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Diabetic and hypertensive retinopathy


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Diabetic and hypertensive retinopathy

  1. 1. Diabetic Retinopathy & Hypertensive Retinopathy By: Ch.Vineela,
  2. 2. Diabetic Retinopathy • Diabetic retinopathy is retinopathy (damage to the retina) caused by complications of diabetes mellitus, which can eventually lead to blindness • It is an ocular manifestation of systematic disease which affects up to 80% of all diabetic patients
  3. 3. DR - Pathogenesis • Damage to capillaries – – formation of microaneurysm (MA) and – leakage leading to • dot & blot haemorrhage, • exudates and • oedema • Changes in blood constituents leading – to decreased blood flow • Micro-vascular or small blood vessel occlusion leading to – capillary non-perfusion • Consequences of ischaemia are – formation of new blood vessels (neo-vascularisation) as retina responds by secreting vascular endothelial growth factor VeGF
  4. 4. Diabetic Retinopathy (DR) – Risk factors • Duration of diabetes • Poor control of Diabetes • Pregnancy • Hypertension • Nephropathy • Obesity and hyperlipidemia • Smoking
  5. 5. Classification 1 ) Non –proliferative -Mild - Moderate - Severe - Very Severe 2) Proliferative 3)Diabetic Maculopathy-- focal exudative -diffuse exudative - ischemic - mixed
  6. 6. Non-proliferative changesclinical • Microaneurysms (MA) – appear as tiny red dots • Oedema – clinically causes thickness »Localised due to leakage from MAs’ »Diffuse due to capillary leakage »Initially located between the OPL and INL »Later involves the INL and NFL »eventually the entire thickness of the retina becomes oedematous »At the fovea, it is cystic in nature
  7. 7. Non-proliferative changes – Clinical Features contd  Exudates: formed at the junction of normal and oedematous retina composed of lipoprotein and lipid-filled macrophages located mainly within the outer plexiform layer
  8. 8. Non-proliferative Clinical Features contd Haemorrhage • ‘Dot and blot’ – in the compact middle layers, from venous end of capillaries • ‘flame shaped’ as they are placed superiorly in nerve fibre layer (RNFL)
  9. 9. Non-proliferative DR Treatment • Usually not required • Only when exudates/oedema in macula (clinically significant macular oedema) • Pt followed up every 6-12 months
  10. 10. Diabetic Maculopathy • Involvement of the fovea by oedema, hard exudates or ischaemia • Most common cause of visual impairment in diabetic patients, with type 2 diabetes. 1.Focal maculopathy • well-circumscribed retinal thickening associated with • complete or incomplete rings of hard exudates 2. Diffuse maculopathy • diffuse retinal thickening, which may be associated with cystoid changes. • landmarks are obliterated by severe oedema which may render localization of the fovea impossible
  11. 11. Focal maculopathy
  12. 12. Diffuse maculopathy
  13. 13. Maculopathy 3. Ischaemic maculopathy • The signs are variable and the macula may look relatively normal despite reduced visual acuity. • In other cases pre-proliferative diabetic retinopathy • FA shows capillary non-perfusion at the fovea and frequently other • Areas of capillary non-perfusion at the posterior pole
  14. 14. Ischaemic Maculopathy
  15. 15. Clinically significant macular oedema 4. CSMO • Retinal oedema within 500μm of the centre of the macula • Hard exudates within 500μm of the centre of the macula, if associated with retinal thickening (which may be outside the 500μm) • Retinal oedema one disc area (1500μm) or larger, any part of which is within one disc diameter of the centre of the macula
  16. 16. Maculopathy Treatment • All cases of CSMO are treated • Aim of treatment is to maintain current level of vision • Argon laser photocoagulation »Focal application »Grid application • Intravitreal Triamcinalone – effect lasts 6/12
  17. 17. Maculopathy – Focal Treatment Focal Treatment Grid Laser Treatment
  18. 18. Non-proliferative Preproliferative changes in DR • DR that exhibits signs of imminent proliferative disease • Clinical signs indicate progressive retinal ischaemi  Cotton-wool spots - composed of accumulations of neuronal debris within the nerve fibre layer. • Signs. Small, whitish, fluffy superficial lesions which obscure underlying blood vessels  Intraretinal microvascular abnormalities (IRMA) are arteriolar-venular shunts that run from retinal arterioles to venules, thus by-passing the capillary bed. Signs. Fine, irregular, red lines that run from arterioles to venules
  19. 19. Non-proliferative Preproliferative changes in DR  Other features a. Venous changes consist of dilatation and tortuosity, looping beading and ‘sausage-like’ segmentation b. Arterial changes include peripheral narrowing c. Dark blot haemorrhages represent haemorrhagic retinal infarcts and are located within the middle retinal layers
  20. 20. NPDR
  21. 21. Proliferative DR (PDR) PDR affects 5– 10% of the diabetic population. Type 1 diabetics are at particular risk with an incidence of about 60% after 30 years.
