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New diabetic retinopathy


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New diabetic retinopathy

  1. 1. Diabetic Retinopathy Waseem Al-Zamil, MD.
  2. 2. <ul><li>the two main types of diabetes : </li></ul><ul><li>Insulin-dependent diabetes (IDD) : </li></ul><ul><li>- known as type 1 . </li></ul><ul><li>- develops most frequently between 10 and 20 years of age . </li></ul><ul><li>Non-insulin-dependent diabetes (NIDD) : </li></ul><ul><li>- also known as type 2. </li></ul><ul><li>- develops most frequently between the ages of 50 and 70 years. </li></ul>
  3. 3. Prevalence <ul><li>Diabetic retinopathy is a leading cause of new cases of blindness in people aged 20 to 74 years . </li></ul><ul><li>It has a considerable impact on both the patient and the society because it typically affects individuals in their most productive years . </li></ul>
  4. 4. Prevalence <ul><li>Blindness is 25 more common in diabetics than non diabetics. </li></ul><ul><li>Prevalence of PDR is much more in type I than type II. </li></ul><ul><li>Diabetic retinopathy more sever in type I than type II. </li></ul>
  5. 5. Prevalence <ul><li>Macular edema : </li></ul><ul><li>NPDR : 2 -6 % </li></ul><ul><li>PDR : 20-63 % </li></ul><ul><li>Macular edema : </li></ul><ul><li>20.1 % in younger onset group. </li></ul><ul><li>25.4 % in older onset group taking insulin </li></ul><ul><li>13.9 % in older onset group not taking insulin </li></ul>
  6. 6. Prevalence <ul><li>The 25-year cumulative rate of progression of DR in Type I was: </li></ul><ul><li>- progression of DR was 83%. </li></ul><ul><li>- progression to PDR was 42%. </li></ul><ul><li>- macular edema was 26%. </li></ul><ul><li>( WESDR Ophthalmology. 2008 Nov;115(11):1859-68 ( </li></ul>
  7. 7. RISK FACTORS <ul><li>The duration of diabetes : </li></ul><ul><li>is the most important factor. </li></ul><ul><li>In patients diagnosed as having diabetes before the age of 30 years, the incidence of DR : </li></ul><ul><li>- after 10 years is 50% </li></ul><ul><li>- after 30 years is 90% </li></ul>
  8. 8. RISK FACTORS <ul><li>It is extremely rare for DR to develop within 5 years of the onset of diabetes. </li></ul><ul><li>about 5% of Type II have NPDR at presentation perhaps due to the lag between onset and diagnosis. </li></ul>
  9. 9. RISK FACTORS <ul><li>2 . Glycemic control : </li></ul><ul><li>Good metabolic control of diabetes will not prevent DR, although it may delay its development by a few years. </li></ul><ul><li>increased severity of diabetic retinopathy is associated with poorer glucose control. </li></ul><ul><li>insulin treatment is associated with a decreased risk of either the development or progression of diabetic retinopathy in patients with type 1 diabetes. </li></ul>
  10. 10. RISK FACTORS <ul><li>With strict control of DM: </li></ul><ul><li>- risk of developing retinopathy was reduced by 75% . </li></ul><ul><li>- 50% reduction in the rate of progression of retinopathy in existing retinopathy </li></ul><ul><li>- early worsening of retinopathy is unlikely to threaten vision . </li></ul><ul><li>Diabetes Control and Complications Trial Research Group N Engl J Med 1993; 329:977-986. </li></ul>
  11. 11. RISK FACTORS <ul><li>3 . Miscellaneous factors : </li></ul><ul><li>- pregnancy. (Hormonal changes ) </li></ul><ul><li>- systemic hypertension. </li></ul><ul><li>- renal disease . </li></ul><ul><li>- anaemia.( ↓oxygen ) </li></ul><ul><li>- elevated serum lipid. </li></ul><ul><li>- carotid artery occlusive disease. </li></ul><ul><li>- Alcohol. ( ? ) </li></ul><ul><li>- Obesity. </li></ul>
