Retinal Detachment (R.D.) is a separation of the sensory retina from the retinal pigment epithelium(R.P.E) by sub retinal fluid(S.R.F)

There are two main types.

1. Rhegmatogenous or Primary R.D.
2. Nonrhegmatous or Secondary R.D.

Secondary R.D sub divided in to two types:

• Tractional R.D.
•  Exudative(Serous) R.D

Rhegmatogenous RD

• Rhegmatogenous R.D is a condition in which fluid from vitreous cavity passes through a full thickness retinal defect in to the sub retinal space to cause separation of the neural retina from the underlying R.P.E
• It affects about 1:10,000 of the population each year

Etiology

• Neural retinal break
• Vitreous liquefaction and detachment
• Vitreoretinal traction
• Intra ocular fluid currents associated with   movement of liquid vitreous and sub retinal  fluid
• History of trauma
• History of previous ocular disease
• History of systemic diseases

Ophthalmic Features

• Age: Common age group is 40-70 years
• Sex: 60 % case comprises by males
• Hereditary: although a no.of pedigree shows familial detachments, most cases are sporadi
• Common complains -
• Flashes of lights(Photopsia)
• Floaters- may be
• Solitary ring shaped opacity(Weiss Ring)
• Cobwebs
• Sudden shower of minute red colored or dark spots
• Localized relative loss in field of vision
• sudden painless loss of vision
• Blurring of distant vision
• Pupil – RAPD
• Fundus Examination – Loss of normal fundal glow
• Retinal breaks:
• Present in about 70% of
• The eyes with tobacco dust.
• appears as red discontinuities in the retinal surface
• Upper temporal quadrant is the commonest site for retinal break

Shape of R.D in relation to primary break

Retinal signs depends on duration of R.D.

1. Fresh R.D
• Detached retina has a convex configuration,slightly opaque and corrugated appearance, undulates freely with eye movements
2. Long standing retinal detachment
• Retinal thinning secondary to atrophy, secondary intraretinal cysts if more than 1 year,  sub retinal  demarcation lines, present after 3 months.

Treatment

1. Cryotherapy
2. Scleral Buckling
3. Pneumatic Retinopexy
4. Vitrectomy

1. Cryo therapy
• Cryotherapy (freezing) or laser photocoagulation  are occasionally used alone to wall off a small area of retinal detachment so that the detachment does not spread.
2. Scleral Buckle surgery
• Scleral buckle surgery is an established treatment in which the eye surgeon sews one or more silicone bands (bands, tyres) to the sclera (the white outer coat of the eyeball). The bands push the wall of the eye inward against the retinal hole, closing the break or reducing fluid flow through it and reducing the effect of vitreous traction thereby allowing the retina to re-attach. Cryotherapy (freezing) is applied around retinal breaks prior to placing the buckle. Often subretinal fluid is drained as part of the buckling procedure. The buckle remains in situ. The most common side effect of a scleral operation is myopic shift.
3. Pneumatic retinopexy
• This operation is generally performed in the doctor's office under local anesthesia. It is another method of repairing a retinal detachment in which a gas bubble (SF6 or C3F8 gas) is injected into the eye after which laser or freezing treatment is applied to the retinal hole. The patient's head is then positioned so that the bubble rests against the retinal hole. Patients may have to keep their heads tilted for several days to keep the gas bubble in contact with the retinal hole. The surface tension of the air/water interface seals the hole in the retina, and allows the retinal pigment epithelium to pump the subretinal space dry and suck the retina back into place. This strict positioning requirement makes the treatment of the retinal holes and detachments that occurs in the lower part of the eyeball impractical. This procedure is usually combined with cryopexy or laser photocoagulation.
4. Vitrectomy
   • Vitrectomy is an increasingly used treatment for retinal detachment. It involves the removal of the vitreous gel and is usually combined with filling the eye with either a gas bubble (SF6 or C3F8 gas) or silicon oil. An advantage of using gas in this operation is that there is no myopic shift after the operation and gas is absorbed within a few weeks. Silicon oil (PDMS), if filled needs to be removed after a period of 2–8 months depending on surgeon's preference. Silicon oil is more commonly used in cases associated with proliferative vitreo-retinopathy (PVR). A disadvantage is that a vitrectomy always leads to more rapid progression of a cataract in the operated eye. In many places vitrectomy is the most commonly performed operation for the treatment of retinal detachment.

• A layer of the retina called the retinal pigment epithelium (RPE) is disrupted by deposits called drusen, or other age-related changes. These changes, if severe enough, may cause vision to deteriorate. When the macula breaks down, you lose your central vision, but it does not affect your peripheral (side) vision.
• A leading cause of severe vision loss in people over 65 years of age ,associated with the aging process; the macula may lose effectiveness over time.

Ophthalmic Features

• Early AMD may be hardly noticeable, and may only occur in one eye.
• Words on a page may look blurred.
• It may be difficult to recognize people’s faces.
• A dark or empty area may appear in the center of vision.
• Straight lines may look distorted.
• With AMD, dark areas may appear in your central vision

Two types of AMD

• Atrophic (Dry) AMD - Caused by aging and thinning of macular tissues when drusen are present.
  • Vision loss is usually gradual.
  • Most common form.
• Exudative (Wet) AMD - Caused when abnormal
  • Blood vessels form underneath the retina. These vessels leak  blood/fluid and blur central vision.
  • Vision loss may be rapid and severe.

