic Retinopathy (DR) is the most common microvascular complication of diabetes mellitus and the leading cause of blindness in working-age adults worldwide. In India — home to one of the world’s largest diabetic populations — the burden of diabetic eye disease is immense and growing. Critically, it causes no symptoms until significant damage has occurred, making annual screening mandatory for every person with diabetes.

The disease is caused by chronic hyperglycaemia (high blood sugar), which progressively damages the walls of the small capillaries supplying the retina. These damaged vessels become leaky, allowing fluid, lipids, and proteins to seep into the retinal tissue, causing macular oedema — swelling at the macula and the most common cause of visual impairment in diabetics. In advanced disease, the retina responds to ischaemia (poor oxygen supply) by releasing Vascular Endothelial Growth Factor (VEGF), which triggers the growth of new, abnormal blood vessels — a process called neovascularisation. These fragile vessels can bleed (vitreous haemorrhage), cause tractional retinal detachment, or lead to rubeosis iridis and neovascular glaucoma.

DR is classified into: Non-Proliferative DR (NPDR) — mild, moderate, or severe — where changes are confined within retinal vessels; and Proliferative DR (PDR), the most advanced stage with new vessel growth outside the retinal surface. Diabetic Macular Oedema (DMO) can occur at any stage and is the major driver of central vision loss.

Risk factors include duration of diabetes, poor glycaemic control (HbA1c >7%), hypertension, dyslipidaemia, nephropathy, pregnancy, and anaemia. At Suraj Eye Institute, comprehensive diabetic eye care includes dilated fundus examination, OCT for DMO assessment, FFA for non-perfusion mapping, and treatments including laser photocoagulation, intravitreal anti-VEGF injections, Ozurdex implants, and vitreoretinal surgery for advanced cases.

Age-Related Macular Degeneration (ARMD) is the leading cause of irreversible central vision loss in adults over 60 in the developed world, and its prevalence is rising rapidly in India as life expectancy increases. It affects the macula — the central 5 mm of the retina responsible for detailed central vision needed for reading, recognising faces, and fine work. ARMD does not cause total blindness (peripheral vision is preserved) but can severely impair quality of life.

Dry ARMD (Atrophic) accounts for approximately 85–90% of all cases. It is characterised by the gradual accumulation of small yellow deposits called drusen beneath the retinal pigment epithelium (RPE), accompanied by progressive degeneration of RPE and photoreceptors. Vision loss is slow and progressive. In its advanced form — geographic atrophy — large areas of the RPE and photoreceptors degenerate completely. There is no curative treatment, though the AREDS2 vitamin supplement formulation (vitamins C and E, lutein, zeaxanthin, zinc) can slow progression in intermediate disease. Complement inhibitors (e.g., Syfovre/pegcetacoplan) are emerging therapies for geographic atrophy.

Wet ARMD (Neovascular) accounts for only 10–15% of cases but causes the majority of severe vision loss. Abnormal new blood vessels — a choroidal neovascular membrane (CNVM) — grow from the choroid through Bruch’s membrane beneath or into the retina. These vessels leak blood and fluid, causing rapid, severe central vision distortion and loss. Without treatment, legal blindness can result within weeks to months. Wet ARMD is now highly treatable: intravitreal anti-VEGF agents (Avastin, Eylea, Pagenax) can stabilise or improve vision in the majority of patients when administered promptly.

Symptoms include distortion of straight lines (metamorphopsia), a central blind or blurred spot (scotoma), and difficulty reading. At Suraj Eye Institute, ARMD is diagnosed and monitored using OCT, OCT-Angiography, FFA, and ICGA, with prompt anti-VEGF treatment initiated at first detection of wet change.

Vitrectomy is a foundational surgical procedure in vitreoretinal surgery. The term derives from “vitreous” (the clear gel filling the eye’s posterior chamber) and “-ectomy” (surgical removal). During vitrectomy, the vitreous gel is carefully removed and replaced with sterile balanced salt solution (BSS), a gas bubble (C3F8 or SF6), or silicone oil — depending on the underlying condition. Removal of the vitreous gives the surgeon unobstructed access to the retina and resolves traction that may be threatening retinal integrity.

