Diabetic Eye Disease

8,634 views
8,273 views

Published on

Published in: Health & Medicine
1 Comment
12 Likes
Statistics
Notes
No Downloads
Views
Total views
8,634
On SlideShare
0
From Embeds
0
Number of Embeds
3
Actions
Shares
0
Downloads
908
Comments
1
Likes
12
Embeds 0
No embeds

No notes for slide

Diabetic Eye Disease

  1. 1. Diabetic Eye Disease
  2. 2. Diabetic Eye Disease <ul><li>Prevalence </li></ul><ul><li>Symptoms </li></ul><ul><li>Diagnostic techniques and signs </li></ul><ul><li>Pathophysiology </li></ul><ul><li>Associated conditions </li></ul><ul><li>Management </li></ul>
  3. 3. Diabetic Retinopathy Introduction <ul><li>Chronic </li></ul><ul><li>Bilateral </li></ul><ul><li>Symmetrical </li></ul><ul><li>Capillary disease </li></ul><ul><li>Caused by systemic Diabetes Mellitus (DM) </li></ul><ul><li>Primary area of effect along with </li></ul><ul><ul><li>Feet </li></ul></ul><ul><ul><li>Lower legs </li></ul></ul><ul><ul><li>Kidneys </li></ul></ul><ul><ul><li>Brain </li></ul></ul>
  4. 4. Diabetic Retinopathy - Prevalence <ul><li>The most common retinal vascular disease </li></ul><ul><li>Leading cause of preventable blindness in the working age population of the western world </li></ul><ul><li>Diabetes Mellitus </li></ul><ul><ul><li>4% in the UK >40 age group </li></ul></ul><ul><ul><li>2% in the UK general population </li></ul></ul><ul><ul><li>10% of DM are Type 1 </li></ul></ul><ul><ul><li>90% of DM are Type 2 </li></ul></ul>
  5. 5. Diabetic Retinopathy Type 1 vs Type 2 <ul><li>Type 1 </li></ul><ul><ul><li>Diagnosed before the age of 30 </li></ul></ul><ul><ul><li>Also known as insulin dependent DM (IDDM) </li></ul></ul><ul><ul><li>Also known as juvenile onset DM </li></ul></ul><ul><ul><li>Autoimmune disease with HLA genetic associations </li></ul></ul><ul><ul><li>Onset principally between 10 and 14 years old </li></ul></ul><ul><li>Type 2 </li></ul><ul><ul><li>Also known as non-insulin dependent DM (NIDDM) </li></ul></ul><ul><ul><li>Also known as adult onset DM </li></ul></ul><ul><ul><li>No HLA association </li></ul></ul><ul><ul><li>Incidence rises with age to 0.6% per year in 7 th decade </li></ul></ul>
  6. 6. Diabetic Retinopathy - Prevalence <ul><li>Diabetic retinopathy in 25% to 33% of DM patients </li></ul><ul><li>Sight threatening DR in 1 / 4 of juvenile onset type 1, 1 / 10 of later onset type 1 and 1 / 30 of type 2 diabetics </li></ul><ul><li>Nearly all (98%) of type 1 diabetics will have DR after 20 years duration of the DM </li></ul><ul><li>Duration of DM is the primary risk factor for the development of DR </li></ul><ul><li>The incidence of DR per year is lower, the earlier the age of diagnosis of DM </li></ul>
  7. 7. Diabetic Retinopathy DM Risk factors for Type 2 <ul><li>Afro-Caribbeans and Asians = relative risk factor 2-3x (Japanese have a relative risk factor <1) </li></ul><ul><li>Family history </li></ul><ul><li>Age </li></ul><ul><li>Hypertension </li></ul><ul><li>Obesity </li></ul><ul><li>Male </li></ul><ul><li>Smoking </li></ul><ul><li>History of DM during pregnancy </li></ul>
  8. 8. Diabetic Retinopathy –Morbidity Risk <ul><li>Myocardial Infarction (heart attack) (2x) </li></ul><ul><li>Cerebral Vascular Accident (stroke) (2x) </li></ul><ul><li>Peripheral vascular disease </li></ul>