Investigations

• Many people do not realize they have a problem until vision blurs.
• Your ophthalmologist can detect early AMD  during an eye exam that includes:
• Ophthalmoscopic examination
  • Fluorescein angiography - Dye is injected into your arm where it travels through the body to the blood vessels in your eye.
  • Special photographs are taken of your eye; dye will highlight abnormal blood vessel growth under the retina

Make most of your vision

• If you have been diagnosed with AMD, you must monitor your vision every day with an Amsler Grid.
• With AMD, Amsler Grid may contain blurry or wavy lines.
• Preserve good vision with regular eye exams

                               
Amsler Grid, as seen through a normal eye      Amsler Grid, as might be seen through an eye with AMD

Treatment (Dry AMD)

• There is no treatment for dry AMD.
• Nutritional supplements may help slow progression and impact of AMD:
• Vitamins C, E
• Beta carotene
• Zinc

(Vitamin supplements are not cures for AMD, nor can they restore vision already lost from AMD.)

Treatment (Wet AMD)

1. Thermal Laser Therapy - Used when abnormal blood vessel growth is not under center of macula. High-energy, focused light beam treats tiny area of retina by “burning” it; destroys abnormal underlying blood vessels, preventing further leakage/bleeding/growth
• Following treatment, your vision may be more blurred than before; will stabilize within a few weeks.
• Scar forms where treatment occurred, creating a permanent blind spot that might be noticeable in your field of vision.
• Likely that 50% of wet AMD patients who have laser procedure will need re-treatment within 3 to 5 years..
2. Photo Dynamic Therapy (PDT) - If abnormal blood vessels grow under center of macula, PDT may be a treatment option. Uses a combination of a light-activated (photo- sensitive) drug and a special low-power (cool) laser.
• Photosensitive drug injected into vein in arm, where it travels throughout the body; attaches to molecules found in abnormal blood vessels. Laser light targeted directly on the abnormal vessels, activating the drug; drug causes damage specifically to those unwanted blood vessels. After PDT, abnormal blood vessels may re-open; multiple treatments may be required.
3. Anti-VEGF treatment - A certain chemical in your   body is critical in causing abnormal blood vessels to grow  under the retina, and is called vascular endothelial growth factor, or VEGF. There are several drugs (anti-VEGF) that can block the trouble-causing VEGF. Blocking VEGF reduces the growth of abnormal blood vessels, slows their leakage, and helps to slow vision loss.
• The anti-VEGF drug is injected into your eye with a very fine needle.(Your ophthalmologist will clean your eye to prevent infection and will administer an anesthetic eye drops to your eye to prevent pain.)
• Patients receive multiple anti-VEGF injections over the course of many months.
• In some cases, your ophthalmologist may recommend combining anti-VEGF treatment with other therapies (i.e. some patients also receive photodynamic laser therapy).

What happens when AMD cannot be treated?

• People with wet or dry AMD who cannot be treated will not become blind—they will still have peripheral (side) vision.

• With special low-vision rehabilitation, devices and services, people can often learn how to “see” again with remaining vision.

Vision Rehabilitation

• Learn new strategies to accomplish daily activities, Skills/devices/techniques help people with advanced AMD regain confidence and live independently despite loss of central vision.
• Low Vision Aids- Optical low-vision devices use lenses to magnify objects:
• Magnifying spectacles
• Hand magnifiers
• Stand magnifiers
• Video magnifiers
• Telescopes
• Large-print books, newspapers, magazines, playing cards, checks
• Writing/signing guides
• High contrast/large number telephones, thermostats, watches, remotes
• Talking books, watches, timers, medical devices

• The clinical picture of branch retinal vein occlusion is retinal hemorrhages that are segmental in distribution.
• The apex of the obstructed tributary vein almost always lies at an arteriovenous crossing. Usually some degree of pathologic arteriovenous nicking is present.
• The occlusion is commonly located one or two disc diameters away from the optic disc. However, the occlusion may lie at a point near the disc edge or, less frequently, may involve one of the smaller, more peripheral tertiary or macular branches.

Etiology

• Systemic Hypertension
• History of cardio vascular disease
• Increased cholesterol
• History of glaucoma
• High serum levels of a2 globulin

Ophthalmic Features

• The clinical picture of branch retinal vein occlusion is retinal hemorrhages that are segmental in distribution.
• The apex of the obstructed tributary vein almost always lies at an arteriovenous crossing. Usually some degree of pathologic arteriovenous nicking is present.
• The occlusion is commonly located one or two disc diameters away from the optic disc. However, the occlusion may lie at a point near the disc edge or, less frequently, may involve one of the smaller, more peripheral tertiary or macular branches