Modern vitrectomy uses a three-port system: a continuous infusion cannula to maintain intraocular pressure; a fibre-optic light pipe for intraocular illumination; and a high-speed vitreous cutter (operating at 5,000–10,000 cuts per minute) that simultaneously cuts and aspirates the vitreous. All three instruments enter through very small incisions in the pars plana — the non-functional periphery of the retina — approximately 3.5 mm behind the limbus in pseudophakic eyes and 4 mm in phakic eyes. Modern microincision vitrectomy surgery (MIVS) using 23-gauge (0.6 mm) or 25-gauge (0.5 mm) instruments allows sutureless, self-sealing incisions with rapid post-operative recovery.

Conditions treated by vitrectomy include: rhegmatogenous and tractional retinal detachment; vitreous haemorrhage (from PDR, trauma, or vascular occlusion); macular holes (Gass stages 2–4); epiretinal membrane (macular pucker); diabetic tractional retinal detachment; posterior segment foreign bodies; dropped nucleus complicating cataract surgery; endophthalmitis; giant retinal tears; and proliferative vitreoretinopathy (PVR).

The procedure is performed under local (peribulbar or sub-Tenon’s) anaesthesia as day-care surgery, typically lasting 30 to 90 minutes. When a gas tamponade is used, patients must maintain a specific head posture (face-down or tilted) for up to 14 days to keep the gas bubble in contact with the repair site. Silicone oil is used for complex detachments and removed in a second procedure after healing. At Suraj Eye Institute, vitrectomy is performed using cutting-edge 25-gauge MIVS platforms with wide-field viewing and intraoperative OCT guidance.

Retinal detachment (RD) is a sight-threatening ocular emergency in which the neurosensory retina — the layer containing the photoreceptors and their supporting cells — separates from the underlying retinal pigment epithelium (RPE) and choroid. Separated from its blood supply, the detached retina progressively degenerates; if not surgically repaired promptly, the result is permanent, irreversible vision loss.

There are three principal types. Rhegmatogenous RD (most common, ~85% of cases) occurs when a break, tear, or hole in the retina allows liquid vitreous to pass through and accumulate in the subretinal space, lifting the retina away from the RPE. Risk factors include high myopia (short-sightedness), prior cataract or other intraocular surgery, blunt or penetrating eye trauma, lattice degeneration, and a family history of RD. The vitreous liquefies and detaches with age (posterior vitreous detachment, PVD), and if it tears a retinal vessel or creates a retinal break during this process, RD may follow. Tractional RD occurs when fibrovascular membranes — most commonly from proliferative diabetic retinopathy — pull the retina off without a primary break. Exudative (serous) RD results from fluid accumulation under the retina without a break or traction, usually from choroidal tumours, inflammation, or severe hypertension.

The cardinal symptoms of RD are: a sudden dramatic increase in floaters (dark spots, strings, or cobwebs in the vision); flashes of light (photopsia), particularly in the temporal peripheral field; and a dark shadow or curtain advancing from the periphery toward the centre of vision — this last symptom indicates the detachment is progressing and the macula may be threatened. A macula-off retinal detachment is a true ocular emergency: the sooner the macula is re-attached, the better the visual outcome. Even a delay of hours can impact the final visual acuity.

Treatment options at Suraj Eye Institute include pneumatic retinopexy (office-based gas injection with laser), scleral buckling (an external silicone explant to indent the eye wall and close the break), and pars plana vitrectomy (PPV) with internal tamponade — all combined with laser photocoagulation or cryotherapy to seal the retinal break. The choice of procedure depends on the type, location, and extent of the detachment and the surgeon’s assessment. If you develop new floaters, flashes, or a visual curtain, please attend our Eye Emergency service immediately. Time is vision.