  9. 9. Diabetic Retinopathy History & Symptoms <ul><li>Possible history of DM </li></ul><ul><ul><li>Type 1 almost certainly </li></ul></ul><ul><ul><li>Type 2 possibly not </li></ul></ul><ul><ul><ul><li>Mild systemic Sx </li></ul></ul></ul><ul><ul><ul><li>4-7 years suffering from condition prior to diagnosis </li></ul></ul></ul><ul><ul><ul><li>20% already have DR at diagnosis </li></ul></ul></ul><ul><li>Lethargy </li></ul><ul><li>Thirst (polydypsia) </li></ul><ul><li>Pee a lot (polyuria) </li></ul><ul><li>Weight loss </li></ul><ul><li>Increased appetite (polyphagia) </li></ul><ul><li>Reduced Visual Acuity </li></ul>
  10. 10. Diabetic Retinopathy History & Symptoms <ul><li>In Type 1, 30% present with diabetic ketoacidosis </li></ul><ul><ul><li>A hyperglycaemic episode </li></ul></ul><ul><ul><li>Sickly sweet breath smell (pear drops) </li></ul></ul><ul><ul><li>Signing respirations </li></ul></ul><ul><ul><li>Abdominal pain </li></ul></ul><ul><ul><li>Reduced consciousness or coma </li></ul></ul><ul><li>Hypoglycaemia is a result of over treatment </li></ul><ul><ul><li>Sweating </li></ul></ul><ul><ul><li>Shaking </li></ul></ul><ul><ul><li>Altered behaviour </li></ul></ul><ul><ul><li>Reduced consciousness levels </li></ul></ul><ul><ul><li>Seizure </li></ul></ul>
  11. 11. Diabetic Retinopathy Diagnostic Techniques & Signs <ul><li>Use the following tests in your eye examination: </li></ul><ul><ul><li>Distance Visual Acuity (right and left) </li></ul></ul><ul><ul><li>Intraocular pressure measurement </li></ul></ul><ul><ul><li>Anterior segment examination with a slit-lamp biomicroscope </li></ul></ul><ul><ul><li>Dilated fundus examination with an indirect ophthalmoscopic method </li></ul></ul><ul><ul><li>Pupil assessment </li></ul></ul>
  12. 12. Diabetic Retinopathy Diagnostic Techniques & Signs <ul><li>The following tests are used by the GP for the diagnosis of type 2 DM: </li></ul><ul><ul><li>Fasting blood glucose levels >7.8 mmol/l </li></ul></ul><ul><ul><li>Glycated haemoglobin (HbAC1) > 7% </li></ul></ul><ul><ul><li>Glucose tolerance test > 11.1 mmol/l 2 hrs after ingesting 75g of glucose </li></ul></ul><ul><ul><li>GTT >7.8 mmol/l suggests IGT, which often progresses to DM and carries the same cardiovascular risks as DM </li></ul></ul>
  13. 13. Diabetic Retinopathy Diagnostic Techniques & Signs <ul><li>The following stages of diabetic retinopathy have been described: </li></ul><ul><ul><li>Mild non-proliferative diabetic retinopathy (NPDR) </li></ul></ul><ul><ul><li>Moderate non-proliferative retinopathy </li></ul></ul><ul><ul><li>Severe non-proliferative retinopathy </li></ul></ul><ul><ul><li>Proliferative diabetic retinopathy (PDR) </li></ul></ul><ul><ul><li>Diabetic maculopathy </li></ul></ul>
  14. 14. Diabetic Retinopathy Diagnostic Techniques & Signs <ul><li>In mild NPDR the only lesions seen in the fundus are microaneurysms (MA) </li></ul><ul><ul><li>Outpouchings of capillary walls </li></ul></ul><ul><ul><li>Tiny, round, sharp-edged red dots </li></ul></ul><ul><ul><li>Most commonly seen in the temporal arcades </li></ul></ul><ul><ul><li>FFA shows them as white dots on a dark background </li></ul></ul><ul><ul><li>Located between the INL and the IPL </li></ul></ul><ul><ul><li>Very hard to differentiate from dot haemorrhages (MA are slightly smaller) without FFA </li></ul></ul>
  15. 15. Diabetic Retinopathy Diagnostic Techniques & Signs MA seen in moderate NPDR
  16. 16. Diabetic Retinopathy Diagnostic Techniques & Signs <ul><li>In moderate NPDR the same microaneurysms are seen plus any of: </li></ul><ul><ul><li>Intra-retinal haemorrhages </li></ul></ul><ul><ul><ul><li>Dot haemorrhages </li></ul></ul></ul><ul><ul><ul><li>Blot haemorrhages </li></ul></ul></ul><ul><ul><ul><li>Flame-shaped haemorrhages </li></ul></ul></ul><ul><ul><li>Intra-retinal lipid exudates </li></ul></ul><ul><ul><li>Cotton wool spots </li></ul></ul>
