1. Brian J. Mihok, D.O. Program Director Ophthalmology Grandview Hospital
Common Eye Problems
Brian J. Mihok, D.O.
Program Director Ophthalmology
Grandview Hospital

2. What is the most common cause of blindness in the United States?
Macular Degeneration *
Diabetic Retinopathy
Cataract
Glaucoma

3. Which of these potentially blinding diseases has early symptoms that the patient may recognize
Macular Degeneration
Diabetic Retinopathy
Glaucoma
None of the above*

5. Topics Anatomy Refresher Most Common Eye Problems The Big 3
Glaucoma, Macular Degeneration and Diabetes

6. Where to Start?
Recent study done at Georgetown University revealed that about 2/3 of internal medicine residents admit to not being comfortable with their ophthalmologic examination.
Also showed that when given a fundus photo 60% could not properly identify the optic nerve

7. The Healthy Eye
Light rays enter the eye through the cornea, pupil and lens. These structures all work to focus light on the retina.
Cornea – clear watch glass in the front of the eye responsible for 2/3 of focusing power of the eye
Lens – responsible for the other 1/3 of the focusing power
Iris – works to filter excess light
Pupil – empty space in the middle of the iris which allows light transmission

8. The Healthy Eye
The retina is a transparent multilayered structure that converts light rays into electrical impulses. This electrical signal is then sent through the optic nerve and eventually to the brain.
The brain then analyzes the information and produces what we perceive as our sight.

9. The Healthy Eye The retina consists of two main areas,
the macula and peripheral retina.
Macula
Small area in center of retina that is located between the retinal arcades.
It allows you to see fine details clearly.
At its center is the fovea, which allows activities like reading small print and recognizing a face.

10. The Healthy Eye Peripheral retina
Everything that doesn’t fall into the macula
Gives you your peripheral vision
Important for night vision
Better at detecting motion than the macula
Normal retina

11. Retina

12. Macula and Foveal Importance
Without the fovea the Best Visual potential is 20/200
The big E, qualifies as legally blind

13. What does 20/200 mean?
20/200
20/15
This patient can see at twenty feet what a normal vision person can see at 15.
Distance at which THIS patient would need to be from an object to be able to see it
Distance at which a patient with NORMAL VISION would need to be from an object to be able to see it

14. Legal Blindness
Defined as best corrected visual acuity of 20/200 or less in the better eye; or a visual field limitation such that the widest diameter of the visual field, in the better eye, subtends an angle no greater than 20 degrees.

15. Overview of the Most Common Eye Diseases

16. World Health Organization Data
Worldwide Most Common Causes of Blindness
Cataract
Glaucoma
Macular Degeneration
Corneal Opacities
Diabetic Retinopathy
Which of those diseases are preventable or curable?

18. What about in the US?
The number one cause of blindness in the US and most developed nations is Macular Degeneration
The most common cause of blindness of people under age 65 in the US is Diabetic Retinopathy
The most common blinding diseases in the United States are
Macular Degeneration, Glaucoma, Diabetic Retinopathy

19. The Big Three (Glaucoma, DM, AMD)
None of these big 3 have early symptoms
Screening is key to preventing vision loss
By the time patients have perceived loss the disease is advanced.

20. Diabetes

21. Diabetes
For Americans under the age of 65 Diabetes is the number one cause of blindness

22. Epidemiology As duration of DM increases so does the prevalence of DR
At 20 years 99% Type I and 60% of Type II have some diabetic retinopathy, with 3.6% of Type I and 1.6% of Type II being legally blind
National Health and Nutrition Examination Survey III
Rates of DR in diabetics over age forty is higher in AA (27%) & Mexican Americans (33%), than Caucasians (18%)

23. Diabetic Retinopathy
Hyperglycemia leads to damaged and incompetent capillaries
These capillaries can
Leak (causing edema, hemorrhages, exudate)
Shut down (ischemia, non-perfusion and neovascularization)

24. Findings in Diabetic Retinopathy
Micro aneurysms
Out pouching of diseased capillary endothelial cells
Intra retinal hemorrhages
Dot blot and flame
Leakage through diseased capillary endothelial cells
Hard exudates
Lipid exudates from leakage out of diseased capillary endothelial cells
Often associated with retinal edema

25. Micro aneurysms and Intra Retinal Heme

26. Hard Exudate

27. Findings in Diabetic Retinopathy
Cotton Wool Spot
Represents a local infarction of nerve fiber layer
White areas with fluffy margins
Have no predictive value in diabetic retinopathy
Venous beading
Tortuous veins and enlargement
Used to determine severity of retinopathy and likely-hood of progressing to severe vision loss

28. Cotton Wool Spots

29. Venous Beading

30. Vision Threatening Changes
Macular Edema
Neovascularization
Macular Ischemia

31. Retinal Edema
Can occur anywhere in the retina but not clinically significant unless in the macula and meets certain criteria
Occurs from leaky capillaries and is induced by vasoproliferative factors
Treatment: Injections or lasers