  12. 12. Ocular Risk Factors <ul><li>PVD : </li></ul><ul><li>due to degenerative changes in the vitreous. </li></ul><ul><li>significantly more common in diabetic subjects. </li></ul><ul><li>complete PVD may prevent the development of PDR because the hyaloid is needed as a scaffold for retinal neovascularization. </li></ul><ul><li>attached posterior hyaloid has also been associated with an increased risk for DME </li></ul>
  13. 13. Ocular Risk Factors <ul><li>High myopia : </li></ul><ul><li>choroidal degeneration and extensive old chorioretinopathy protect against DR. </li></ul><ul><li>believed to act in the same manner as pan retinal photocoagulation by reducing the metabolic needs of the retina </li></ul>
  14. 14. Ocular Risk Factors <ul><li>Removal of cataract : </li></ul><ul><li>DR may progress after cataract surgery. </li></ul><ul><li>Patient who have CSME, SNPDR or PDR should undergo photocoagulation if the media is sufficiently clear. </li></ul><ul><li>If the cataract preclude retina evaluation and treatment, prompt postoperative retinal evaluation and treatment should considered. </li></ul>
  15. 15. PATHOGENESIS <ul><li>Diabetic retinopathy is a microangiopathy affecting the retinal precapillary arterioles, capillaries and venules . </li></ul><ul><li>Retinopathy has features of both: </li></ul><ul><li>- microvascular leakage. (mild- mod NPDR) </li></ul><ul><li>- microvascular occlusion .(sever NPDR-PDR) </li></ul>
  16. 17. PATHOGENESIS <ul><li>Microvascular occlusion : </li></ul><ul><li>thickening of the capillary basement membrane. </li></ul><ul><li>capillary endothelial cell damage and proliferation. </li></ul><ul><li>changes in red blood cells leading to defective oxygen transport, and increased stickiness and aggregation of platelets </li></ul>
  17. 18. PATHOGENESIS <ul><li>Fibrous glial cell </li></ul><ul><li>proliferation </li></ul>Microvascular occlusion retinal ischaemia retinal hypoxia Arteriovenous shunts ( IRMA ) Neovascularization
  18. 19. New vessel proliferation Fibrous glial tissue proliferaion Tractional RD RD IRMA
  19. 20. PATHOGENESIS <ul><li>Microvascular leakage : </li></ul><ul><li>- due to reduction in the number of pericytes . </li></ul><ul><li>- The pericytes are wrapped around the capillaries and are thought to be responsible for the structural integrity of the vessel wall. </li></ul><ul><li>- Development of retinal edema requires accumulation of fluid which occurs if : </li></ul>Leakage : Absorption : - Microanurerysms. - Incompetent capillaries - Uptake from adjusent capillaries - Healthy RPE cells
  20. 21. PATHOGENESIS Loss pericytes Microvascular leakage haemorrhage retinal oedema Diffuse Localized Microanurysm ” ”
  21. 22. CLINICAL FEATURES <ul><li>Microaneurysms : </li></ul><ul><li>- located in the inner nuclear layer . </li></ul><ul><li>- the first clinically detectable lesions . </li></ul><ul><li>- small round dots .(20-200 μ ) </li></ul><ul><li>- mostly located near and temporal to the macula. </li></ul><ul><li>- When coated with blood they may be indistinguishable from dot haemorrhages. </li></ul>
  22. 23. CLINICAL FEATURES <ul><li>Haemorrhages : </li></ul><ul><li>The clinical appearance depending on location </li></ul><ul><li>- 'dot' and 'blot' : </li></ul><ul><li>* originating from the venous end of the capillaries. *located in the compact middle layers of the retina . </li></ul><ul><li>- Flame-shaped : </li></ul><ul><li>* originate from the more superficial precapillary arterioles, follow the course of the retinal nerve fibre layer. (liner disribution) </li></ul>
  23. 24. CLINICAL FEATURES <ul><li>Hard exudates : </li></ul><ul><li>- located between the inner plexiform and inner nuclear layers of the retina. (OPL) </li></ul><ul><li>- They are often distributed in a (circinate pattern) . </li></ul><ul><li>- The centres of rings of hard exudates usually contain microaneurysms . </li></ul><ul><li>- Made up of accumulated lipoproteins . </li></ul>