  17. 17. Diabetic Retinopathy Diagnostic Techniques & Signs Intra-retinal haemorrhages seen in moderate NPDR
  18. 18. Diabetic Retinopathy Diagnostic Techniques & Signs Intra-retinal lipid exudates seen in moderate NPDR
  19. 19. Diabetic Retinopathy Diagnostic Techniques & Signs Little effect on VA until extensive foveal coverage Affect VA if at fovea Rare before 45 years old Present at any age Random patterns Form streaks or circles Do not re-absorb Can re-absorb At posterior pole Near vascular lesions No vascular disease Vascular disease In Bruch’s membrane, poorly defined edges In OPL and sharp-edged Drusen Intra-retinal lipid exudates
  20. 20. Diabetic Retinopathy Diagnostic Techniques & Signs Cotton wool spots seen in moderate NPDR
  21. 21. Diabetic Retinopathy Diagnostic Techniques & Signs <ul><li>In severe NPDR extensive spread of the same features as mild NPDR are seen plus any of: </li></ul><ul><ul><li>Intra-retinal microvascular abnormalities (IRMA) </li></ul></ul><ul><ul><li>Venous beading/loops/segmentation </li></ul></ul><ul><ul><li>The 4-2-1 rule </li></ul></ul>
  22. 22. Diabetic Retinopathy Diagnostic Techniques & Signs Venous loop seen in severe NPDR Venous beading and IRMA seen in severe NPDR
  23. 23. Diabetic Retinopathy Diagnostic Techniques & Signs <ul><li>Proliferative Diabetic Retinopathy </li></ul><ul><ul><li>A sight-threatening retinopathy </li></ul></ul><ul><ul><li>Characterised by the growth of new blood vessels on the retina </li></ul></ul><ul><ul><li>New vessels within 1DD of the disc (NVD) </li></ul></ul><ul><ul><li>Or elsewhere (NVE) </li></ul></ul><ul><ul><li>Filamentous loops, from a single vein, form a seafan </li></ul></ul><ul><ul><li>Grow internal to the ILM and cover retinal vessels </li></ul></ul>
  24. 24. Diabetic Retinopathy Diagnostic Techniques & Signs NVD seen in PDR NVE seen in PDR
  25. 25. Diabetic Retinopathy Diagnostic Techniques & Signs <ul><li>New vessels </li></ul><ul><ul><li>Very leaky </li></ul></ul><ul><ul><li>Release substances that create a fibrous skeleton </li></ul></ul><ul><ul><li>Fibrous contraction pulls on the vessel </li></ul></ul><ul><ul><li>Rupture causes pre-retinal or vitreous haemorrhage </li></ul></ul><ul><ul><li>Further contraction causes traction retinal detachment or retinal tears and rhegmatogenous retinal detachment </li></ul></ul>
  26. 26. Diabetic Retinopathy Diagnostic Techniques & Signs Pre-retinal haemorrhage seen in PDR Vitreous haemorrhage seen in PDR
  27. 27. Diabetic Retinopathy Diagnostic Techniques & Signs Traction retinal detachment seen in PDR
  28. 28. Diabetic Maculopathy Diagnostic Techniques & Signs <ul><li>The most common cause of blindness in DM </li></ul><ul><li>Prevalence 30% after 20 years in both type 1 and type 2 DM </li></ul><ul><li>More prevalent in type 2 </li></ul><ul><li>Classified as: </li></ul><ul><ul><li>Focal </li></ul></ul><ul><ul><li>Diffuse </li></ul></ul><ul><ul><li>Ischaemic </li></ul></ul>
  29. 29. Diabetic Maculopathy Diagnostic Techniques & Signs Focal Maculopathy
  30. 30. Diabetic Maculopathy Diagnostic Techniques & Signs <ul><li>Diffuse maculopathy </li></ul><ul><ul><li>No obvious site of vascular leakage </li></ul></ul><ul><ul><li>Causes macular oedema </li></ul></ul><ul><ul><li>Causes loss of the foveal light reflex </li></ul></ul><ul><ul><li>Detectable only with stereoscopic viewing or FFA </li></ul></ul>