32. Macular Edema

33. Neovascularization
An attempt by the retina to reperfuse ischemic tissue
Often a cause of vitreous hemorrhage
Can lead to Tractional Retinal Detachments or Neovascular Glaucoma
Treatment: PRP
Kills ischemic tissue

34. Neovascularization

35. PRP

36. Macular Ischemia End result of decreased perfusion to the macula
Causes permanent vision loss

37. Macular Ischemia

38. Initial Screening and Follow up
Type I rarely have DR within the first 5 years of diagnosis however a number of Type II patients have retinopathy at the time of diagnosis
Type I
Initial exam should be with in the first 5 years of diagnosis then annually after 5 years
Type II
Initial visit at the time of diagnosis
Follow up varies depending on degree of retinopathy
Varies between annually down to monthly
Pregnant Diabetics
Seen during the 1st trimester and follow up as directed

39. Best Treatment of All Diabetic Retinopathy
Prevention
Diabetes Control and Complications Trial (DCCT) and the United Kingdom Prospective Diabetes Study (UKPDS) showed that intensive glycemic control decreased rate of onset and progression of Diabetic Retinopathy
UKPDS also showed that strict blood pressure control in conjunction with intensive glycemic control slows the progression of DR and vision loss

40. Glaucoma

41. Glaucoma Anatomy Refresher
Two main fluid compartments of the eye
Aqueous humor
Vitreous humor

42. Glaucoma Anatomy Refresher
Aqueous Humor is made by the ciliary body and travels through the pupil and drains our of our trabecular meshwork and into Schlems canal
Aqueous is made at a rate that can completely turn over all the aqueous in about 90 minutes.

43. Glaucoma 2nd leading cause of blindness in the world
Late detection is a major risk factor for blindness
Tends to be inherited
Number one risk factor for Glaucoma is AGE

44. Glaucoma
Now defined as an “Optic Neuropathy” which is often associated with increased intraocular pressure (IOP)
Increased IOP doesn’t mean glaucoma!!!!
Can have high IOP and never have glaucoma
Ocular hypertension
Can have normal IOP and have glaucoma
Normal Tension Glaucoma

45. Glaucoma Types Chronic problem Blindness typically over many years
Open Angle
Angle Closure
Chronic problem
Blindness typically over many years
Painless and often symptomless
VERY COMMON
Acute problem
Blindness can occur in hours
Red painful eye, photophobia and fixed dilated pupil
VERY UNCOMMON

46. Open Angle Glaucoma Findings
Normal vision
Normal or near normal visual fields
+/- increased IOP
Glaucomatous cupping of the optic disc

47. Angle Closure Findings
“Hot” eye
Red, painful
Blurry vision
Corneal edema
Nausea, Vomiting and abdominal pain

48. What Causes the Increase in IOP?
Open Angle
Angle Closure
Decreased drainage through the trabecular meshwork.
Exact reason is unknown.
Pupillary block
Given the right circumstances the iris can limit the flow of aqueous through the pupil
This causes the iris to bow forward, and narrow or completely occlude the drainage angle

49. Treatment Medications: Either increase outflow or decrease production
Open Angle
Angle Closure
Medications: Either increase outflow or decrease production
Laser: Thought to cause inflammatory response which “cleans” out the drain
Surgery: Create a fistulous passage for aqueous
Medications:
Used to help lower IOP in an the acute attack.
Pilocarpine may help prevent closure from starting
Laser: Create a new passage for fluid
Surgery: Cataract removal will provide more space between iris and lens

50. Treatment Early identification is key
If treated early most open angle glaucoma will never lead to significant visual dysfunction
If at risk patients are identified by screening angle closure can be prevented

51. Age-Related Macular Degeneration
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Age-Related Macular Degeneration

52. AMD Facts #1 cause of blindness in the US
Affects more than 30 Million people world wide
Inherited (multiple genes most as AD)
Twice as common as Alzheimer's in people over 60
Responsible for 50% of all blindness in developed nations

53. AMD Facts
In 2010 the world wide direct health care expenditure because of AMD was 255 billion dollars.
Smokers are 2-3x’s more likely to have AMD
Obesity and Hypertension are also risk factors for AMD

54. Retinal Anatomy

55. Macular Degeneration
A disease primarily of the Retinal Pigmented Epithelium.
The retina is secondarily injured

56. Retinal Pigmented Epithelium (RPE)
Primary function is to serve as a support cell to the metabolically active photoreceptors
Helps supply nutrients to the photoreceptors
Helps remove waste
Phagocytize old outer segments of the photoreceptors
Vitamin A cycle
Other functions
Absorb scattered
light and heat

57. Bruch’s Membrane
The anatomical barrier between the highly vascular Choroid and the RPE and Retina
The Choroid has more blood vessels per square mm than any where else in the body

58. What is age-related macular degeneration (AMD)?
Over time the RPE has difficulty keeping up with the high metabolic demand of the photoreceptors.
Waste materials from the retina accumulate between the RPE and the underlying Bruchs’ Membrane.
These are clinically seen as drusen
These drusen lead to inflammation
The drusen and inflammatory mediators are toxic to both the overlying RPE and the underlying Bruch’s membrane.

