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Diabetic Retinopathy. Waseem Al-Zamil, MD. the two main types of diabetes : Insulin-dependent diabetes (IDD) : - known as type 1 . - develops most frequently between 10 and 20 years of age . Non-insulin-dependent diabetes (NIDD) : - also known as type 2.

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Diabetic Retinopathy


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    1. Diabetic Retinopathy Waseem Al-Zamil, MD.

    2. the two main types of diabetes : • Insulin-dependent diabetes (IDD): - known as type 1 . - develops most frequently between 10 and 20 years of age . • Non-insulin-dependent diabetes (NIDD): - also known as type 2. - develops most frequently between the ages of 50 and 70 years.

    3. Prevalence • Diabetic retinopathy is a leading cause of new cases of blindness in people aged 20 to 74 years . • It has a considerable impact on both the patient and the society because it typically affects individuals in their most productive years .

    4. Prevalence • Blindness is 25 more common in diabetics than non diabetics. • Prevalence of PDR is much more in type I than type II. • Diabetic retinopathy more sever in type I than type II.

    5. Prevalence • Macular edema : NPDR : 2 -6 % PDR :20-63 % • Macular edema : 20.1 % in younger onset group. 25.4 % in older onset group taking insulin 13.9 % in older onset group not taking insulin

    6. Prevalence • The 25-year cumulative rate of progression of DR in Type I was: - progression of DR was 83%. - progression to PDR was 42%. - macular edema was 26%. ( WESDR Ophthalmology. 2008 Nov;115(11):1859-68 (

    7. RISK FACTORS • The duration of diabetes : • is the most important factor. • In patients diagnosed as having diabetes before the age of 30 years, the incidence of DR : - after 10 years is 50% - after 30 years is 90%

    8. RISK FACTORS • It is extremely rare for DR to develop within 5 years of the onset of diabetes. • about 5% of Type II have NPDR at presentation perhaps due to the lag between onset and diagnosis.

    9. RISK FACTORS 2 . Glycemic control : • Good metabolic control of diabetes will not prevent DR, although it may delay its development by a few years. • increased severity of diabetic retinopathy is associated with poorer glucose control. • insulin treatment is associated with a decreased risk of either the development or progression of diabetic retinopathy in patients with type 1 diabetes.

    10. RISK FACTORS • With strict control of DM: - risk of developing retinopathy was reduced by 75% . - 50% reduction in the rate of progression of retinopathy in existing retinopathy - early worsening of retinopathy is unlikely to threaten vision . Diabetes Control and Complications Trial Research Group N Engl J Med 1993; 329:977-986.

    11. RISK FACTORS 3 . Miscellaneous factors : - pregnancy. (Hormonal changes ) - systemic hypertension. - renal disease . - anaemia.( ↓oxygen ) - elevated serum lipid. - carotid artery occlusive disease. - Alcohol. ( ? ) - Obesity.

    12. Ocular Risk Factors • PVD : • due to degenerative changes in the vitreous. • significantly more common in diabetic subjects. • complete PVD may prevent the development of PDR because the hyaloid is needed as a scaffold for retinal neovascularization. • attached posterior hyaloid has also been associated with an increased risk for DME

    13. Ocular Risk Factors • High myopia : • choroidal degeneration and extensive old chorioretinopathy protect against DR. • believed to act in the same manner as pan retinal photocoagulation by reducing the metabolic needs of the retina

    14. Ocular Risk Factors • Removal of cataract : • DR may progress after cataract surgery. • Patient who have CSME, SNPDR or PDR should undergo photocoagulation if the media is sufficiently clear. • If the cataract preclude retina evaluation and treatment, prompt postoperative retinal evaluation and treatment should considered.