Vascular Endothelial Growth Factor (VEGF) is a signalling protein that regulates the formation and growth of blood vessels. In the diseased retina, excess VEGF drives the growth of abnormal, leaky, fragile new blood vessels (neovascularisation) and increases vascular permeability, causing fluid accumulation (macular oedema) and haemorrhage — the hallmarks of wet ARMD, diabetic macular oedema, and retinal vein occlusions. Anti-VEGF therapy — the intravitreal injection of agents that block VEGF — has been one of the most transformative advances in ophthalmology of the past two decades, converting conditions that previously caused inevitable blindness into treatable diseases.

At Suraj Eye Institute, we offer three leading anti-VEGF agents: Avastin (bevacizumab), originally developed as a systemic cancer therapy (bevacizumab inhibits tumour angiogenesis), repurposed as an intravitreal agent after clinical studies demonstrated its efficacy for wet ARMD. Multiple large randomised controlled trials (CATT, IVAN, GEFAL) have confirmed it to be as effective as ranibizumab. It is the most widely used and most affordable option. Eylea (aflibercept) is a recombinant fusion protein that binds VEGF-A, VEGF-B, and placental growth factor (PlGF) with higher affinity than native receptors, offering more sustained suppression of VEGF activity. Studies (VIEW 1&2, PROTOCOL T) show it may require less frequent injections — every 8 weeks after loading doses — and it is particularly effective for diabetic macular oedema. Pagenax (ranibizumab biosimilar) is a biosimilar of ranibizumab — the first anti-VEGF agent specifically designed for intravitreal use and formally licensed for the treatment of wet ARMD, DMO, and retinal vein occlusions.

The procedure is performed in a sterile procedure room. After application of topical anaesthetic drops, the eye is prepared with povidone-iodine antiseptic solution, and 0.05 mL of the anti-VEGF agent is injected into the vitreous cavity through the pars plana using a fine 30-gauge needle. The procedure takes 5–10 minutes. Most patients receive a loading dose of 3 monthly injections, followed by maintenance injections guided by disease activity on OCT and clinical examination (treat-and-extend or PRN protocols).

Conditions treated include: wet ARMD, diabetic macular oedema (DMO), branch and central retinal vein occlusion, myopic choroidal neovascularisation, retinopathy of prematurity (bevacizumab), and radiation retinopathy. The most important potential risks are endophthalmitis (intraocular infection, ~1 in 3000), retinal detachment, traumatic cataract, and ocular hypertension — all managed by strict aseptic technique and post-injection monitoring.

Ozurdex (dexamethasone intravitreal implant, 0.7 mg, Allergan/AbbVie) is an innovative, biodegradable sustained-release intravitreal drug delivery system. It contains the potent corticosteroid dexamethasone embedded in a biodegradable PLGA (poly lactic-co-glycolic acid) polymer matrix. After injection into the vitreous cavity, the polymer matrix gradually breaks down over approximately 6 months, releasing dexamethasone in a controlled, sustained manner directly at the site of action — the retina. This eliminates the need for the frequent monthly or bi-monthly injections required with anti-VEGF agents in many patients.

Dexamethasone is a broad-spectrum anti-inflammatory agent that acts through multiple mechanisms. It reduces vascular permeability by downregulating inflammatory mediators such as prostaglandins and leukotrienes; it suppresses VEGF and other cytokine production; it stabilises the tight junctions of the blood-retinal barrier; and it promotes apoptosis of inflammatory cells. This multi-target approach makes Ozurdex particularly effective in conditions where both inflammation and VEGF drive macular oedema.

Approved clinical indications for Ozurdex include: macular oedema due to branch retinal vein occlusion (BRVO) and central retinal vein occlusion (CRVO), where Ozurdex has shown significant improvement in visual acuity in phase III GENEVA trials; diabetic macular oedema (DMO), particularly in pseudophakic patients or those who have shown inadequate response to anti-VEGF injections; and non-infectious uveitis affecting the posterior segment of the eye.