Treatment

1. Medical treatment of branch retinal vein occlusion (BRVO) is not effective. In the past, anticoagulants, fibrinolytic agents, clofibrate capsules (Atromid-S), and carbogen inhalation have been used but without success.
2. Intravitreal injection of Bevacizumab- Bevacizumab is a humanized recombinant monoclonal IgG antibody that binds and inhibits all VEGF isoforms. Several small retrospective and uncontrolled case series suggest that intravitreal bevacizumab at doses up to 2.5 mg are effective in improving visual acuity and reducing central macula thickness in eyes with macular edema secondary to BRVO. These results are often seen within 1 month of injection. However, most of the eyes will require additional injections to maintain the effects of bevacizumab.
3. Intravitreal injection of Ranibizumab- A multicenter, prospective, phase III trial comparing intravitreal ranibizumab and sham injections demonstrated the value of VEGF inhibition in eyes with macular edema secondary to BRVO. In this study, eyes were randomized to monthly sham injections, 0.3 mg of ranibizumab and 0.5 mg of ranibizumab, for the first 6 months. Eyes were eligible for rescue laser at month 3 if the hemorrhages had sufficiently cleared to allow safe treatment and if the visual acuity remained at 20/40 or less and the central macular thickness was 250 µm or less.
4. Intravitreal injection of  Triamcinolone - Intravitreal injection of triamcinolone has been used to treat macular edema of different etiologies because of its potent antipermeability and anti-inflammatory properties. A few cases of macular edema secondary to BRVO treated with an intravitreal triamcinolone injection have been reported. The exact dose remains unclear. Doses from 4 mg to 25 mg have been reported to be effective.
5. Macular grid laser photocoagulation- Macular grid laser photocoagulation remains the criterion standard treatment of eyes with perfused macular edema secondary to BRVO
6. Vitrectomy & arteriovenous decompression - Several surgeons have reported resolution of macular edema secondary to BRVO after vitrectomy with or without peeling of the internal limiting membrane.
• Vitrectomy and posterior hyaloid separation improved the visual acuity in eyes with macular edema secondary to BRVO.

The actual mechanisms producing the clinical picture of central retinal vein occlusion may be roughly divided into those conditions that produce a physical blockage at the level of the lamina cribrosa, and those conditions in which hemodynamic factors result in an obstruction to the flow of blood. These mechanisms probably coexist in many patients with Central Vein Occlusion.

Etiology

• An increased risk of central retinal vein occlusion was found in patients with systemic hypertension, diabetes mellitus, and open-angle glaucoma; the risk of central vein occlusion was decreased for patients with increasing levels of physical activity and increasing levels of alcohol consumption.
• For women, the risk decreased with the use of postmenopausal estrogen and increased with a higher erythrocyte sedimentation rate.

Two types of CRVO

• Ischemic CRVO - Patients with an ischemic pattern are usually aware of a sudden, painless decrease in visual acuity. Vision ranges from 20/400 to hand movements.
• The onset, however, is generally not as rapid or the visual loss as extensive as in central retinal artery occlusion.
• Exceptional cases have been noted in which patients with an acute onset had reasonably good vision and yet demonstrated a picture of ischemic central retinal vein occlusion.
• Non Ischemic CRVO - Nonischemic central retinal vein occlusion is a much milder and more variable disease in appearance, symptoms, and course compared with ischemic central retinal vein occlusion

Ophthalmic Features

Confluent hemorrhages are the most prominent ophthalmoscopic feature of an acute ischemic central retinal vein occlusion These hemorrhages occur in a wide variety of shapes and sizes; they are usually concentrated in the posterior pole, but may be seen throughout the retina. Many hemorrhages are flame shaped, reflecting the orientation of the nerve fibers. Dot and punctate hemorrhages are interspersed and indicate involvement of the deeper retinal layers. Bleeding may be extensive, erupting through the internal limiting membrane to form a preretinal hemorrhage or extending into the vitreous. Small dot hemorrhages may be seen either isolated or clustered around small venules. The entire venous tree is tortuous, engorged, dilated, and dark. The retina is edematous, particularly in the posterior pole; some of this edema may obscure portions of the retinal vessels. Cotton-wool patches (soft exudates) are often present.

The disc margin is blurred or obscured, and the precapillary arterioles appear engorged. Splinter hemorrhages and edema are present on the disc surface and extend into the surrounding retina. The physiologic cup is filled, and the venous pulse is absent. The arterioles, often overlooked because of the other more striking pathologic features, are frequently narrowed. Sometimes in central retinal vein occlusion of acute onset, the fundus picture is less dramatic, and all of the findings previously discussed may be present, but to a lesser degree. Vision depends on extent of macular involvement

Investigations

• All patients with central retinal vein occlusion should have a comprehensive ophthalmic evaluation, including an appropriate evaluation for glaucoma. In addition, they should be referred to their primary care physician for an evaluation of cardiovascular risk factors, including hypertension and diabetes
• Standard investigations-FBC, PV, ESR
• U+E, Creatinine
• LFT, Protein Electrophoreseis
• Random Glucose, Lipid
• Urine analysis
• Ophthalmic investigations – FFA, Colour Doppler

FFA

• The intravenous fluorescein angiogram pattern of an ischemic central retinal vein occlusion is usually characterized by a delayed filling time of the venous tree of the retina, capillary and venous dilation, and extensive leaking of fluorescein into the retina, particularly in the macular area and in the area adjacent to the larger venous trunks and capillary nonperfusion may not be noted at the time of initial occlusion, but are usually manifest shortly thereafter. Late-phase photographs show patchy extravascular areas of fluorescence and staining of the retinal veins.
• Microaneurysms may not be noted at the time of initial occlusion, but are usually manifest shortly thereafter.
• Late-phase photographs show patchy extravascular areas of fluorescence and staining of the retinal veins. Fluorescence in the macula indicates capillary leakage and edema; this not only may account for much of the initial visual loss in the acute phase, but may eventually result in permanent structural changes.
• Fluorescence in the macula indicates capillary leakage and edema; this not only may account for much of the initial visual loss in the acute phase, but may eventually result in permanent structural changes
• The most serious complication of central retinal vein occlusion is neovascularization.
• Neovascularization elsewhere (NVE) occurs less frequently than neovascularization of the iris (NVI), and usually only in ischemic occlusions.

