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DIABETES 
AND 
THE EYE 
PRESENTED BY: DR. HUSSEIN ZAINAB
INTRODUCTION 
 The term “diabetes mellitus” describes a metabolic disorder of 
multiple etiology characterized by chronic hyperglycemia with 
disturbances of carbohydrate, fat and protein metabolism 
resulting from defects in insulin secretion , insulin action, or both. 
 The effects of diabetes mellitus include long-term damage 
,dysfunction and failure of various organs.
classification 
 There are two main types of diabetes 
 Type 1 diabetes (T1B): 
 usually develops a childhood and adolescence and 
patients require life long insulin injection for survival. 
 has an abrupt onset, with thirst , increased appetite , 
excessive urination and weight loss occurring over a 
period of several days.
 Type 2 diabetes (T2B): 
 usually develops in adulthood and is related to 
obesity. Lack of physical activity , and unhealthy 
diets. 
 This is the more common type of diabetes 
(representing 90% of diabetes cases worldwide) 
 Treatment may involve lifestyle changes and 
weight loss alone, or oral medication or even 
insulin injections.
 Another classification : 
 Insulin-dependent diabetes mellitus (IDDM). 
 Known as type 1. 
 Develops most frequently between 10 and 20 years of age. 
 Non-insulin-dependent diabetes mellitus (NIDDM). 
 Also known as type 2. 
 Develops most frequently between the ages of 50 and 70 
years. 
Now… the (ADA) uses the term IMMUNE-MEDIATED DIABETIS 
instead of TYPE1.
Epidemiology 
 The most common cause of blindness in developed countries is AMD, while 
in developing ones is diabetic retinopathy 
(because of a increase in the average of age and a good healthy care ) 
 Diabetes is the major systemic disease that causes blindness in 
the United States and is the leading cause of blindness in individual 40 to 
60 years of the age. 
 In USA 4 millions of diabetic patients of 40 years old or more have DR, 1 
million of them have threatened of blindness … 
 The rate of blindness among diabetic persons is 20 times that of the 
general population.
pathogenesis 
Disease of the capillaries and small vessels (microangiopathy) causes 
retinopathy, nephropathy, neuropathy , and heart diseases .
 High blood glucose levels cause endothelial cells lining the blood vessels to 
take in more glucose than normal (these cells do not depend on insulin) 
They then form more glycoproteins on their surface than normal 
 Also cause the basement membrane to grow thicker and weaker . 
 The walls of the vessels become abnormally thick but weak, and 
therefore they bleed ,leak protein, and slow the flow of blood through 
the body.
 
PATHOGENESIS
Ocular effects of diabetes 
Diabetes can cause changes to virtually all 
structures of the eye. 
 1. Cornea + tears 
 2. Aqueous 
 3. Iris 
 4. Lens 
 5. Vitreous 
 6. Retina 
 7. Internal muscles 
 8. External muscles 
6 
1 
3 
3 
5 
8 
8 
7 
4 
7 
2
Lids and conjunctiva 
 prone to infections due to high blood sugar level. 
 Recurrent styes and blepharoconjunctivitis . 
 Loss of tear 
 Xanthelasma,
CORNEA 
 Corneal sensitivity is commonly impaired in diabetes, This sensory deficit 
may predispose to bacterial corneal ulcers, neurotropic ulcers and difficulties 
with contact lenses.
 Intrinsic abnormalities of the epithelial basement membrane 
complexes , with impaired barrier function lead to: 
 Superficial punctate keratitis . 
 Poor healing after trauma
Pupil abnormalities 
 Rigid pupils – difficult mydriasis: 
The cause is an autonomic neuropathy, partially 
denervating both the sphincter and the dilator muscles ..
Iris 
 Hydrops of the iris. 
 Rubeosis iridis : 
• Neovascularization of iris 
• Retinal hypoxia 
• Release of vasoproliferative substance 
(angiogenic factor)
Intraocular Pressure 
 Glaucoma : 
is a complication of Rubeosis of 
the iris. 
 A low intraocular pressure : 
is associated with diabetic 
acidosis.
Lens 
 Refractive error :
Collection of the sugar alcohol sorbitol 
in the lens, due to increased aldose 
reductase activity , causes the lens to 
swell and changes its refractive power.