60. Drusen

61. Two types of AMD Atrophic (“dry”) macular degeneration.
Exudative (“wet”) macular degeneration.

62. Dry AMD The most common form of AMD
Wet AMD arises out of Dry AMD so everyone with Wet AMD also has Dry AMD
Vision loss is slow
Over many years

63. Dry AMD Drusen formation and RPE changes are the first signs of AMD.
Asymptomatic to the patient
As the process continues the waste products slowly cause death of photo receptors
This is irreversible.
Small central scotoma
Metamorphopsia

64. Dry AMD
Eventually enough RPE is damaged that patient ends up with geographic atrophy

65. Wet AMD Arises out of Dry AMD Vision loss may be rapid and severe.
10-15% of people with Dry AMD will go on to develop Wet AMD
Vision loss may be rapid and severe.
Causes about 80% of blindness because of AMD

66. With wet AMD, abnormal blood vessels are present under the retina
If Bruch’s membrane gets damaged enough it can form small breaks
These breaks act as an entryway for new blood vessel growth under the retina from the vascular choroid.
These new vessels leak blood/fluid into the retina and blur the central vision.
With wet AMD, abnormal blood vessels are present under the retina

67. Wet AMD

68. Age Related Eye Disease Study (AREDS)
AREDS investigated whether or not anti-oxidants had an effect on cataracts and macular degeneration.
No effect on cataracts
Slows progression of dry AMD and decrease risk of conversion to wet AMD in moderate to severe AMD:
Vitamins C, E, Beta Carotene, Zinc
500mg Vitamin C, 400 IU Vitamin E, 15mg Beta Carotene (25,000 IU Vitamin A), 80mg Zinc, 2mg of Copper
Zinc only group did almost as well
Lutein and Xeazanthine now replace beta carotene and have been shown to be equally beneficial
AREDS 2 showed no benefit from Omega 3 FA’s on top of antioxidants

70. Treatment of Dry AMD
Currently the only thing we can do are preventative
Smoking cessation
Vitamin supplementation
AREDS vitamins (I-Caps, PreserVision, Ocuvite)
Diet full of dark green vegetables
Exercise and weight loss
Blood pressure control
MANY new investigational therapies
including injections.

71. Anti-VEGF treatment for wet AMD
Currently the gold standard treatment
Largest drawback is frequency of treatment
Q monthly injections for as long as it takes
Earlier treatments worked to limit how bad final visual out come was. This works to halt progression from worsening from its current state.
Some people will even get
improvement
Given via a pars plana
intravitreal injection

72. Recommendations for patients with AMD
Change Modifiable Risk Factors
Smoking cessation
Vitamin supplementation
AREDS vitamins (I-Caps, PreserVision, Ocuvite)
Diet full of dark green vegetables
Exercise and weight loss
Blood pressure control
Daily Monitoring with Amsler Grid.
Early detection to stabilize at a higher start point
Amsler Grid, as seen through a normal eye
Amsler Grid, as might be seen through an eye with AMD

73. Blindness From the Big 3
AMD – leads to loss of central vision. Despite poor central vision most maintain full peripheral vision
Have difficulty with reading, watching TV, recognizing faces
Worst case: no central vision, but preserved periphery
Glaucoma – leads to loss of peripheral vision and if severe enough central vision.
Can have “legal blindness” and still have 20/20 vision
Worst case: Lights Out Dark Blind.
Diabetes – can cause loss of both peripheral vision and central vision.
Worst case: Lights Out Dark Blind

74. An Ounce of Prevention
Whether we are talking about Diabetes, AMD, or Glaucoma the best and most important thing we can do is screening exams
Most Ophthalmologic findings in Diabetic Retinopathy, AMD, and Glaucoma are asymptomatic to the patient. Patients don’t often times notice problems until the disease is advanced.

75. American Academy of Ophthalmology guidelines for eye exams
Age years: At least once during this period
Those with risk factors for glaucoma (African Americans or people with a family history of glaucoma) should be seen every 3-5 years.
Age years: At least twice during this period
Those with risk factors for glaucoma should be seen every 2-4 years.
Age years: Every 2-4 years.
Age 65 years or older: At least once a year.

76. Conclusions AMD is the #1 cause of blindness in the US
Control modifiable risk factors
Screening exams are vital as disease is often asymptomatic until conversion to wet AMD
Diabetes is the # 1 cause of blindness in the US for year olds
Screening exams are vital as disease is often asymptomatic until there is proliferative retinopathy
Glaucoma is the #2 cause of blindness worldwide
Most people with Open angle glaucoma have no idea they have a problem
With screening angle closure is preventable!