Treatment

1. Medical management- No known effective medical treatment is available for either the prevention of or the treatment of central retinal vein occlusion (CRVO). Identifying and treating any systemic medical problems to reduce further complications is important. Because the exact pathogenesis of the CRVO is not known, various medical modalities of treatment have been advocated by multiple authors with varying success in preventing complications and in preserving vision.
2. Intravitreal Bevacizumab- In patients with macular edema, injection of bevacizumab (0.05 mL/1.25 mg) into the vitreous cavity through pars plana has been shown to be effective not only in resolving the edema but also in corresponding improvement in vision.
• Also, in patients with neovascular glaucoma, a similar dose has shown significantly decreased angle neovascularization and improved intraocular pressure control, both medically and surgically.
• Even though the exact mechanism of action of intravitreal injections of bevacizumab is not known, bevacizumab probably reduces VEGF concentrations in the vitreous cavity. This leads to a reduction in capillary permeability and macular edema. The main drawback of these injections is post treatment recurrences of macular edema, requiring repeat injections.
• Significant complications reported due to the injection of bevacizumab include cataract, glaucoma, retinal detachment, vitreous hemorrhage, and endophthalmitis
3. Intravitreal injection of ranibizumab -
• Vascular endothelial growth factor (VEGF) expression is upregulated by hypoxia and was noted to be elevated in the ocular fluids of patients with CRVO. One of the potent effects of VEGF is to increase vascular permeability in the macula leading to visually significant macular edema.
• Ranibizumab is a humanized, affinity-matured VEGF antibody fragment that binds to and neutralizes all isoforms of VEGF. Ranibizumab showed improved visual outcomes in patients with neovascular age-related vascular degeneration due to its anti-VEGF activity. The role of ranibizumab in the management of CRVO was reported in multiple studies. Intraocular injections of 0.3 mg or 0.5 mg ranibizumab provided rapid improvement in 6-month visual acuity and macular edema following CRVO, with low rates of ocular and nonocular safety events.Long-term follow-up of these patients is needed to know the persistence of these gains for more than 6 months.
4. 4) Dexamethasone intravitreal implant
• Dexamethasone is a potent, water-soluble corticosteroid that can be delivered to the vitreous cavity by the dexamethasone intravitreal implant (DEX implant; OZURDEX, Allergan; Irvine, Calif). A DEX implant is composed of a biodegradable copolymer of lactic acid and glycolic acid containing micronized dexamethasone. The drug-copolymer complex gradually releases the total dose of dexamethasone over a series of months after insertion into the eye through a small pars plana puncture using a customized applicator system.

                     

5. Intravitreal injection of triamcinolone
• In patients with macular edema, injection of triamcinolone (0.1 mL/4 mg) into the vitreous cavity through pars plana has been shown to be effective not only in resolving the edema but also in corresponding improvement in vision.
• Even though the exact mechanism of action of intravitreal injections of corticosteroids is not known, the triamcinolone crystals in the vitreous cavity probably reduce VEGF concentrations in the vitreous cavity. This leads to a reduction in capillary permeability and macular edema. The main drawback of an injection of triamcinolone was post treatment recurrences of macular edema, requiring repeat triamcinolone injections, typically every 3-6 months.
• In addition, significant complications reported due to the injection of triamcinolone include cataract, glaucoma, retinal detachment, vitreous hemorrhage, and endophthalmitis.
6. Laser photocoagulation-
• Laser photocoagulation is the known treatment of choice in the treatment of various complications associated with retinal vascular diseases (eg, diabetic retinopathy, branch retinal vein occlusion). Panretinal photocoagulation (PRP) has been used in the treatment of neovascular complications of CRVO for a long time. However, no definite guidelines exist regarding exact indication and timing of PRP
• Argon green laser usually is used. Laser parameters should be about 500-µm size, 0.1-0.2 second duration, and power should be sufficient to give medium white burns. Laser spots are applied around the posterior pole, extending anterior to equator. They should be about 1 burn apart and total 1200-2500 spots.
• If ocular media is hazy for laser to be applied, cryoablation of the peripheral fundus is performed. About 16-32 transscleral cryo spots are applied from ora serrata posteriorly

• Epidemiology -
• Men > Women
• Bilateral in 1 – 2 %
•  May have other retinal vascular disease
• History-
•  Occurs over period of seconds
•  May have prior history of amaurosis fugax
• Painless
• Sudden loss of vision