 MYOPIA SHIFT: 
 Increase in blood sugar level 
 Hyperglycemia 
 Increase in osmotic pressure of 
crystalline lens 
 Increase in refractive index of lens
 HYPERMETROPIC SHIFT: 
 Decrease in blood sugar level 
 Hypoglycemia 
 Decrease in osmotic pressure 
of crystalline lens 
 Decrease in refractive index 
of lens.
 Cataract : 
 Cataract is a major cause of vision impairment in 
people with diabetes. 
 It occurs 10-20 years after the onset of insulin dependent 
diabetes. 
 Control of the diabetes with restoration of normal blood 
glucose levels stops progression of the opacity.
True diabetes cataract (snow-  
flake/snow-storm catarct) 
Pre-senile cataract 
Diabetic papillopathy 
 Diabetic papillopathy is an uncommon ocular manifestation of 
diabetes mellitus (DM). 
 The underlying pathogenesis is unclear but it maybe the result of 
small vessel disease . 
 Presentation is usually with mild optic nerve dysfunction and slow 
progression .
 VA: 5/10 or better. 
 Non specific unilateral or 
bilateral mild disc swelling and 
hyperemia. 
 It usually resolves spontaneously 
within several months.
DIABITICS NEUROPATHY 
 Paralysis of ocular muscles innervated by the third or sixth nerve. 
 Sudden onset of diplopia and painful muscle paralysis 
associated with a homolateral headache . 
 Short duration of hyperglycemia in diabetic, the paralysis 
disappears spontaneously with several weeks . 
 Long time of hyperglycemia in diabetic , it persists up to 6 
months.
Diabetic pupillary defect 
 Medical lesion in diabetes usually spare the pupil, 
comparing with surgical lesion(aneurysm …) which 
involve the pupil.
 This is because of the microangiopathy which 
involves the vasa nervorum .., causing ischemia of the 
main trunk of nerve, and sparing the superficial 
pupillary fibers .. 
While spare the pial vessels 
which supply the superficial 
Pupillomotor parasympathetic 
fibers
Diabetic Retinopathy 
 Retinopathy is the most important ocular 
complication of diabetes 
 Prevalence of DR of any severity in the diabetic 
population is 30% and prevalence of blindness 
due to DR is approximately 5%
RISK FACTORS 
• Duration of DM 
• Control of DM. Will not prevent but delays 
• Hypertension 
• Renal Disease 
• Pregnancy 
• Obesity, hyperlipidaemia, smoking, anaemia
0% 
Duration and Diabetic retinopathy 
40% 
100% 
5% 
85% 
100% 
120% 
100% 
80% 
60% 
40% 
20% 
0% 
PRESNTAION AFTER 10-15 Y AFTER 30 Y 
Type 1 Type 2
DR Pathogenesis 
loss of pericytes 
thickening of basement membrane 
Proliferative and damage endothelial cells 
Increased capillary permeability/ 
abnormal vasoproliferation
Normal Diabetic
CLASSIFICATION 
 Non-proliferative : 
 Mild 
 Moderate 
 Severe 
 Proliferative :
Nonproliferative diabetic retinopathy 
 Mild : 
 Indicated by the presence 
of at least 1 micro aneurysm. 
 Referral : review in 1-2 years.
 Moderate: 
 Includes the presence of 
hemorrhages, micro - 
aneurysms, and hard exudates 
Cotton wool spot. 
 Referral : 
review in 6 months – 1 year ; 
or refer to ophthalmologist 
Exudate 
Microaneurysm 
Cotton wool
 Severe: 
 The (4-2-1) rule; one or more of: 
• hemorrhages and microaneurysms 
in 4 quadrants. 
• venous beading in at least 2 
quadrants. 
• intraretinal microvascular 
abnormalities in at least 1 quadrant 
 Referral : review in 4 months . 
IRMA 
Beading
Proliferative diabetic retinopathy 
 severe non-proliferative DR and one or more 
of the following : 
 Neovascularization : NVE , NVD. 
 Vitreous / Preretinal hemorrhage .
