RETINA Dr. G. Rajasekhar D.N.B, FRCS (Glasgow). RETINA  ARTERY OCCLUSIONS  VEIN OCCLUSIONS  DIABETIC RETINOPATHY  CENTRAL SEROUS RETINOPATHY  HYPERTENSIVE.

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Presentation transcript:

RETINA Dr. G. Rajasekhar D.N.B, FRCS (Glasgow)

RETINA  ARTERY OCCLUSIONS  VEIN OCCLUSIONS  DIABETIC RETINOPATHY  CENTRAL SEROUS RETINOPATHY  HYPERTENSIVE RETINOPATHY  MACULAR DEGENERATION

RETINA ARTERY OCCLUSION  CENTRAL RETINAL ARTERY OCCLUSION  BRANCH RETINAL ARTERY OCCLUSION

RETINA CRAO  Sudden painless loss of vision  h/o suggestive of risk factors like HTN, DM or embolic disease  Vision PL +  Relative afferent pupillary defect

RETINA CRAO: RAPD

RETINA CRAOFundus: Gross thinned out vessels artery > vein Some times emboli may be seen Segmentation of blood column- “cattle truck appearance” Diffuse clouding of macula with “cherry red spot” Primary optic atrophy develops after few weeks

RETINA CRAO

RETINA CRAO

RETINA CRAO WITH CILIO RETINA ARTERY SPARING

RETINA CRAO FFA

RETINA  BRAO  Sudden painless loss of visual field  h/o suggestive of risk factors like HTN, DM or embolic disease  Visual field defect corresponding to site of occlusion respecting horizontal meridian  Relative afferent pupillary defect

RETINA BRVO

RETINA ARTERY OCCLUSION Management  No proven effective treatment  Measures to reduce IOP  Ocular massage  IV acetzolamide  Carbogen (95% oxygen + 5% CO 2 ) inhalation  Paracentasis  Evaluate for sourse of emboli and other risk factors

RETINA CRVO  Sudden painless loss of vision  h/o suggestive of risk factors like HTN, DM or embolic disease  Vision 6/12 to 2/60  Relative afferent pupillary defect +/-

RETINA CRVO  ISCHAEMIC TYPE  NON-ISCHAEMIC TYPE

RETINA CRVOISCHAEMIC

RETINA CRVO ISCHAEMIC

RETINA CRVONON-ISCHAEMIC

RETINA CRVO NON-ISCHAEMIC

RETINA  BRVO  Sudden painless loss of visual field  h/o suggestive of risk factors like HTN, DM or embolic disease  Visual field defect corresponding to site of occlusion respecting horizontal meridian

RETINA BRVO

RETINA  COMPLICATIONS  MACULAR EDEMA  NEOVASCULARISATION OF RETINA  NEOVASCULARISATION OF IRIS

RETINA N V I

RETINA VEIN OCCLUSION Management At regular intervals  Observe the patient for development of NVD / NVE / NVI  Monitor IOP  FFA and LASER photocoagulation if there develops NVD / NVE / NVI  Grid LASER burns for persistant macular edema Evaluate for risk factors

RETINA CENTRAL SEROUS RETINOPATHY Painless rapid dimisision of vision Meta morphopsia Central haziness in the visual field

RETINA CENTRAL SEROUS RETINOPATHY  Vision 6/9 to 6/36  Vision gets corrected with addition of +1 to 1.50 D galsses  Central scotoma  Well circumscribed shallow elevation of retina in macula +/- sub retinal precipitates  “RING SIGN”  May include optic disc

RETINA CENTRAL SEROUS RETINOPATHY

RETINA CENTRAL SEROUS RETINOPATHY FFA

RETINA CENTRAL SEROUS RETINOPATHY Treatment:  Observation  Rule out any source of tuberculosis  Focal laser photo coagulation if CSR persists for more than 4 months or early recovery is required

Diabetic Eye Disease Anterior Segment  Manifest refractive changes  Recurrent corneal epithelial erosions and reduced corneal sensitivity  Blepharitis, styes and chalazion  Conjunctival hyperaemia and MA  Rubeosis Iridis & NVG  Cataract formation  III rd and VI th cranial nerve palsies

DIABETIC RETINOPATHY RISK FACTORS DURATIONDURATION LEVEL OF CONTROLLEVEL OF CONTROL ASSOCIATED RISK FACTORS LIKEASSOCIATED RISK FACTORS LIKE SmokingSmoking PregnancyPregnancy HypertensionHypertension Renal failureRenal failure Carotid diseaseCarotid disease

DIABETIC RETINOPATHY PATHOGENESIS  Loss of pericytes  Thickening of basement membrane  Endothelial cell damage,proliferation  Platelet aggregation  Micro vascular occlusion  Release of growth factors