  31. 31. Diabetic Maculopathy Diagnostic Techniques & Signs <ul><li>Ischaemic maculopathy </li></ul><ul><ul><li>Extensive ischaemia and vascular leakage </li></ul></ul><ul><ul><li>Resulting from capillary closure </li></ul></ul><ul><ul><li>Multiple intra-retinal haemorrhages </li></ul></ul><ul><ul><li>Multiple cotton wool spots </li></ul></ul><ul><ul><li>IRMA </li></ul></ul><ul><ul><li>Venous abnormalities </li></ul></ul>
  32. 32. Diabetic Maculopathy Diagnostic Techniques & Signs Clinically Significant Macular Oedema
  33. 33. Diabetic Eye Disease Anterior Segment Diagnostic Techniques & Signs <ul><li>Manifest refractive changes </li></ul><ul><ul><li>1.5x more likely to be myopic </li></ul></ul><ul><ul><li>Investigate in adult-onset myopia </li></ul></ul><ul><li>Cataract formation </li></ul><ul><ul><li>More commonly cortical cataract </li></ul></ul><ul><ul><li>Predictive of mortality </li></ul></ul><ul><li>III rd and VI th cranial nerve palsies </li></ul><ul><ul><li>Esop and isolated SR palsy </li></ul></ul><ul><ul><li>Resolve in 2-6 months </li></ul></ul><ul><ul><li>No pupil involvement </li></ul></ul><ul><ul><li>Classic recent onset incommitant strabismus Sx </li></ul></ul>
  34. 34. Diabetic Eye Disease Anterior Segment Diagnostic Techniques & Signs <ul><li>Recurrent corneal epithelial erosions and reduced corneal sensitivity </li></ul><ul><ul><li>Trauma </li></ul></ul><ul><ul><li>CL fitting </li></ul></ul><ul><li>Conjunctival hyperaemia and MA </li></ul><ul><li>Blepharitis, styes and chalazion </li></ul><ul><li>Rubeosis Iridis </li></ul><ul><ul><li>Sign of advanced diabetic eye disease </li></ul></ul><ul><ul><li>Growth starts at pupil margin </li></ul></ul><ul><ul><li>Leads to acute ACG </li></ul></ul>
  35. 35. Diabetic Eye Disease Anterior Segment Diagnostic Techniques & Signs Rubeosis Iridis
  36. 36. Diabetes Mellitus Pathophysiology <ul><li>Failure in glucose metabolism </li></ul><ul><ul><li>Hyperglycaemia, following food intake </li></ul></ul><ul><li>Aetiology is different between type 1 and 2 </li></ul><ul><li>Insulin deficiency or insulin receptor resistance are the causes </li></ul>
  37. 37. Diabetes Mellitus Pathophysiology <ul><li>Insulin </li></ul><ul><ul><li>Created in the pancreas (beta cells) </li></ul></ul><ul><ul><li>Promotes cellular glucose uptake </li></ul></ul><ul><ul><li>Promotes conversion of glucose to glycogen </li></ul></ul><ul><ul><li>Promotes conversion of glucose to lipids </li></ul></ul><ul><li>Glucagon </li></ul><ul><ul><li>Created in the pancreas (alpha cells) </li></ul></ul><ul><ul><li>Opposite action to insulin </li></ul></ul>
  38. 38. Diabetes Mellitus Pathophysiology <ul><li>Type 1 diabetes </li></ul><ul><ul><li>Beta cells are destroyed by an inappropriate immune response to an antigen </li></ul></ul><ul><ul><li>Complete absence of insulin production </li></ul></ul><ul><ul><li>Cow’s milk additives in infant feeds and viruses implicated as possible antigens </li></ul></ul><ul><ul><li>Many associated HLA genes on chromosome 6 </li></ul></ul><ul><ul><li>Environment and heredity important – 30% concordance in identical twins </li></ul></ul>
  39. 39. Diabetes Mellitus Pathophysiology <ul><li>Type 2 diabetes </li></ul><ul><ul><li>Beta cells are less effective at secreting insulin </li></ul></ul><ul><ul><li>Insulin receptors in the body’s cells are less stimulated by a given amount of insulin </li></ul></ul><ul><ul><li>No HLA associated genetic component </li></ul></ul><ul><ul><li>Heredity very important – 100% concordance in identical twins </li></ul></ul>