Etiology

• Systemic Hypertension 66%
•  Diabetes mellitus 25%
•  Cardiac valve disease 25%
•  Carotid atherosclerosis 45%

Ophthalmic Features

• Vision CF to Light Perception (90%)
• Rarely No Light Perception
• Afferent pupillary defect
• Cherry Red Spot- Opacification of ganglion cells around fovea, takes hours to develop and fades in 4-6 weeks. May be “brown” in blacks.
• Both arteries & veins gets thinned.
• May develop rubeosis & glaucoma within 1 month
• Occurs in up to 15-20%
•  Retinal neovascularization occurs but rarely
•  Ipsilateral carotid obstruction

Ophthalmic Features

• Fundus Fluorescein Angiography (FFA)
• Electro Retinogram (ERG)
• Visual fields

FFA

• Delayed A-V transit time
• Staining of optic nerve or point of embolus
•     Rare retinal vessel staining
• Normal choroidal pattern
• Complete lack of filling, rare in only 2%

ERG

• B-wave origin is inner retina, thus CRAO gives, B wave reduction.
•  A-wave is normal, since photoreceptors perfused
• Compare with flat ERG seen in ophthalmic artery occlusion

Visual fields

• Often have a preserved temporal island
• Spared islands corresponding to cilioretinal sparring

Treatment

• Digital massage to dislodge embolus
• A/C Paracentesis
•  IV acetazolamide
•  Gas Inhalation: Carbogen, Oxygen
•  Retrobulbar vasodilators
•  Inject Fibrinolytic in supraorbital artery
•  Emergent TPPV with/without PFCL
•  YAG laser embolysis

• A Chorioretinal disorder characterized by an idiopathic localized serous detachment of the neural retina in the macular region.
• Usually unilateral

Etiology

• Age: 20 – 50 years
• Gender: Male > female
• Increased incidence in:
• Emotional stress
• Type A personality
• Physical Strains
• People engaged in visually demanding work
• Also found to be associated with vasoconstrictive agents, endogenous hypercortisolism, Systemic corticosteroids, SLE, Hypertension

Ophthalmic Features

• Presentation:
• Unilateral blurred vision with a relative scotoma in the central visual field
• Unilateral metamorphopsia and/or micropsia
• Patients with extrafoveal involvement may be asymptomatic
• Visual acuity:
• V/A ranges from 6/5 to 6/60, usually 6/9 – 6/12
• Acquired hyperopia
• Disparity between retinoscopy and refraction



• Fundus:
• A round to oval sensory retinal detachment is present at the posterior pole
• SRF: clear or turbid ± Precipitates in the posterior surface of the sensory detachment
• In some small PED within the serous detachment may be evident
• Other features:
• Impaired Dark adaptation
• Colour desaturation
• Increased retinal recovery time to bright light
• Patients may present as bullous inferior peripheral retinal detachment (non-rhegmatogenous), with a tract of atrophic RPE from macular region (seen best with FFA)

Investigations

• Fundus Fluorescein Angiography (FFA)
• Slit Lamp Biomicroscopy
• Optical Coherence Tomography ( OCT)

FFA

• Characteristic features:
• Smoke-stack appearance:
• Small hyperfluorescent spot in the early phase due to leakage of dye through the RPE
• Fluorescein passes into the subretinal space and ascends vertically until the upper border, like a smoke-stack, in the late venous phase
• The dye then spreads laterally, taking on a “mushroom” or “umbrella” configuration until entire area of detachment is filled
• Ink-blot appearance: less common
• Hyperfluorescent spot in early phase , which enlarges centrifugally until the entire detachment is filled with dye

Smoke stack appearance

Ink blot appearance

Slit Lamp Biomicroscopy

• Transparent blister in the posterior pole between neural retina and RPE
• Beam splitting as the light traverses the serous space
• Increased distance between the retinal vessels and their shadows
• Absent foveal reflex
• Small dot like deposits in the posterior of retina which is believed to be the precipitates of plasma proteins including fibrin

OCT

Treatment

• Observation: 3-4 months in most first episodes of unilateral CSCR
• Laser photocoagulation
• Systemic beta blockers: may have a beneficial role, but not well proven

• Because of failure of RPE cells edema occurs in the eye.
• Macular edema comprises:-
• Cystoid Macular Edema (CME)
• Neovascularisation
• Diabetic Edema

CME

• Vasculature and Inflammatory diseases
• Extracellular accumulation of fluid.

Symptoms

• Visual impairment
• Metamorphopsia
• Flickering
• Macropsia/Micropsia

Diagnosis

• Slit lamp examination
• FFA - Fluorescein angiography images show your Eye M.D. if any blood vessels are leaking and how much leakage there is.
• OCT - Because macular edema occurs inside the layers of retina tissue, you may have a test called fluorescein angiography, or another called optical coherence tomography (OCT) to help make an accurate diagnosis.
• It measures the thickness of the retina and is also very sensitive at detecting swelling and fluid.