Ozurdex is especially advantageous in: patients with inadequate response to anti-VEGF agents (so-called “VEGF-independent” oedema driven predominantly by inflammation); patients who require a longer interval between clinic visits; bilateral disease requiring treatment in both eyes in the same sitting; and patients in whom the burden of frequent injections is problematic. The implant is injected through the pars plana using a specially designed single-use applicator. The procedure takes 5–10 minutes under topical anaesthesia. Effect begins within 1–2 weeks and typically lasts 4–6 months, after which a repeat implant may be considered. Key side effects include raised intraocular pressure (IOP) — monitored at regular intervals — and acceleration of cataract in phakic patients. At Suraj Eye Institute, all Ozurdex patients are followed up with regular IOP checks and OCT imaging.

Optical Coherence Tomography (OCT) is arguably the most significant diagnostic advance in ophthalmology in the past three decades. Introduced in 1991 by Huang et al., OCT uses near-infrared light (typically 840 nm wavelength) and the principle of low-coherence interferometry to produce high-resolution, cross-sectional, tomographic images of the retina — analogous to ultrasound imaging, but using light rather than sound waves, and achieving 10–100 times superior axial resolution (3–10 microns) that can delineate individual retinal layers.

The OCT beam is split: one portion scans the tissue of interest (sample arm), the other reflects off a reference mirror (reference arm). When the two beams recombine, interference patterns are generated that encode the depth and reflectivity of structures within the retina. Spectral-domain OCT (SD-OCT), the current standard, simultaneously acquires information across a broad spectrum, enabling ultra-fast scan speeds (25,000–80,000 A-scans per second) and acquisition of dense volumetric macular maps. Enhanced Depth Imaging OCT (EDI-OCT) uses image averaging to visualise the choroid in detail. OCT-Angiography (OCTA), a newer technique, detects motion contrast from flowing blood cells to generate angiographic maps of the retinal and choroidal microvasculature without any dye injection — a major advantage over FFA and ICGA.

In retinal disease, OCT enables precise, non-invasive, real-time visualisation of every layer of the retina. The key layers visible include: the internal limiting membrane (ILM), retinal nerve fibre layer (RNFL), ganglion cell complex (GCC), inner and outer plexiform layers, inner and outer nuclear layers, the ellipsoid zone (EZ) — the bright line corresponding to the photoreceptor inner/outer segment junction, a marker of photoreceptor integrity — the retinal pigment epithelium (RPE) / Bruch’s membrane complex, and the choroid.

Critical clinical applications include: measurement of central macular thickness (CMT) — the standard metric for monitoring treatment response in DMO and wet ARMD; detection of intraretinal fluid (IRF) and subretinal fluid (SRF); staging of macular holes; visualisation of epiretinal membranes and vitreomacular traction; characterisation of drusen in ARMD; assessment of sub-RPE deposits; diagnosis of CSCR; and RNFL analysis for glaucoma. At Suraj Eye Institute, OCT is the cornerstone of all retinal assessment and is used at every follow-up visit to guide treatment decisions precisely.

Fundus Fluorescein Angiography (FFA) is a dynamic, photographic technique that provides a detailed, real-time map of the retinal circulation — revealing blood flow patterns, vascular anatomy, areas of leakage, non-perfusion, and neovascularisation that are not visible on routine fundus examination alone. It remains the gold standard for characterising retinal vascular disease and planning targeted treatments.

The procedure works as follows: sodium fluorescein dye (2 mL of 25% or 5 mL of 10% solution) is injected rapidly into an antecubital (cubital fossa) vein. Fluorescein circulates through the systemic vasculature and reaches the ocular circulation in approximately 8–12 seconds. A fundus camera equipped with a blue-green excitation filter (~490 nm) illuminates the retina, exciting the fluorescein molecules, which then emit yellow-green fluorescent light (~520–530 nm) captured through a barrier filter and recorded as a time-sequenced series of photographs.