  40. 40. Diabetic Retinopathy Pathophysiology <ul><li>A disease of the retinal microvasculature causing capillary leakage and occlusion </li></ul><ul><li>Larger retinal vessels are located in the NFL and GCL </li></ul><ul><li>Smaller retinal capillaries are located as deep as the INL </li></ul><ul><li>The RPE and the retinal vasculature form the Blood-Retinal barrier </li></ul><ul><ul><li>Tight junctions </li></ul></ul><ul><ul><li>No fenestrations </li></ul></ul><ul><ul><li>Pericytes to control growth and provide support </li></ul></ul><ul><ul><li>Basement membrane </li></ul></ul>
  41. 41. Diabetic Retinopathy Pathophysiology <ul><li>Abnormal changes to the microvasculature </li></ul><ul><ul><li>Thickening of the basement membrane </li></ul></ul><ul><ul><li>Loss of pericytes </li></ul></ul><ul><ul><li>Endothelial cell changes </li></ul></ul><ul><li>Basement membrane effect is accelerated ageing </li></ul><ul><li>75% pericyte loss removes support and allows bulging of the vessel wall (saccular MA) </li></ul><ul><li>Extra growth of endothelial cells, forming tight loop MAs </li></ul><ul><li>Loss of tight junctions breaks down the blood-retinal barrier </li></ul>
  42. 42. Diabetic Retinopathy Pathophysiology <ul><li>Intra-retinal lipid exudates </li></ul><ul><ul><li>From leakage of plasma proteins and lipo-proteins </li></ul></ul><ul><ul><li>Located in OPL and form streaks or circles around areas of leakage </li></ul></ul><ul><ul><li>Leakage at macula leads to visible oedema (focal and diffuse) </li></ul></ul>
  43. 43. Diabetic Retinopathy Pathophysiology <ul><li>Further leakage causes: </li></ul><ul><ul><li>Intra-retinal haemorrhages </li></ul></ul><ul><ul><li>Flame-shaped haemorrhages when from superficial capillary bed </li></ul></ul><ul><ul><li>Dot and blot haemorrhages when from deep capillary bed. </li></ul></ul>
  44. 44. Diabetic Retinopathy Pathophysiology <ul><li>Capillary blockage due to: </li></ul><ul><ul><li>Thickening of basement membrane </li></ul></ul><ul><ul><li>Sticky endothelial cell </li></ul></ul><ul><ul><li>Increased blood viscosity as platelets aggregate and red blood cells change </li></ul></ul><ul><ul><li>Causes local retinal hypoxia and nerve cell death </li></ul></ul><ul><ul><li>Metabolic debris accumulates in the nerve fibres as axoplasmic transport fails </li></ul></ul><ul><ul><li>This material is located at the edges of ischaemic retina and appears as cotton wool spots </li></ul></ul>
  45. 45. Diabetic Retinopathy Pathophysiology <ul><li>The retinal hypoxic response </li></ul><ul><ul><li>Vascular endothelial growth factor is released from veins in areas of retinal hypoperfusion </li></ul></ul><ul><ul><li>Initial response is limited to the capillary bed, in the dilation of pre-existing arterio-venous connections (IRMA) </li></ul></ul><ul><ul><li>Later, outgrowths from the veins begin to grow through the ILM and across the face of the posterior vitreous forming new vessels (PDR) </li></ul></ul>
  46. 46. Diabetic Retinopathy Pathophysiology <ul><li>New vessels </li></ul><ul><ul><li>Immature, without normal pericytes numbers or tight junctions, but with fenestrations </li></ul></ul><ul><ul><li>Prone to bleeding and leakage </li></ul></ul><ul><ul><li>Accompanied by fibroblasts, forming fibrous attachments between vessels and vitreous </li></ul></ul><ul><ul><li>Fibrous contraction causes: </li></ul></ul><ul><ul><ul><li>Bleeding </li></ul></ul></ul><ul><ul><ul><li>Retinal detachment </li></ul></ul></ul><ul><ul><ul><li>Retinal tears </li></ul></ul></ul><ul><ul><ul><li>Rhegmatogenous retinal detachment </li></ul></ul></ul><ul><li>VEGF leads to new vessel formation on the iris (rubeosis iridis) </li></ul>