    15. PATHOGENESIS • Diabetic retinopathy is a microangiopathy affecting the retinal precapillary arterioles, capillaries and venules . • Retinopathy has features of both: - microvascular leakage. (mild- mod NPDR) - microvascular occlusion .(sever NPDR-PDR)

    16. PATHOGENESIS • Microvascular occlusion : • thickening of the capillary basement membrane. • capillary endothelial cell damage and proliferation. • changes in red blood cells leading to defective oxygen transport, and increased stickiness and aggregation of platelets

    17. PATHOGENESIS Fibrous glial cell proliferation Microvascular occlusion retinal ischaemia retinal hypoxia Arteriovenous shunts ( IRMA ) Neovascularization

    18. IRMA New vessel proliferation Fibrous glial tissue proliferaion Tractional RD RD

    19. PATHOGENESIS • Microvascular leakage : - due to reduction in the number of pericytes . - The pericytes are wrapped around the capillaries and are thought to be responsible for the structural integrity of the vessel wall. - Development of retinal edema requires accumulation of fluid which occurs if : Absorption : Leakage : - Uptake from adjusent capillaries - Healthy RPE cells - Microanurerysms. - Incompetent capillaries

    20. PATHOGENESIS Loss pericytes Microvascular leakage haemorrhage retinal oedema Localized Microanurysm”” Diffuse

    21. CLINICAL FEATURES • Microaneurysms : - located in the inner nuclear layer . - the first clinically detectable lesions . - small round dots .(20-200 μ) - mostly located near and temporal to the macula. - When coated with blood they may be indistinguishable from dot haemorrhages.

    22. CLINICAL FEATURES • Haemorrhages : The clinical appearance depending on location - 'dot' and 'blot' : * originating from the venous end of the capillaries. *located in the compact middle layers of the retina . - Flame-shaped : * originate from the more superficial precapillary arterioles, follow the course of the retinal nerve fibre layer. (liner disribution)

    23. CLINICAL FEATURES • Hard exudates : - located between the inner plexiform and inner nuclear layers of the retina. - They are often distributed in a (circinate pattern) . - The centres of rings of hard exudates usually contain microaneurysms . - Made up of accumulated lipoproteins .

    24. CLINICAL FEATURES • Retinal oedema : • located between the outer plexiform and inner nuclear layers. • Later it may involve the inner plexiform and nerve fibre layers, until eventually the entire thickness of the retina may become oedematous. • with further accumulation of fluid, the fovea assumes a cystoid appearance .

    25. Macular edema types: (FFA + Clinical) Focal ME :which has identifiable leakage source. Diffuse ME: which has multiple unidentifiable source of leakage. Cystoid ME: in which fluid accumulate in OPL and INL to form cystoid spaces.

    26. Optical coherence tomographic patterns of diabetic macular edema • (1) spongelike retinal swelling. • (2) cystoid macular edema (CME). • (3) serous retinal detachment (SRD). Kim BY, Smith SD, Kaiser PK: Optical coherence tomographic patterns of diabetic macular edema. Am J Ophthalmol 142(3):405-412, 2006

    27. CLINICAL FEATURES • Vascular changes : • venous changes :in the form of 'beading', 'looping' and 'sausage-like' segmentation. • It represent endothelial cell proliferation. • arterioles may also be narrowed and even obliterated, resembling a BRAO . - The most powerful predictors for development of PDR.

    28. CLINICAL FEATURES • Cotton-wool spots : (Soft exudates ) - Nerve fiber layer infarction. - caused by capillary occlusion in the retinal nerve fibre layer. • The interruption of axoplasmic flow caused by the ischaemia, and subsequent build-up of transported material within the nerve axons, is responsible for the white and opaque appearance of these lesions. • Disappear within weeks to months.

    29. CLINICAL FEATURES • Intraretinalmicrovascular abnormalities (lRMA) : • Dilated, tortous retinal capillaries that act as a shunt between arterioles and venules. • frequently seen adjacent to areas of capillary closure. • IRMA may resemble focal areas of flat NVE . But in IRMA : • intraretinal location. • absence of profuse leakage on fluorescein angiography. • failure to cross over major retinal blood vessels.