• Preventive
• Medical
• Surgical

• Keep underlying Systemic diseases well Controlled-
• DM
• HIV/CMV
• BP/Lipid control

• Topical Therapy – NSAIDS, Steroids
• Systemic Therapy-NSAIDS, Steroids, Diuretics
• Unique Posterior Segment Drug Delivery
• Trans-scleral
• Intravitreal – ( Kenalog, Macugen,Lucentis, Avastin)
• Injection
• Implant (Biodegradable / Nonbiodegradable)

• Nd:YAG vitreolysis
• Pars Plana Vitrectomy/Membrane Peel
• Focal/Grid Photocoagulation
• Photo-Dynamic Therapy (PDT)

• Synonyms: macular cyst, retinal hole, retinal perforation
• A macular hole is a full-thickness defect of retinal tissue.
• It runs from the internal limiting membrane to the outer segment of the photoreceptor layer. It involves the fovea, so affects central visual acuity (VA).

• Usually idiopathic (<10% have a history of trauma). The most widely accepted theory suggests that age-related focal shrinkage of the prefoveolar vitreous cortex causes traction on the foveal area, leading to foveal detachment and subsequent macular hole formation.
• Other risk factors include cystoid macular edema, retinal detachment, laser injury, hypertension, very high myopia and diabetic retinopathy.

• It may rarely be an incidental finding. Symptoms appear gradually over days/weeks:
• Distorted vision as well as visual loss.
• Visual acuity (VA) will depend on the site of the hole.
• Look for a tiny well-defined 'punched out' area of the macula which can be hard to detect. There may be yellow-white deposits at the base with a grey margin around it representing oedema.
• Slit Lamp Examinattion will show 'a round excavation with well-defined borders' interrupting the beam of the slit lamp.
• Most patients also have a semi-translucent tissue over the hole, which may be surrounded by a grey halo caused by detachment of the retina.
• Gass Biomicroscopic Classification
• Stage 1a Seen as a yellow spot. This is not specific for macular hole - can be associated with central serous chorioretinopathy, cystoid macular oedema, and solar maculopathy.
• Stage 1b Occult hole: doughnut-shaped yellow ring (approximately 200-300 μm) centred on the foveola. Approximately 50% of holes progress to stage 2.
• Stage 2 Full thickness macular hole (<400 μm). Prefoveolar cortex usually separates eccentrically creating a semi-transparent opacity, often larger than the hole, and the yellow ring disappears. These generally progress to stage 3.
• Stage 3 Holes >400 μm associated with partial vitreomacular separation.
• Stage 4 Complete vitreous separation from the entire macula and optic disc

• Diagnosis is usually made clinically; however, the following may be useful:
• Ocular coherence tomography (OCT) provides high-resolution cross-sectional imaging of the retina and is useful in predicting prognosis.
• Fluorescein angiography (FA), although not usually necessary, may be useful in differentiating macular holes from cystoid macular oedema and choroidal neovascularisation (CNV).
• It typically shows a window defect early in the angiogram that does not expand with time, and there is no leakage or accumulation of dye.
• There may be Amsler grid abnormalities. However, plotting small central scotomas is often difficult.

Treatment

• About 50% of stage 1 holes resolve spontaneously, but almost all stage 2 (and above) progress without surgery.
• The chosen surgery depends on the staging of the hole. Surgical closure of the hole is considered up until stage 3 or 4 associated with a visual acuity (VA) of 6/18 or worse. If the macular hole has been present for 1-3 years, then surgery is likely to work. If it has been present for 5 years or longer, then results may be more variable.
• Vitrectomy may relieve traction on the edge of the hole. The vitreous ± internal limiting membrane are removed and a long-acting gas bubble is introduced to tamponade the macula back into position. Short periods of postoperative prone posturing are being used in some centres in selected patients to aid surgical procedures associated with intraocular gas tamponade to achieve macular hole closure and there is increasing evidence to support its use.
• Vitrectomy (with fluid-gas exchange for stage 2, 3, and 4 holes) improves vision compared with conservative treatment. Series of patients have been variously reported with hole closure rates of 73-95%. Most patients' VA improves by two lines of the Snellen chart.
• Success is also possible if the hole is long-standing (6 months-2 years) or if the patient is aged >80 years.
• Occasionally more than one operation is required to close the hole.
• Standard vitrectomy with internal limiting membrane (ILM) maculorrhexis (peeling) has been performed in patients with stage 3 or 4 idiopathic macular holes. The retina is massaged to approximate the edges of the hole as closely as possible. This technique gives a good anatomical and functional result.
• For those patients who have a condition that precludes surgery, visual rehabilitation may be the only option with, for example, referral to low visual aids clinics if needed.

• A macular pucker is scar tissue that has formed on the eye's macula, located in the center of the eye's light-sensitive tissue called the retina. The macula provides the sharp, central vision we need for reading, driving, and seeing fine detail. A macular pucker can cause blurred and distorted central vision.
• Macular pucker is also known as epiretinal membrane, preretinal membrane, cellophane maculopathy, retina wrinkle, surface wrinkling retinopathy, premacular fibrosis, and internal limiting membrane disease.

• When the vitreous pulls away from the retina, there is microscopic damage to the retina's surface (Note: This is not a macular hole). When this happens, the retina begins a healing process to the damaged area and forms scar tissue, or an epiretinal membrane, on the surface of the retina. This scar tissue is firmly attached to the retina surface. When the scar tissue contracts, it causes the retina to wrinkle, or pucker, usually without any effect on central vision. However, if the scar tissue has formed over the macula, our sharp, central vision becomes blurred and distorted.