  47. 47. Diabetic Retinopathy Pathophysiology <ul><li>The link between impaired glucose metabolism and microvascular pathophysiology is through the sorbitol pathway </li></ul><ul><li>In the presence of hyperglycaemia, aldose reductase catalyses the conversion of glucose into sorbitol </li></ul><ul><li>Osmotic changes cause the lens pathology </li></ul><ul><li>Toxic sorbitol destroys the capillary pericytes causing the microvascular changes </li></ul>
  48. 48. Diabetic Retinopathy Management <ul><li>Two-fold approach: </li></ul><ul><ul><li>Prevention through management of DM </li></ul></ul><ul><ul><li>Screening and direct treatment with laser photocoagulation when appropriate </li></ul></ul><ul><li>Control of DM is through good control of blood glucose levels and reduction of risk factors through lifestyle changes: </li></ul><ul><ul><li>Reduce lipid intake </li></ul></ul><ul><ul><li>Reduce sugar intake </li></ul></ul><ul><ul><li>Reduce obesity </li></ul></ul><ul><ul><li>Increase exercise </li></ul></ul><ul><ul><li>Reduce tobacco and ETOH intake </li></ul></ul>
  49. 49. Diabetes Mellitus Management <ul><li>Type 1: </li></ul><ul><ul><li>Self-administered sub-cutaneous insulin injections </li></ul></ul><ul><ul><li>Blood glucose monitoring </li></ul></ul><ul><li>Type 2: </li></ul><ul><ul><li>Lifestyle modification for 3 months </li></ul></ul><ul><ul><li>Patient urine glucose checks, GP blood glucose checks </li></ul></ul><ul><ul><li>HbAC1 blood tests </li></ul></ul><ul><ul><li>If control is insufficient use medical therapy </li></ul></ul>
  50. 50. Diabetes Mellitus Management <ul><li>Type 2 medical therapy: </li></ul><ul><ul><li>Sulphonylureas </li></ul></ul><ul><ul><ul><li>Glibenclamide </li></ul></ul></ul><ul><ul><ul><li>Gliclazide </li></ul></ul></ul><ul><ul><ul><li>Tolbutamide </li></ul></ul></ul><ul><ul><li>Biguadine </li></ul></ul><ul><ul><ul><li>Metformin (for obese, but not renal dysfunction) </li></ul></ul></ul><ul><ul><li>Intestinal glucosidase inhibitor </li></ul></ul><ul><ul><ul><li>Acarbose </li></ul></ul></ul><ul><ul><li>Thiazolidinediones </li></ul></ul><ul><ul><ul><li>Pioglitazone </li></ul></ul></ul><ul><ul><li>Prandial glucose regulators </li></ul></ul><ul><ul><ul><li>Repaglinide </li></ul></ul></ul><ul><ul><li>10% end up using insulin </li></ul></ul>
  51. 51. Diabetic Retinopathy Management <ul><li>NICE guideline for detecting DR: </li></ul><ul><ul><li>Test requirement: </li></ul></ul><ul><ul><ul><li>> 80% sensitivity </li></ul></ul></ul><ul><ul><ul><li>> 95% specificity </li></ul></ul></ul><ul><ul><ul><li>< 5% technical failure </li></ul></ul></ul><ul><ul><li>Suggested tests: </li></ul></ul><ul><ul><ul><li>Retinal photography </li></ul></ul></ul><ul><ul><ul><li>Indirect ophthalmoscopy with Volk lens and SLE by trained personnel </li></ul></ul></ul><ul><ul><li>Suggested procedure: </li></ul></ul><ul><ul><ul><li>Dilation with 1% tropicamide prior to application of test </li></ul></ul></ul>
  52. 52. Diabetic Retinopathy Management <ul><li>NICE guideline for screening protocol in DR: </li></ul><ul><ul><li>Recall system for annual review in type 2 DM </li></ul></ul><ul><ul><li>Appropriate and acceptable screening test to be applied to all type 2 diabetics </li></ul></ul><ul><ul><li>Participation in opportunistic screening is not an adequate substitute for formal screening and should be used only where formal screening is impossible </li></ul></ul>