  24. 26. CLINICAL FEATURES <ul><li>Retinal oedema : </li></ul><ul><li>located between the outer plexiform and inner nuclear layers. </li></ul><ul><li>Later it may involve the inner plexiform and nerve fibre layers, until eventually the entire thickness of the retina may become oedematous. </li></ul><ul><li>with further accumulation of fluid, the fovea assumes a cystoid appearance . </li></ul>
  25. 27. <ul><li>Macular edema types: (FFA + Clinical) </li></ul><ul><li>Focal ME :which has identifiable leakage source. </li></ul><ul><li>Diffuse ME : which has multiple unidentifiable source of leakage. </li></ul><ul><li>Cystoid ME : in which fluid accumulate in OPL and INL to form cystoid spaces. </li></ul>
  26. 28. Optical coherence tomographic patterns of diabetic macular edema <ul><li>(1) spongelike retinal swelling. </li></ul><ul><li>(2) cystoid macular edema (CME). </li></ul><ul><li>(3) serous retinal detachment (SRD). </li></ul>Kim BY, Smith SD, Kaiser PK: Optical coherence tomographic patterns of diabetic macular edema. Am J Ophthalmol 142(3):405-412, 2006
  27. 29. CLINICAL FEATURES <ul><li>Vascular changes : </li></ul><ul><li>venous changes :in the form of 'beading', 'looping' and 'sausage-like' segmentation. </li></ul><ul><li>It represent endothelial cell proliferation. </li></ul><ul><li>arterioles may also be narrowed and even obliterated, resembling a BRAO . </li></ul><ul><li>- The most powerful predictors for development of PDR. </li></ul>
  28. 30. CLINICAL FEATURES <ul><li>Cotton-wool spots : (Soft exudates ) </li></ul><ul><li>- Nerve fiber layer infarction. </li></ul><ul><li>- caused by capillary occlusion in the retinal nerve fibre layer. </li></ul><ul><li>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. </li></ul><ul><li>Disappear within weeks to months. </li></ul>
  29. 31. CLINICAL FEATURES <ul><li>Intraretinal microvascular abnormalities (lRMA) : </li></ul><ul><li>Dilated, tortous retinal capillaries that act as a shunt between arterioles and venules. </li></ul><ul><li>frequently seen adjacent to areas of capillary closure. </li></ul><ul><li>IRMA may resemble focal areas of flat NVE . But in IRMA : </li></ul><ul><li>intraretinal location. </li></ul><ul><li>absence of profuse leakage on fluorescein angiography. </li></ul><ul><li>failure to cross over major retinal blood vessels. </li></ul>
  30. 32. CLINICAL FEATURES <ul><li>New Vessels: </li></ul><ul><li>Unlike IRMA, they arise on the retinal surface and may extend or be pulled into the vitreous cavity. </li></ul><ul><li>NVD : NV appears on or within one DD of disc margin . </li></ul><ul><li>NVE : any other location . </li></ul>
  31. 33. CLINICAL FEATURES <ul><li>Fibrous Glial proliferation : </li></ul><ul><li>Accompained growth of new vessels. </li></ul><ul><li>It is proliferation between the posterior vitreous gel and the ILM. </li></ul><ul><li>Derived from retinal glial cells and fibrocytes. </li></ul>
  32. 34. Classification of severity of diabetic retinopathy <ul><li>Nonproliferative DRP : </li></ul>4 : 2 : 1 Rule Microaneurysms, retinal hemorrhage and hard exudate Mild NPDR Mild NPDR plus cotton wool spots . Moderate NPDR <ul><li>Moderate NPDR plus one of : </li></ul><ul><li>Intraretinal Hges in four quadrants . </li></ul><ul><li>marked venous beading in two or more quadrants </li></ul><ul><li>IRMA one or more quadrants. </li></ul>Severe NPDR Two or more of the above features described in severe NPDR Very severe NPDR