• Vision loss from a macular pucker can vary from no loss to severe loss, although severe vision loss is uncommon.
• People with a macular pucker may notice that their vision is blurry or mildly distorted, and straight lines can appear wavy.
•  They may have difficulty in seeing fine detail and reading small print.
• There may be a gray area in the center of your vision, or perhaps even a blind spot.

• A macular pucker usually requires no treatment. In many cases, the symptoms of vision distortion and blurriness are mild, and no treatment is necessary. People usually adjust to the mild visual distortion, since it does not affect activities of daily life, such as reading and driving. Eye drops,  medications, nor nutritional supplements will improve vision distorted from macular pucker. Sometimes the scar tissue--which causes a macular pucker--separates from the retina, and the macular pucker clears up.
• Rarely, vision deteriorates to the point where it affects daily routine activities. However, when this happens, surgery may be recommended. This procedure is called a vitrectomy in which the vitreous gel is removed to prevent it from pulling on the retina and replaced with a salt solution (Because the vitreous is mostly water, you will notice no change between the salt solution and the normal vitreous). Also, the scar tissue which causes the wrinkling is removed. A vitrectomy is usually performed under local anesthesia.
• After the operation, you will need to use medicated eye drops to protect against infection

Retinitis pigmentosa is the most common of a group of hereditary progressive retinal degenerations or dystrophies. There is considerable variation and overlap among the various forms of retinitis pigmentosa. Common to all of them is progressive degeneration of the retina, specifically of the light receptors, known as the rods and cones. The rods of the retina are involved earlier in the course of the disease, and cone deterioration occurs later. In this progressive degeneration of the retina, the peripheral vision slowly constricts and central vision is usually retained until late in the disease.

• Retinitis pigmentosa is an inherited condition which involves both eyes. If it starts in one eye, the other eye usually develops the same condition in a number of years. Most cases are familial, inherited in a variety of ways, including dominant, recessive, and sex-linked recessive. Some cases are sporadic and lack a family history of the disease.

• Since retinitis pigmentosa begins as rod degeneration, the patient first notices increasing difficulty in night vision, followed by difficulty seeing in the periphery. Slowly progressive constriction of the visual field leads to tunnel vision. A small area of central vision in both eyes usually persists for years. Generally night blindness precedes tunnel vision by years or even decades. Total blindness eventually ensues in most cases. The age of appearance of legal blindness ranges from as early as childhood to as late as the 40s.

Diagnosis

• The history (especially the possibility of retinitis pigmentosa appearing in other family members) and complaints of the patient may make one suspect RP, it is primarily diagnosed by examination. The patient may complain of difficulty seeing at night or in low light condition. At some point, the ophthalmologist observes relatively characteristic bone spicule pigment during the fundus examination
• Visual fields -will find defects in the peripheral (side vision) with the degree of loss related to defects in relation to the damage occurring in this disease. Over time, the visual field may reduce to a small central island of vision causing "tunnel vision." The final progression may be the complete loss of the remaining central vision.
• Electoretinogram -Responses to flashes of light are measured via electrodes placed on the surface of the eye. It is a painless test. The electroretinogram(ERG), in conjunction with the visual field exam, will usually make the diagnosis. This will also determine if there is any cone involvement.
• Recently, gene testing for defects is being done to clarify the basic cause for RP and assist in ultimately finding a treatment

• As of now there is no specific cure for retinitis pigmentosa. For years, vitamin A therapy has been recommended for many RP patients, based on research dating back to the early 1990s. A randomized, controlled trial of vitamins A and E found that 15,000 IU a day of vitamin A palmitate could slow the course of the condition among adults with typical forms of RP. Vitamin E, however, at a 400 IU a day dose appeared to have an adverse effect on the course of RP in the same study.
• Another study among adult patients with RP has shown that an omega-3-rich diet containing docosahexaenoic acid can further slow disease progression. Such a diet includes one to two 3-ounce servings per week of oily fish such as salmon, tuna, herring, mackerel, or sardine

Toxoplasmosis is a disease provoked by the obligate intracellular protozoan Toxoplasma gondii. It is found in a variety of mammal and bird hosts. The most common intermediate host is the cat. It is one of the most frequent causes of retinochoroiditis in humans, with more than 60 percent of the United States population and up to 75 percent of the world's general population possessing some seropositive findings

• Human infection may occur from ingestion of contaminated or undercooked meat and dairy products, direct or indirect ingestion of cat feces and transplacental transmission from an infected mother to the fetus. Toxoplasmosis can only be transmitted to a fetus during maternal parastemia. Congenital toxoplasmosis accounts for the majority of cases encountered in clinical practice.
• In most cases, the body is primed for infection or toxoplasmosis reactivation by an immune system failure. This may occur following contraction of human immunodeficiency syndrome (HIV) or with medical immunosupression following organ transplantation.

          

• The symptoms associated with ocular toxoplasmosis include unilateral, mild ocular pain, blurred vision and new onset of floating spots. Patients often describe their vision as hazy.
• Clinical findings may include granulomatous iritis, vitritis, optic disc swelling, neuroretinitis, vasculitis and retinal vein occlusion in the vicinity of the inflammation, in the actively involved eye.
• Funduscopically, active toxoplasmosis presents with white-yellow, choreoretinal lesions and vitreous cells. There may be old, inactive lesions in the fellow eye.
• Toxoplasmosis can produce cystoid macular edema and choroidal neovascularization.