  22. 22. PDR • Pathogenesis - Primary feature is neovascularization caused by angiogenic growth factors elaborated by hypoxic retinal tissue in an attempt to re-vascularize hypoxic retina. • Clinically »New vessels at the disc (NVD) »New vessels elsewhere (NVE) • Leaks in FA
  23. 23. PDR NVD NVE
  24. 24. PDR • Treatment • Laser therapy is aimed at inducing involution of new vessels and preventing visual loss • Pan retinal laser photocoagulation PRP – delivery at slit lamp or via Indirect Ophthalmoscope • About 2500 burns over 2 sessions
  25. 25. PDR - treatment
  26. 26. PDR - consequences • Vitreous Haemorrhage – retrohyaloid, intragel or both • Tractional RD • Rubeosis Iridis and Neovascular Glaucoma (NVG)
  27. 27. Treatment of Complications of PDR • Persistent Vit Haem » Vitrectomy » Endophotocoagulation • Tractional RD » Vitrectomy » +/- Oil • Rubeosis Iridis / NVG » » » » Adequate PRP +/- Intravitreal Avastin (anti-angiogenic factor) Medical management of glaucoma Surgical management of glaucoma Cyclodestructive laser
  28. 28. Screening • All diabetic patients aged over 12 years and/or entering puberty should be screened General screening and referral to Specialist • 1. Annual review 􀁍 Normal fundus. 􀁍 Mild NPDR with small haemorrhages and/or small hard exudates more than one disc diameter from the fovea. • 2. Routine referral (weeks) 􀁍 NPDR with large exudates within the major temporal arcades but not threatening the fovea. 􀁍 NPDR without maculopathy but with reduced visual acuity impairment. • 3. Early referral (days) 􀁍 CSMO 􀁍 Severe and very severe NPDR. • 4. Urgent referral (same day) 􀁍 PDR. 􀁍 Preretinal or vitreous haemorrhage. 􀁍 Rubeosis iridis. 􀁍 Retinal detachment Screening in pregnancy Diabetic retinopathy can significantly worsen during pregnancy.
  29. 29. HT Retinopathy • Untreated systemic hypertension is associated with – retinopathy, – optic neuropathy, and – choroidopathy. • Retinopathy consists of a spectrum of retinal vascular changes that are pathologically related to microvascular damage from elevated blood pressure.
  30. 30. Pathogenesis Arteriolar narrowing • Arteriolar narrowing may be focal or generalized; • Ophthalmoscopic diagnosis of generalized narrowing is difficult, although the presence of focal narrowing makes it highly probable that blood pressure is raised. • Severe hypertension may lead to the development of cotton-wool spots
  31. 31. Vascular leakage • Vascular leakage leads to flame-shaped retinal haemorrhages and retinal oedema • Chronic retinal oedema may result in the deposition of hard exudates around the fovea with a macular star configuration • Swelling of the optic nerve head is the hallmark of accelerated hypertension
  32. 32. Grades of HT Retinopathy • Grade 1 consists of ‘mild’ generalized retinal arteriolar narrowing; • Grade 2 consists of ‘more severe’ generalized narrowing, focal areas of arteriolar narrowing and arterio-venous (AV) nicking; • Grade 3 consists of grade 1 and 2 signs plus the presence of retinal haemorrhages, microaneurysms, hard exudates and cotton-wool spots; • Grade 4, also called accelerated (malignant) hypertensive retinopathy, consists of signs in the preceding three grades plus optic disc swelling
  33. 33. Treatment • Major aim of treatment is to prevent,limit patient ‘s high blood pressure and reduce high risk of cardiovascular disease and death. • Anti –hypertensive drug treatment required to control the high blood pressure