  53. 53. Diabetic Retinopathy Management <ul><li>Diabetics can reduce the risk of DR by: </li></ul><ul><ul><li>Controlling BP and blood glucose levels </li></ul></ul><ul><ul><li>Losing/managing weight </li></ul></ul><ul><ul><li>Maintaining good levels of physical activity </li></ul></ul><ul><ul><li>Reduce cholesterol intake </li></ul></ul><ul><ul><li>Stopping/reducing smoking and alcohol intake </li></ul></ul><ul><li>Important especially for: </li></ul><ul><ul><li>Men </li></ul></ul><ul><ul><li>Asians and Afro-Caribbeans </li></ul></ul><ul><ul><li>Older people </li></ul></ul>
  54. 54. Diabetic Retinopathy Management Minimal or Mild Background DR Low risk Background DR Routine Care Recall for annual review <ul><li>Occurrence/worsening of lesions since previous assessment </li></ul><ul><li>Scattered exudates >1DD from fovea </li></ul><ul><li>People at high risk of progression </li></ul><ul><li>Sudden improvement in glycaemic control </li></ul><ul><li>Renal disease </li></ul><ul><li>Hypertension </li></ul>Early Review Recall and review every 3 - 6 months Unexplained drop in VA Hard exudates within 1DD of fovea Macular oedema Unexplained retinal findings Pre-proliferative or severe DR Referral Ophthalmologist within 4 weeks New vessels Pre-retinal and/or vitreous haemorrhage Rubeosis Iridis Urgent Referral Ophthalmologist within 1 week Sudden loss of vision Retinal detachment Emergency Referral Ophthalmologist same day Condition Action
  55. 55. Diabetic Retinopathy Management <ul><li>Laser photocoagulation: </li></ul><ul><ul><li>Argon laser, with a contact or Volk lens at a SL </li></ul></ul><ul><ul><li>Targeting laser and foot control </li></ul></ul><ul><ul><li>Topical anaesthesia </li></ul></ul><ul><ul><li>Light of 514nm </li></ul></ul><ul><ul><li>500 μm, 200mW, 0.1 secs exposure </li></ul></ul><ul><ul><li>Energy absorbed by blood and retinal pigment causes local heating </li></ul></ul><ul><ul><li>Burning kills retinal cells and seals blood vessels </li></ul></ul>
  56. 56. Diabetic Retinopathy Management <ul><li>The effect of the burn: </li></ul><ul><ul><li>Reduced local and global retinal oxygen demand </li></ul></ul><ul><ul><li>Enhanced transmission of oxygen from choroid </li></ul></ul><ul><ul><li>Breaks the metabolic chain of events leading to advanced diabetic eye disease </li></ul></ul>
  57. 57. Diabetic Retinopathy Management <ul><li>When to use Laser photocoagulation: </li></ul><ul><ul><li>No advantage to Tx at severe NPDR stage </li></ul></ul><ul><ul><li>Monitor every 4/12 and instigate Tx immediately PDR appears </li></ul></ul><ul><ul><li>Tx earlier if: </li></ul></ul><ul><ul><ul><li>One-eyed </li></ul></ul></ul><ul><ul><ul><li>Hx of fellow-eye PDR </li></ul></ul></ul><ul><ul><ul><li>Local circumstances prevent 4/12 follow-up </li></ul></ul></ul><ul><ul><li>NVD > ¼ disc area </li></ul></ul><ul><ul><li>NVD with pre-retinal/vitreous haemorrhage </li></ul></ul><ul><ul><li>NVE with pre-retinal/vitreous haemorrhage </li></ul></ul><ul><ul><li>Rubeosis Iridis </li></ul></ul><ul><ul><li>Extensive retinal hypoxia on FFA </li></ul></ul>
  58. 58. Diabetic Retinopathy Management <ul><li>How to use Laser photocoagulation: </li></ul><ul><ul><li>Usually pan-retinal photocoagulation (PRP) </li></ul></ul><ul><ul><li>1200-1600 (sometimes many more) individual burns </li></ul></ul><ul><ul><li>500 μm spacing </li></ul></ul><ul><ul><li>Outside temporal arcades </li></ul></ul><ul><ul><li>500 μm beyond nasal margin of disc </li></ul></ul><ul><ul><li>2 or more visits </li></ul></ul><ul><ul><li>Limited NVE may use more localised treatment </li></ul></ul>
  59. 59. Diabetic Retinopathy Management Pan-retinal photocoagulation