  33. 35. Classification of severity of diabetic retinopathy <ul><li>Proliferative DRP : </li></ul>New vessels and/or fibrous proliferations; or preretinal and/or vitreous hemorrhage Early PDR <ul><li>NVD ≥ 1/3 of DD. </li></ul><ul><li>less extensive NVD, if vitreous or preretinal hemorrhage is present . </li></ul><ul><li>NVE ≥ half disc area, if vitreous or preretinal hemorrhage is present </li></ul>PDR with HRC <ul><li>Extensive vitreous hemorrhage precluding grading. </li></ul><ul><li>retinal detachment involving the macula. </li></ul><ul><li>phthisis bulbi . </li></ul>Advanced PDR
  34. 36. Diagnostic Testing <ul><li>Fluorescein Angiography : </li></ul><ul><li>Not needed to identify CSME or PDR. </li></ul><ul><li>But : </li></ul><ul><li>As a guide during CSME treatment. </li></ul><ul><li>Identify macular capillary nonperfusion. </li></ul><ul><li>Identify subtle areas of NV causing recurrent vitreous hemorrhage despite full PRP. </li></ul>
  35. 37. Diagnostic Testing <ul><li>Color Fundus photography : </li></ul><ul><li>For Documentation purpose . </li></ul><ul><li>Ultrasonography : </li></ul><ul><li>When opaque media preclude retinal examination. </li></ul><ul><li>Useful in ruling out : </li></ul><ul><li>RD. </li></ul><ul><li>Traction threatening macular detachment. </li></ul>
  36. 38. Diagnostic Testing <ul><li>Color vision assessment: </li></ul><ul><li>DM associated with acquired blue-Yellow defect caused by diabetes it self and macular edema. (patients unable accurately match in self –monitored color-dependant urine or blood-glucose tests) </li></ul>
  37. 39. Diagnostic Testing <ul><li>Visual Felid: </li></ul><ul><li>Diabetic individuals often complaining of night vision loss and felid constriction due to: </li></ul><ul><li>Retinopathy. </li></ul><ul><li>Retinal non perfusion. </li></ul><ul><li>Laser surgery. </li></ul><ul><li>- Higher risk of developing glaucoma. </li></ul>
  38. 40. Complications of proliferative diabetic retinopathy <ul><li>Persistent vitreous haemorrhage . </li></ul><ul><li>Retinal detachment . </li></ul><ul><li>Opaque membranes . </li></ul><ul><li>Rubeosis iridis . </li></ul>
  39. 41. MANAGEMENT OF DIABETIC RETINOPATHY <ul><li>Medical Therapy : </li></ul><ul><li>Glycemic control : </li></ul><ul><li>DCCT , Tight control decrease risk of progression of retinopathy , nephropathy and neuropathy. </li></ul><ul><li>Blood pressure control. </li></ul><ul><li>Blood lipids control. </li></ul>
  40. 42. MANAGEMENT OF DIABETIC RETINOPATHY <ul><li>Laser surgery : </li></ul><ul><li>The treatment of depends on the severity of retinopathy and the presence or absence of CSME, which may be present at any stage . </li></ul>
  41. 43. Macular oedema <ul><li>defined as the presence of any retinal thickening or hard exudates within one disc diameter (i.e. 1500 µ m) of the centre of the fovea. </li></ul><ul><li>clinically insignificant macular oedema do not require treatment, only should be followed up at 6 monthly intervals. </li></ul>
  42. 44. Clinically significant macular oedema (CSMO) <ul><li>defined as the presence of one or more of the following features: </li></ul><ul><li>Retinal oedema within 500 µ m of the centre of the fovea . </li></ul><ul><li>Hard exudates within 500 µ m of the fovea, if associated with adjacent retinal thickening (which may be outside the 500 µ m limit) . </li></ul><ul><li>Retinal oedema that is one disc area (1500 µ m) or larger, any part of which is within one disc diameter of the centre of the fovea. </li></ul>
  43. 46. Focal laser photocoagulation <ul><li>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%. </li></ul>
  44. 47. Focal laser photocoagulation <ul><li>Poor visual outcome after focal laser associated with : </li></ul><ul><li>Macular ischemia . </li></ul><ul><li>Hard exudates deposit in the fovea. </li></ul><ul><li>Marked cystoid macular edema. </li></ul><ul><li>Diffuse fluorescin leakage . </li></ul>