NVD 
Neovascularization
Visual loss in diabetic retinopathy : 
 Caused by : 
 Macularpathy 
 Vitreous hemorrhage 
 Retinal detachment
Macularpathy : 
Main cause to visual loss in diabetic retinopathy 
 edema 
 ischemic 
 exudate
Cotton wool 
Macularpathy 
exudate 
ischemic 
Normal
OCT 
Normal Macular edema
Vitreous hemorrhage
Retinal detachment
Management 
 Medical treatment . 
 Observation. 
 Laser therapy . 
 Anti VEGF 
 Vitrectomy.
 Medical treatment: 
 glucose control : 
 controlling diabetes. 
 maintaining the HbA1C level in the 6-7% range. 
 Level of activity : 
maintaining a healthful lifestyle with regular exercise can 
help reduce the complication of diabetes and DR. 
 Blood pressure control. 
 Lipid-lowering therapy.
 Follow up: 
Retinal finding Suggested follow-up 
Normal Annually 
Mild NPDR 1 year 
6 months - 1year or refer to 
ophthalmologist. 
Moderate NPDR 
Sever NPDR Every 4 months 
DME Every 2-4 months 
PDR Every 2-3 months
 Laser therapy: 
 reduces severe visual loss. 
 reduces legal blindness by 90% in people with severe 
nonproliferative or proliferative retinopathy. 
 Indications: 
 Proliferative diabetic retinopathy PRP. 
 Diabetic macular edema focal laser.
Panretinal photocoagulation 
PRP
Panretinal photocoagulation 
(PRP) 
Before After
Focal laser 
Before After
Anti VEGF 
 Bevacizumab Avastin ® 
 Ranibizumab lucentis® 
 Aflibercept Eylea®
Avastin ® : Bevacizumab 
 Is part of a class of drugs that block the growth of 
abnormal blood vessels. 
 Was initially approved by (FDA) as a treatment for 
different types of cancer. 
 Its use “off-label” to treat eye disease such as DR, RVO 
and wet-AMD. 
 This drug can stop the blood vessels leaking and growing 
.
 Avastin benefits in DR includes 
PDR and DME. 
 It could complement the focal 
photocoagulation in DME, 
 and an adjuvant agent to PRP in PDR therapy 
..
 Vitrectomy: 
 Removes blood 
 Removes Traction 
 Allows PRP
Vitrectomy
Aspirin in diabetic eye 
 Aspirin use did not alter progression of diabetic 
retinopathy. 
 Aspirin use did not increase risk of vitreous 
hemorrhage. 
 Aspirin use did not affect visual acuity. 
 Aspirin use reduced risk of cardiovascular morbidity 
and mortality.
Arteriolosclerosis 
Hypertension retinopathy 
IV 
III 
Normal 
Diabetic retinopathy
THANKS

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Diabetes and the Eye: A Guide to Diabetic Retinopathy

  • 1. DIABETES AND THE EYE PRESENTED BY: DR. HUSSEIN ZAINAB
  • 2. INTRODUCTION  The term “diabetes mellitus” describes a metabolic disorder of multiple etiology characterized by chronic hyperglycemia with disturbances of carbohydrate, fat and protein metabolism resulting from defects in insulin secretion , insulin action, or both.  The effects of diabetes mellitus include long-term damage ,dysfunction and failure of various organs.
  • 3. classification  There are two main types of diabetes  Type 1 diabetes (T1B):  usually develops a childhood and adolescence and patients require life long insulin injection for survival.  has an abrupt onset, with thirst , increased appetite , excessive urination and weight loss occurring over a period of several days.
  • 4.  Type 2 diabetes (T2B):  usually develops in adulthood and is related to obesity. Lack of physical activity , and unhealthy diets.  This is the more common type of diabetes (representing 90% of diabetes cases worldwide)  Treatment may involve lifestyle changes and weight loss alone, or oral medication or even insulin injections.
  • 5.  Another classification :  Insulin-dependent diabetes mellitus (IDDM).  Known as type 1.  Develops most frequently between 10 and 20 years of age.  Non-insulin-dependent diabetes mellitus (NIDDM).  Also known as type 2.  Develops most frequently between the ages of 50 and 70 years. Now… the (ADA) uses the term IMMUNE-MEDIATED DIABETIS instead of TYPE1.