    30. CLINICAL FEATURES • New Vessels: • Unlike IRMA, they arise on the retinal surface and may extend or be pulled into the vitreous cavity. • NVD : NV appears on or within one DD of disc margin . {most important prognostic factor for the risk of sever visual loss in DR, DRStudy} • NVE : any other location .

    31. CLINICAL FEATURES • Fibrous Glial proliferation : • Accompained growth of new vessels. • It is proliferation between the posterior vitreous gel and the ILM. • Derived from retinal glial cells and fibrocytes.

    32. Classification of severity of diabetic retinopathy • NonproliferativeDRP : 4 : 2 : 1 Rule

    33. Classification of severity of diabetic retinopathy • ProliferativeDRP :

    34. Diagnostic Testing • Fluorescein Angiography : • Not needed to identify CSME or PDR. • But : • As a guide during CSME treatment. • Identify macular capillary nonperfusion. • Identify subtle areas of NV causing recurrent vitreous hemorrhage despite full PRP.

    35. Diagnostic Testing • Color Fundus photography : • For Documentation purpose . • Ultrasonography : • When opaque media preclude retinal examination. • Useful in ruling out : • RD. • Traction threatening macular detachment.

    36. Diagnostic Testing • Color vision assessment: • DM associated with acquired blue-Yellow defect caused by diabetes itself and macular edema. (patients unable accurately match in self –monitored color-dependant urine or blood-glucose tests)

    37. Diagnostic Testing • Visual Felid: • Diabetic individuals often complaining of night vision loss and felid constriction due to: • Retinopathy. • Retinal non perfusion. • Laser surgery. - Higher risk of developing glaucoma.

    38. Complications of proliferative diabetic retinopathy • Persistent vitreous haemorrhage . • Retinal detachment . • Opaque membranes . • Rubeosis iridis .

    39. MANAGEMENT OF DIABETIC RETINOPATHY • Medical Therapy : • Glycemic control : DCCT , Tight control decrease risk of progression of retinopathy , nephropathy and neuropathy. • Blood pressure control. • Blood lipids control.

    40. MANAGEMENT OF DIABETIC RETINOPATHY • Laser surgery : The treatment of depends on the severity of retinopathy and the presence or absence of CSME, which may be present at any stage .

    41. Macular oedema • defined as the presence of any retinal thickening or hard exudates within one disc diameter (i.e. 1500 µm) of the centre of the fovea. • clinically insignificant macular oedema do not require treatment, only should be followed up at 6 monthly intervals.

    42. Clinically significant macular oedema (CSMO) • defined as the presence of one or more of the following features: • Retinal oedema within 500 µm of the centre of the fovea . • Hard exudates within 500 µm of the fovea, if associated with adjacent retinal thickening (which may be outside the 500 µm limit) . • Retinal oedema that is one disc area (1500 µm) or larger, any part of which is within one disc diameter of the centre of the fovea.

    43. Focal laser photocoagulation • All eyes with CSMO should be considered for treatment with laser photocoagulation irrespective of the level of visual acuity because treatment reduces the risk of visual loss by 50%.

    44. Focal laser photocoagulation • Poor visual outcome after focal laser associated with : • Macular ischemia . • Hard exudates deposit in the fovea. • Marked cystoid macular edema. • Diffuse fluorescin leakage .

    45. Direct treatment • involves applying laser burns to microaneurysms and microvascular lesions in the centre of rings of hard exudates located between 500 and 3000 µm (two disc diameters) from the centre of the fovea. • - The spot size is : 50-100 µm . - The duration of : 0.10 second or less. - The power : sufficient power to obtain a gentle whitening or darkening of the microaneurysm. - Wave length : green – yallow Argon

    46. 1500 mirco 3000 micro 500 micro

    47. Direct treatment • Treatment of lesions between 300 and 500 µm from the centre of the fovea should be considered if CSMO persists, in spite of previous treatment and, if visual acuity is less than 6/12.