  45. 48. Direct treatment <ul><li>involves applying laser burns to microaneurysms and microvascular lesions in the centre of rings of hard exudates located between 500 and 3000 µ m (two disc diameters) from the centre of the fovea. </li></ul><ul><li>- The spot size is : 50-100 µ m . </li></ul><ul><li>- The duration of : 0.10 second or less. </li></ul><ul><li>- The power : sufficient power to obtain a gentle whitening or darkening of the microaneurysm. </li></ul><ul><li>- Wave length : green – yallow Argon </li></ul>
  46. 49. 1500 mirco 500 micro 3000 micro
  47. 50. Direct treatment <ul><li>Treatment of lesions between 300 and 500 µ m 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. </li></ul>
  48. 51. Grid treatment <ul><li>used for areas of diffuse retinal thickening located more than 500 µ m from the centre of the fovea and 500 µ m from the temporal margin of the optic disc. </li></ul><ul><li>- The spot size is : 50 - 100 µ m . </li></ul><ul><li>- The exposure time : 0.10 second. </li></ul><ul><li>- The burns should be of very light intensity and one burn width apart. </li></ul><ul><li>- Wave length : green – yallow Argon . </li></ul>
  49. 52. Macular oedema treatment <ul><li>It should be emphasized that the main aim of treatment is to preserve the patient's current visual level. </li></ul><ul><li>Only about 15% of eyes show improvement. </li></ul><ul><li>It may take up to 4 months for the oedema to resolve, re-treatment should not be considered prematurely . </li></ul>
  50. 53. Focal Laser Side Effects <ul><li>Paracentral scotoma. </li></ul><ul><li>Transient increased edema and decresed vision. </li></ul><ul><li>Choroidal neovascularization. </li></ul><ul><li>Subretinal fibrosis. </li></ul><ul><li>Scar expansion. </li></ul><ul><li>Foveolar burns. </li></ul>
  51. 54. Anti-VGEF & Macular Edema
  52. 55. Anti-VGEF & Macular Edema
  53. 56. Algorithm for panretinal scatter coagulation of the retina
  54. 57. laser photocoagulation <ul><li>The following are the clinical features of eyes at high risk PDR: </li></ul><ul><li>NVD or neovascularization within one disc diameter of the optic disc more than one-quarter disc in area . </li></ul><ul><li>Less extensive NVD associated with vitreous or preretinal haemorrhage. </li></ul><ul><li>NVE more than one-half disc in area in association with vitreous or preretinal haemorrhage. </li></ul>
  55. 58. laser photocoagulation <ul><li>The aim of treatment is to: </li></ul><ul><li>induce involution of new vessels . </li></ul><ul><li>prevent vitreous haemorrhage. </li></ul><ul><li>Initial treatment involves the placement of about 2000-3000 burns in a scatter pattern, extending from the posterior fundus to cover the peripheral retina in one or more sessions. </li></ul>
  56. 59. laser photocoagulation <ul><li>The technique of PRP is as follows: </li></ul><ul><li>Topical corneal anaesthesia is adequate in most patients. </li></ul><ul><li>- The spot size :depends on which contact lens is being used. (500 - 200 µ m). </li></ul><ul><li>- The duration : between 0.10 and 0.05 second </li></ul><ul><li>- The power level : produces a gentle burn </li></ul>
  57. 60. laser photocoagulation <ul><li>3. burns spaced about one half burn apart. </li></ul><ul><li>4. the power is increased by 50 mW increments until a grey-white burn of gentle intensity is produced . </li></ul><ul><li>Follow-up : </li></ul><ul><li>- is after an interval of 4-8 weeks. </li></ul><ul><li>- In eyes with severe NVD, several treatment sessions with 5000 or more burns may be required. - the most important cause of persistent neovascularization is inadequate treatment. </li></ul>