• The goal of management is twofold: (1) eradicate the parasite and (2) suppress the inflammatory response.
• Alternative antibiotic treatments include: (1) clindamycin, 300mg, PO QID used with sulfadiazine, for four to six weeks, (2) tetracycline, 2g loading then 250mg PO QID and sulfadiazine for four to six weeks, or (3) trimethoprim/sulfamethoxazole 160/800mg, one tablet PO BID, with or without clindamycin or prednisone, for the same duration.
• In otherwise normal individuals, after beginning antibiotic therapy, add oral steroids at a dose of 20 to 80mg PO daily for four to six weeks. Periocular steroids are never indicated. Oral steroids without systemic antibiotics are expressly contraindicated.

Lattice degeneration is a disease of the eye where peripheral retina becomes atrophic in a lattice pattern and may develop tears / breaks / holes, which may further progress to retinal detachment. It is an important cause of retinal detachment in young myopic individuals. The cause is not known but pathology reveals vascular insufficiency resulting in ischemia and fibrosis.

• The etiology of lattice is questionable. It appears to be due to dropout of peripheral retinal capillaries with resulting ischemia, which induces thinning of all retinal layers. There is sclerosis of the larger vessels, with their lumen being filled with extracellular glial tissue, giving lattice degeneration its characteristic fibrotic appearance.
• Lattice degeneration occurs in eight to 11 percent of the general population. It presents as a linear trail of fibrosed vessels within atrophied retina in a "lattice" pattern. It nearly always runs circumferentially between the equator and the ora serrata

• Typical lattice consists of sharply demarcated spindle-shaped areas of retinal thinning usually located between the equator of the retina and the posterior border of the vitreous base. This is more frequently located in the temporal half of the retina and is seen more superiorly than inferiorly.
• Atypical lattice is characterised by radial lesions which appear continuous with the peripheral blood vessels. This type is typically seen in patients with Stickler syndrome.

• The main concern with lattice degeneration is the chance of progression to rhegmatogenous retinal detachment. With many types of retinal breaks, the area is often prophylactically sealed with laser photocoagulation or cryoretinopexy to prevent this. In lattice degeneration alone, prophylactic treatment is not practical in that the risk of detachment is only 0.1 to 0.7 percent in the phakic eye. Atrophic holes in phakic eyes with lattice degeneration also do not require prophylactic treatment, as the risk of progression to detachment is two percent or less.
• Furthermore, prophylactic treatment of lattice lesions in eyes with greater than 6.00D of myopia yields no benefit. These lesions need only routine, yearly monitoring with the patient educated about signs and symptoms of retinal detachment. However, a linear tractional tear forming at the posterior border of a lattice lesion has about a 37 percent risk of progression to retinal detachment and therefore should receive prophylactic therapy.

• Floaters - Small specks or clouds moving in your field of vision are called floaters. You may see them more clearly when looking at a plain background, such as a blank wall.
• Flashes -When the vitreous gel inside your eye rubs or pulls on the retina, you may see what look like flashing lights or lightning streaks. You may have experienced this same sensation if you have ever been hit in the eye and seen "stars".

• Floatres - Posterior vitreous detachments or PVDs are common causes of vitreous floaters. Far less commonly, these symptoms can be associated with retinal tears or detachments that may be linked to PVDs.
• Flashes  - Ordinarily, light entering your eye stimulates the retina. This produces an electrical impulse, which the optic nerve transmits to the brain. The brain then interprets this impulse as light or some type of image. When the retina is tugged, torn or detached from the back of the eye, a flash or flicker of light commonly is noticed. Depending on the extent of the tear or detachment, these flashes of light might be short-lived or continue indefinitely until the retina is repaired.
• Vitreous detachments with accompanying vitreous floaters also may occur in circumstances such as:
• Inflammation in the eye's interior-
• Nearsightedness
• Cataract surgery
• YAG laser eye surgery
• Diabetes (diabetic retinopathy)
• CMV retinitis

• You should see your ophthalmologist as soon as possible if:
• One new, large floater or "showers" of floaters appear suddenly
• You see sudden flashes of light
• You notice other symptoms, such as the loss of side vision.
• Floaters and flashes of light become more common as we grow older. While not all floaters and flashes are serious, you should always have a medical eye examination by an ophthalmologist to make sure there has been no damage to your retina

• Because there's a risk of a torn retina, call your ophthalmologist if a new floater appears suddenly. Floaters can get in the way of clear vision, which may be quite annoying, especially when reading.
• While some floaters may remain in your vision, many of them will fade over time and become less bothersome. Even if you have had some floaters for years, you should have an eye examination immediately if you notice new ones.
• There is no specific treatment for separation of the vitreous gel from the retina. Medications can be used to help alleviate symptoms from migraine. Laser therapy or surgery may be required for retinal tears.
• The treatment for floaters and flashes depends on the underlying condition. While not all floaters and flashes are serious, you should always have a medical eye examination by an ophthalmologist to make sure there has been no damage to your retina.