The angiogram proceeds through characteristic phases: the choroidal phase (pre-arterial, ~10 sec), when dye fills the choriocapillaris first; the arterial phase (~12 sec), retinal arteries fill bright; the arteriovenous (AV) phase (~15–20 sec), simultaneous arterial and venous filling with laminar flow visible in veins; the venous phase (~25–30 sec), veins fill completely; and the late phase (~5–10 min), when most dye has washed out but areas of hyperfluorescence (leakage from damaged vessels or CNV) persist as bright spots. Areas of non-perfusion appear as dark areas (hypofluorescence) surrounded by bright vessels.

The principal clinical uses of FFA include: diabetic retinopathy assessment — mapping microaneurysms, areas of capillary non-perfusion (ischaemia), and neovascularisation, and guiding laser photocoagulation; characterisation of CNVM in ARMD; assessment of extent and non-perfusion in branch and central retinal vein occlusion; identification of the leakage point in central serous chorioretinopathy (CSCR); assessment of retinal vasculitis and uveitis; and choroidal and retinal tumour assessment. FFA is a generally safe procedure; common side effects include transient nausea (10–15%), skin and urine discolouration (yellow-orange) for 24–48 hours, and rarely, itching. Serious anaphylactic reactions are rare (approximately 1 in 10,000 injections). FFA is contraindicated in pregnancy. At Suraj Eye Institute, FFA is performed by trained ophthalmic photographers and interpreted by experienced vitreoretinal specialists.

Indocyanine Green Angiography (ICGA) is a specialised retinal imaging technique that visualises the choroidal circulation — the rich vascular network lying beneath the retinal pigment epithelium (RPE) and supplying the outer retinal layers, including the photoreceptors. While Fluorescein Angiography (FFA) excels at imaging the retinal vasculature in the inner retina, it is limited in its ability to penetrate the RPE to reveal the deeper choroidal pathology. ICGA was developed specifically to overcome this limitation.

The physics underpinning ICGA’s superiority for choroidal imaging is the near-infrared (NIR) fluorescent property of the ICG dye. ICG absorbs light at approximately 790 nm and emits at ~835 nm — wavelengths in the near-infrared spectrum that penetrate the retinal pigment epithelium, the xanthophyll pigment of the macula, thin subretinal haemorrhages, and other opacities that completely block the shorter-wavelength fluorescein used in FFA. Moreover, ICG is almost entirely (98%) protein-bound in the bloodstream, which significantly retards its leakage from choroidal vessels compared to fluorescein — allowing sustained imaging of the choroidal vasculature architecture over time.

ICGA is the investigation of choice — and often the gold standard — for several important conditions: Polypoidal Choroidal Vasculopathy (PCV), a condition characterised by branching choroidal vascular networks terminating in polyp-like aneurysmal dilations at their tips. PCV can clinically mimic wet ARMD and is common among Asian populations, including Indians. The distinction is critical because PCV responds better to photodynamic therapy (PDT) in combination with anti-VEGF, rather than anti-VEGF alone. ICGA is essential for diagnosing PCV, as the polyps are not adequately visible on FFA or OCT alone. Central Serous Chorioretinopathy (CSCR), where ICGA identifies areas of choroidal hyperpermeability and the specific leakage points, guiding laser or PDT treatment. Occult choroidal neovascularisation in wet ARMD, where ICGA delineates vessels not clearly visible on FFA. Other uses include choroidal vasculitis, inflammatory choroiditis, choroidal tumours, and assessment of choroidal vascular insufficiency.

ICGA is typically performed in the same session as FFA using a combined scanning laser ophthalmoscope (SLO)-based system, providing complementary information about both retinal and choroidal circulations simultaneously. At Suraj Eye Institute, combined FFA/ICGA provides the most comprehensive vascular assessment, ensuring the most accurate diagnosis and individually tailored treatment plan for each patient.