VASCULAR CHANGES DIABETIC RETINOPATHY IS A MICRO ANGIOPATHY AFFECTING MAINLY CAPILLARIES  INTRA RETINAL CAPILLARY CLOSURE  RETINAL ISCHAEMIA  NEW VESSEL FORMATION IN RETINA & IRIS  INCREASED VASCULAR PERMEABILITY  DIFFUSE RETINAL OEDEMA  LOCALISED RETINAL OEDEMA  HARD EXUDATES

CLASSIFICATION Non-proliferative Proliferative

NON-PROLIFERATIVE DIABETIC RETINOPATHY STAGES Mild NPDR Mild NPDR Moderate NPDR Moderate NPDR Severe NPDR Severe NPDR Very severe NPDR Very severe NPDR

MILD NPDR At least one microaneurysm

MODERATE NPDR MODERATE NPDR Hemorrhages and / or MA Soft exudates, venous beading

SEVERE NPDR  H/Ma in all 4 quadrants  VB in two or more quadrants  IRMA in at least one quadrant quadrant  The rule

VERY SEVERE NPDR Any two or more of severe NPDR

PROLIFERATIVE DIABETIC RETINOPATHY  NVD or NVE or NVI  Preretinal or vitreous haemorrhage  Fibrous tissue proliferation

NVD or NVE NVD or NVE

NVD or NVE

Preretinal &Vitreous Haemorrhage

NVD >1/3 –1/2DA

NVE  1/2DA And pre retinal or vitreous hemorrhage

Traction retinal detachment seen in PDR Advanced Diabetic Retinopathy

MACULAR EDEMA  Retinal thickening within 2 disc diameters of the centre of the macula.

Focal diabetic maculopathy Circumscribed retinal thickening Associated complete or incomplete circinate hard exudates Focal leakage on FA Focal photocoagulation Good prognosis

Diffuse diabetic maculopathy Diffuse retinal thickening Generalized leakage on FA Guarded prognosis Grid photocoagulation Frequent cystoid macular oedema Variable impairment of visual acuity

Ischaemic diabetic maculopathy Macula appears relatively normal Capillary non-perfusion on FA Poor visual acuity Treatment not appropriate

Thickening of the retina located  500µm from the center of the macula

Hard exudates with thickening of the adjacent Retina

A zone of retinal thickening, 1DA or larger in size located  1DA from the center of the macula

ROLE OF FLOURESCEIN ANGIOGRAPHY CSMECSME Capillary loss Capillary loss Flourescein leakage Flourescein leakage

ROLE OF FLOURESCEIN ANGIOGRAPHY Capillary loss leakage leakage Capillary loss leakage leakage Ischemic maculopathy CSMENVE Ischemic maculopathy CSMENVE

MANAGEMENT

Diabetic Retinopathy Management The effect of the photocoagulation burn: Reduced local and global retinal oxygen demandReduced local and global retinal oxygen demand Enhanced transmission of oxygen from choroidEnhanced transmission of oxygen from choroid Breaks the metabolic chain of events leading to advanced diabetic eye diseaseBreaks the metabolic chain of events leading to advanced diabetic eye disease

CSME  All areas of macular thickening must be treated  For leakage - focal photocoagulation  For diffuse thickening - macular grid photocoagulation  Do not treat avascular zones

Treatment of clinically significant macular edema For microaneurysms in centre of hard exudate rings located  m from centre of fovea Focal treatment Gentle whitening or darkening of microaneurysm (  m, 0.10 sec) For diffuse retinal thickening located more than 500  m from centre of fovea and 500  m from temporal margin of disc Grid treatment Gentle burns (  m, 0.10 sec), one burn width apart

Spot size (  m ) depends on contact lens magnification Gentle intensity burn ( sec) Follow-up 4 to 8 weeks Area covered by complete PRP Initial treatment is burns Laser panretinal photocoagulation

Indications for vitreo retinal surgery Retinal detachment involving macula Severe persistent vitreous haemorrhage Dense, persistent premacular haemorrhage Progressive proliferation despite laser therapy

HYPERTENSIVE RETINOPATHY A set of vascular and retinal changes seen in hypertensives as a response to chronic rise of blood pressure. Fundus changes seen are Narrowing Leakage AV crossing changes Choiroidal changes

HYPERTENSIVE RETINOPATHY Narrowing

HYPERTENSIVE RETINOPATHY Leakage

HYPERTENSIVE RETINOPATHY AV crossing changes

HYPERTENSIVE RETINOPATHY AV crossing changes

HYPERTENSIVE RETINOPATHY Stageing of retinopathy Stage 1: focal narrowing of areteries Stage 2: generalised narrowing with AV crossing changes Stage 3: stage 2 + haemorrhages and exudates Stage 4: stage 3 + papilloedema

HYPERTENSIVE RETINOPATHY Choridal: Infarcts

HYPERTENSIVE RETINOPATHY Choridal: Pigmentary changes

HYPERTENSIVE RETINOPATHY Choridal: Rarely bilateral exudative retinal detachment can occur ( E.g.: Toxemia of pregnancy) Hypertensive retinopathy occurs in pure form only in younger individuals with out vascular sclerosis

Retinopathy of prematurity

Thank you