  • 6. Epidemiology  The most common cause of blindness in developed countries is AMD, while in developing ones is diabetic retinopathy (because of a increase in the average of age and a good healthy care )  Diabetes is the major systemic disease that causes blindness in the United States and is the leading cause of blindness in individual 40 to 60 years of the age.  In USA 4 millions of diabetic patients of 40 years old or more have DR, 1 million of them have threatened of blindness …  The rate of blindness among diabetic persons is 20 times that of the general population.
  • 7. pathogenesis Disease of the capillaries and small vessels (microangiopathy) causes retinopathy, nephropathy, neuropathy , and heart diseases .
  • 8.  High blood glucose levels cause endothelial cells lining the blood vessels to take in more glucose than normal (these cells do not depend on insulin) They then form more glycoproteins on their surface than normal  Also cause the basement membrane to grow thicker and weaker .  The walls of the vessels become abnormally thick but weak, and therefore they bleed ,leak protein, and slow the flow of blood through the body.
  • 10. Ocular effects of diabetes Diabetes can cause changes to virtually all structures of the eye.  1. Cornea + tears  2. Aqueous  3. Iris  4. Lens  5. Vitreous  6. Retina  7. Internal muscles  8. External muscles 6 1 3 3 5 8 8 7 4 7 2
  • 11. Lids and conjunctiva  prone to infections due to high blood sugar level.  Recurrent styes and blepharoconjunctivitis .  Loss of tear  Xanthelasma,
  • 12. CORNEA  Corneal sensitivity is commonly impaired in diabetes, This sensory deficit may predispose to bacterial corneal ulcers, neurotropic ulcers and difficulties with contact lenses.
  • 13.  Intrinsic abnormalities of the epithelial basement membrane complexes , with impaired barrier function lead to:  Superficial punctate keratitis .  Poor healing after trauma
  • 14. Pupil abnormalities  Rigid pupils – difficult mydriasis: The cause is an autonomic neuropathy, partially denervating both the sphincter and the dilator muscles ..
  • 15. Iris  Hydrops of the iris.  Rubeosis iridis : • Neovascularization of iris • Retinal hypoxia • Release of vasoproliferative substance (angiogenic factor)
  • 16. Intraocular Pressure  Glaucoma : is a complication of Rubeosis of the iris.  A low intraocular pressure : is associated with diabetic acidosis.
  • 18. Collection of the sugar alcohol sorbitol in the lens, due to increased aldose reductase activity , causes the lens to swell and changes its refractive power.
  • 19.  MYOPIA SHIFT:  Increase in blood sugar level  Hyperglycemia  Increase in osmotic pressure of crystalline lens  Increase in refractive index of lens
  • 20.  HYPERMETROPIC SHIFT:  Decrease in blood sugar level  Hypoglycemia  Decrease in osmotic pressure of crystalline lens  Decrease in refractive index of lens.
  • 21.  Cataract :  Cataract is a major cause of vision impairment in people with diabetes.  It occurs 10-20 years after the onset of insulin dependent diabetes.  Control of the diabetes with restoration of normal blood glucose levels stops progression of the opacity.
  • 22. True diabetes cataract (snow-  flake/snow-storm catarct) Pre-senile cataract 
  • 23. Diabetic papillopathy  Diabetic papillopathy is an uncommon ocular manifestation of diabetes mellitus (DM).  The underlying pathogenesis is unclear but it maybe the result of small vessel disease .  Presentation is usually with mild optic nerve dysfunction and slow progression .
  • 24.  VA: 5/10 or better.  Non specific unilateral or bilateral mild disc swelling and hyperemia.  It usually resolves spontaneously within several months.
  • 25. DIABITICS NEUROPATHY  Paralysis of ocular muscles innervated by the third or sixth nerve.  Sudden onset of diplopia and painful muscle paralysis associated with a homolateral headache .  Short duration of hyperglycemia in diabetic, the paralysis disappears spontaneously with several weeks .  Long time of hyperglycemia in diabetic , it persists up to 6 months.
  • 26. Diabetic pupillary defect  Medical lesion in diabetes usually spare the pupil, comparing with surgical lesion(aneurysm …) which involve the pupil.