  58. 62. laser photocoagulation <ul><li>Signs of involution : </li></ul><ul><li>regression of neovascularization leaving only 'ghost' vessels or fibrous tissue. </li></ul><ul><li>decrease in venous dilatation. </li></ul><ul><li>absorption of retinal haemorrhages . </li></ul><ul><li>disc pallor . </li></ul><ul><li>Treatment of recurrence : </li></ul><ul><li>Further argon laser PRP filling in any gaps between previous laser scars. </li></ul>
  59. 63. PARS PLANA VITRECTOMY INDICATIONS <ul><li>Severe persistent vitreous haemorrhage . </li></ul><ul><li>Tractional retinal detachment involving the macula. </li></ul><ul><li>Combined tractional and rhegmatogenous retinal detachment . </li></ul><ul><li>Progressive fibrovascular proliferation . </li></ul><ul><li>Rubeosis iridis associated with vitreous haemorrhage . </li></ul>
  60. 64. PARS PLANA VITRECTOMY INDICATIONS <ul><li>6. Dense, persistent, premacular, subhyaloid haemorrhage . </li></ul><ul><li>7. Red Blood Cell-induced glaucoma. </li></ul><ul><li>8. Bilateral vitreous haemorrhage . </li></ul><ul><li>9. Dense cataract associated with vitreous haemorrhage . </li></ul>
  61. 65. Follow up Suggested follow-up Retinal Finding Annually Normal Every 9 months Mild NPDR Every 6 months Moderate NPDR Every 4 months Sever NPDR Every 2- 4 months CSME Every 6 months CNSME Every 2-3 months PDR
  62. 66. Aspirin & DRP <ul><li>Is Aspirin effective in preventing progression of diabetic retinopathy ? </li></ul><ul><li>Aspirin use did not alter progression of diabetic retinopathy . </li></ul><ul><li>Aspirin use did not increase the risk of vitreous hemorrhage . </li></ul><ul><li>Aspirin use did not effect visual acuity. </li></ul><ul><li>Aspirin use reduce the cardiovascular morbidity and mortality . </li></ul>
  63. 67. Sorbinil & DRP <ul><li>Sorbinil is an aldose reductase inhibitor. </li></ul><ul><li>Sorbinil does not affect the progression of DRP or Diabetic neuropathy. </li></ul>
  64. 68. Practical Points <ul><li>Pregnancy : </li></ul><ul><li>DR accelerate during pregnancy and improve postpartum. </li></ul><ul><li>Do not hesitate to treat with laser when indicated. </li></ul><ul><li>FFA should be avoided in all but the most difficult cases of macular edema. </li></ul>
  65. 69. Practical Points <ul><li>PRP : </li></ul><ul><li>Three-mirror lens can be used for both focal laser and PRP. </li></ul><ul><li>Do not forget lens magnification , in most lenses use 200 μ m to produce 500 μ m spot in the retina. </li></ul><ul><li>Do not count the spots but fill up an appropriate region of retina . </li></ul>
  66. 70. Practical Points <ul><li>Usually PRP performed in 2 sessions spaced 2-4 weeks apart. </li></ul><ul><li>If possible start with inferior retina. </li></ul><ul><li>If patient discomfortable during PRP: </li></ul><ul><li>Reassure the patient it is expected and the treatment going well. </li></ul><ul><li>Decrease the duration to about 0.05 s. </li></ul><ul><li>Do it in more but shorter sessions. </li></ul><ul><li>Retrobulbar anesthetic can be used. </li></ul>
  67. 71. Practical Points <ul><li>Major reason for under treatment is not well dilated pupil. </li></ul><ul><li>If NV recur after complete PRP : </li></ul><ul><li>Add more PRP in the periphery or between previous laser burns. </li></ul><ul><li>Vitrectomy . </li></ul>
  68. 72. Practical Points <ul><li>CSME + Capillary non perfusion : </li></ul><ul><li>Some recommend doing grid laser for area with capillary non perfusion (decrease possibility of NV ) </li></ul><ul><li>Lowering serum lipid and ME : </li></ul><ul><li>Clofibrate (in several British study) </li></ul><ul><li>Reduce amount of hard exudate but macular edema edema persist with only modest improvement in VA . </li></ul>
  69. 73. Remember <ul><li>Argon blue : 488 nm. </li></ul><ul><li>Argon green : 514 nm. </li></ul><ul><li>Dye yellow : 577 nm. </li></ul><ul><li>Krypton red : 647 nm. </li></ul>