  60. 60. Diabetic Retinopathy Management <ul><li>PRP – The good: </li></ul><ul><ul><li>Reduces rate of severe visual loss to 50% of what it would be untreated </li></ul></ul><ul><ul><li>Causes regression of new vessels after 2-3 weeks </li></ul></ul><ul><ul><li>Returns venous circulation to normal </li></ul></ul><ul><ul><li>Can be re-applied </li></ul></ul><ul><li>PRP – The bad: </li></ul><ul><ul><li>Destroys retina </li></ul></ul><ul><ul><li>Causes extensive visual field loss </li></ul></ul><ul><ul><li>Causes loss of night vision </li></ul></ul><ul><ul><li>May cause reduction in VA if burns are too close to the fovea </li></ul></ul><ul><ul><li>May cause arcuate scotomata if burn energy is too high </li></ul></ul>
  61. 61. Diabetic Maculopathy Management <ul><li>More photocoagulation </li></ul><ul><ul><li>Less intense and smaller burns than PRP </li></ul></ul><ul><ul><li>Within the temporal arcades </li></ul></ul><ul><ul><li>Over area of retinal ischaemia and leakage in focal maculopathy </li></ul></ul><ul><ul><li>Tx area often surrounded by circinate exudates </li></ul></ul><ul><ul><li>Grid pattern for CSMO in diffuse maculopathy, with 100-150 burns in macular area </li></ul></ul><ul><ul><li>No Tx is useful for ischaemic maculopathy. 30% develop PDR within 2 years </li></ul></ul><ul><ul><li>Avoid the area within 375 μm of the fovea </li></ul></ul><ul><ul><li>Tx, if possible, reduces moderate visual loss to 40% of untreated condition </li></ul></ul>
  62. 62. Diabetic Maculopathy Management Grid pattern photocoagulation at macula, just post-treatment
  63. 63. Diabetic Eye Disease Management <ul><li>Vitrectomy: </li></ul><ul><ul><li>Removal of blood, vascular and fibrous material and vitreous from the vitreous </li></ul></ul><ul><ul><li>Replacement with clear fluid (silicone oil or saline) </li></ul></ul><ul><ul><li>Use when: </li></ul></ul><ul><ul><ul><li>Non-clearing vitreous haemorrhage (6/12) </li></ul></ul></ul><ul><ul><ul><li>Traction retinal detachment involving macula </li></ul></ul></ul><ul><ul><ul><li>Combined traction/rhegmatogenous retinal detachment </li></ul></ul></ul><ul><ul><li>Monitored using ultrasonography </li></ul></ul><ul><ul><li>Type 1 diabetics have the greater risk without Tx </li></ul></ul><ul><li>Detachment and tear repair </li></ul>
  64. 64. Diabetic Eye Disease Associated Conditions <ul><li>Primary open-angle glaucoma </li></ul><ul><li>Secondary angle-closure glaucoma </li></ul><ul><li>Vitreous haemorrhage </li></ul><ul><li>Traction retinal detachment </li></ul><ul><li>Rhegmatogenous retinal detachment </li></ul><ul><li>Cataract </li></ul><ul><li>Myopia </li></ul>
  65. 65. Diabetic Eye Disease Associated Conditions <ul><li>Myocardial infarction </li></ul><ul><li>Transient ischaemic attacks </li></ul><ul><li>Reversible ischaemic neurological deficit </li></ul><ul><li>Stroke </li></ul><ul><li>Peripheral neuropathy </li></ul><ul><li>Foot ulceration </li></ul><ul><li>Gangrene </li></ul><ul><li>Nephropathy </li></ul>
  66. 66. Diabetic Eye Disease Clinical Pearls <ul><li>Maculopathy is the commonest cause of blindness in diabetes mellitus </li></ul><ul><li>Clinically significant macular oedema is unrelated to visual acuity and can exist in the presence of ‘normal’ 6/6 vision. It can only be identified through observation using stereoscopic indirect biomicroscopy </li></ul><ul><li>FFA is only used for treatment , it is not a tool for diagnosis. Angiography is not required for treating proliferative disease since PRP does not require precise aiming of the laser </li></ul><ul><li>The development of diabetic retinopathy is time-dependent </li></ul>

×