  • 27.  This is because of the microangiopathy which involves the vasa nervorum .., causing ischemia of the main trunk of nerve, and sparing the superficial pupillary fibers .. While spare the pial vessels which supply the superficial Pupillomotor parasympathetic fibers
  • 28. Diabetic Retinopathy  Retinopathy is the most important ocular complication of diabetes  Prevalence of DR of any severity in the diabetic population is 30% and prevalence of blindness due to DR is approximately 5%
  • 29. RISK FACTORS • Duration of DM • Control of DM. Will not prevent but delays • Hypertension • Renal Disease • Pregnancy • Obesity, hyperlipidaemia, smoking, anaemia
  • 30. 0% Duration and Diabetic retinopathy 40% 100% 5% 85% 100% 120% 100% 80% 60% 40% 20% 0% PRESNTAION AFTER 10-15 Y AFTER 30 Y Type 1 Type 2
  • 31. DR Pathogenesis loss of pericytes thickening of basement membrane Proliferative and damage endothelial cells Increased capillary permeability/ abnormal vasoproliferation
  • 33. CLASSIFICATION  Non-proliferative :  Mild  Moderate  Severe  Proliferative :
  • 34. Nonproliferative diabetic retinopathy  Mild :  Indicated by the presence of at least 1 micro aneurysm.  Referral : review in 1-2 years.
  • 35.  Moderate:  Includes the presence of hemorrhages, micro - aneurysms, and hard exudates Cotton wool spot.  Referral : review in 6 months – 1 year ; or refer to ophthalmologist Exudate Microaneurysm Cotton wool
  • 36.  Severe:  The (4-2-1) rule; one or more of: • hemorrhages and microaneurysms in 4 quadrants. • venous beading in at least 2 quadrants. • intraretinal microvascular abnormalities in at least 1 quadrant  Referral : review in 4 months . IRMA Beading
  • 37. Proliferative diabetic retinopathy  severe non-proliferative DR and one or more of the following :  Neovascularization : NVE , NVD.  Vitreous / Preretinal hemorrhage .
  • 39. Visual loss in diabetic retinopathy :  Caused by :  Macularpathy  Vitreous hemorrhage  Retinal detachment
  • 40. Macularpathy : Main cause to visual loss in diabetic retinopathy  edema  ischemic  exudate
  • 41. Cotton wool Macularpathy exudate ischemic Normal
  • 45. Management  Medical treatment .  Observation.  Laser therapy .  Anti VEGF  Vitrectomy.
  • 46.  Medical treatment:  glucose control :  controlling diabetes.  maintaining the HbA1C level in the 6-7% range.  Level of activity : maintaining a healthful lifestyle with regular exercise can help reduce the complication of diabetes and DR.  Blood pressure control.  Lipid-lowering therapy.
  • 47.  Follow up: Retinal finding Suggested follow-up Normal Annually Mild NPDR 1 year 6 months - 1year or refer to ophthalmologist. Moderate NPDR Sever NPDR Every 4 months DME Every 2-4 months PDR Every 2-3 months
  • 48.  Laser therapy:  reduces severe visual loss.  reduces legal blindness by 90% in people with severe nonproliferative or proliferative retinopathy.  Indications:  Proliferative diabetic retinopathy PRP.  Diabetic macular edema focal laser.
  • 52. Anti VEGF  Bevacizumab Avastin ®  Ranibizumab lucentis®  Aflibercept Eylea®
  • 53. Avastin ® : Bevacizumab  Is part of a class of drugs that block the growth of abnormal blood vessels.  Was initially approved by (FDA) as a treatment for different types of cancer.  Its use “off-label” to treat eye disease such as DR, RVO and wet-AMD.  This drug can stop the blood vessels leaking and growing .
  • 54.  Avastin benefits in DR includes PDR and DME.  It could complement the focal photocoagulation in DME,  and an adjuvant agent to PRP in PDR therapy ..
  • 55.  Vitrectomy:  Removes blood  Removes Traction  Allows PRP
  • 57. Aspirin in diabetic eye  Aspirin use did not alter progression of diabetic retinopathy.  Aspirin use did not increase risk of vitreous hemorrhage.  Aspirin use did not affect visual acuity.  Aspirin use reduced risk of cardiovascular morbidity and mortality.
  • 58. Arteriolosclerosis Hypertension retinopathy IV III Normal Diabetic retinopathy