Slide 1 - MOA Internal Server

							The Essentials for Paraoptometric
  Personnel in Understanding
       Medical Optometry

          Jeff D. Miller, O.D.
         Stillwater, Oklahoma
     millereyedoc@cockrelleyecare.com
Baby Boomers

• Approximately 80 Million
• 7,918 people turn 60 each day in 2006
• That’s 330/hour
• Every day until 2014, 10,000 Americans
  turn 50
• 1/8 Americans are 65 or older
Health of Americans

• Diabetes –epidemic in children
• HTN – steep rise
• CVD – linked w/HTN
• Obesity – 15% in 1980 - 33% in 2004
• Obesity doubles the risk of vision loss
 AMD, Glaucoma, Cataracts, Diabetes
Ocular Disease -TODAY

• Diabetic Retinopathy is the leading cause
 of blindness ages 25-74

• AMD is the most common cause of
 blindness in Americans 60 and older

• Cataracts are the leading cause of
 blindness in the world
Ocular Disease-TODAY

• Glaucoma – 2.2 million cases diagnosed, 2
  million undiagnosed

• 1 Million blind, 2.4 million visually
  impaired (2/3 are female)

• By far the most common ocular disorder:
    “Ocular Surface Disease” or OSD
Ocular Disease Estimates
In The Year 2020
• NEI Eye Prevention Research Group
• Diabetic Retinopathy – 50% increase
• AMD – 70% increase
• Glaucoma – 3.36 million – 53% increase
• Legal Blindness – 70% increase

• In 2036 all today’s numbers will double
REMEMBER- OF THE EYE DISEASES WE ARE
COVERING TODAY THEY REPRESENT:
 A. THE LEADING CAUSE OF BLINDNESS IN THE USA
    AGES 25-74.

 B. THE LEADING CAUSE OF CENTRAL VISION LOSS IN
    PATIENTS OVER 60

 C. THE SECOND LEADING CAUSE OF PREVENTABLE
    BLINDNESS IN THE USA (CATARACTS ARE FIRST)

 AND THERE IS NO WAY TO TELL YOU HAVE THEM BASED ON THE
  WAY YOU FEEL! THEY ARE ONLY DETECTABLE THROUGH AN EYE
                    HEALTH EVALUATION
GLAUCOMA
• Glaucoma is a group of diseases that can damage the
  eye’s optic nerve and result in irreversible vision loss and
  blindness.

• Glaucoma is multifactorial – it is not a single disease
  process. Rather it is a large group of disorders.

• The term glaucoma should only be used in reference to
  the entire group of disorders, just as the term cancer is
  used to encompass many clinical entities with certain
  common denominators.
GLAUCOMA
• The common denominator in glaucoma is
  optic nerve damage/death which derives
  from various risk factors.
• Glaucoma is the leading cause of
  preventable blindness in the US.
• There are several forms of glaucoma, the
  most common is Primary Open Angle
  Glaucoma or POAG.
Forms of Glaucoma
• POAG, Primary Open Angle Glaucoma
• LTG or NTG, Low Tension or Normotensive
    Glaucoma
•   Angle Closure Glaucoma
•   Congenital Glaucoma
•   Secondary Glaucoma’s – Pigmentary Glaucoma,
    Neovascular Glaucoma, and Inflammatory or
    Uveitic Glaucoma, Angle Recession Glaucoma
Risk Factors for Glaucoma
•   Intraocular Pressure, IOP
•   Genetics - Family History
•   Age (increases after 40yrs and 60 yrs)
•   Race (African American, Hispanics)
•   Gender (men or women?)
•   Diabetes Mellitus
•   Cardiovascular Disorders
•   Obstructive Sleep Apnea
Glaucoma Diagnosis
• Traditionally: IOP, optic nerve changes, visual field
  defect – treat or monitor.
• Risk factors are better known today and play a large role
  in treatment initiation.

• Today’s technology also allows much earlier diagnosis
  and treatment initiation through various
  tests/technology:IOP, stereoscopic optic nerve
  evaluation, optic nerve topography, nerve fiber layer
  analysis with scanning lasers and OCT, central corneal
  thickness, gonioscopy, Visante OCT, blood flow analysis,
  and visual fields.
Diagnosis
• IOP – “normal” 10-22mmHg
• Remember LTG or NTG, IOP appears
    in the normal range
•   ONH evaluation –characteristic changes
•   CCT - central corneal thickness obtained via pachymetry
    - normal is 555 microns
•   Gonioscopy – evaluates where the aqueous fluid drains
•   Nerve Fiber layer Analysis: GDx VCC, HRT II and III,
    OCT (i.e.Stratus,Cirrus)
•   Visual Fields
ONH EVALUATION

Normal Healthy Optic Nerve
Grading cup to disc ratio
Normal Healthy Optic Nerve
   with small C/D Ratio
SUSPICIOUS ONH
GLAUCOMATOUS
ADVANCED GLAUCOMA WITH OPTIC ATROPHY
ADVANCING GLAUCOMA WITH
NOTCHING OF SUPERIOR RIM
                                  EMGTS-patients with
                                  exfoliation or recurrent
                                  disc hemorrhage may
                                  have worse prognosis
                                  and need greater tx and
                                  closer observation.



                                      CNTGS-”strongly
                                      predictive of disease
                                      progression”



OHTS-detection of disc hemorrhages-
84% were detected only by photos
16% by exam and photos. Increased
risk of glaucoma development found
however, 86.7% w/disc hem have not
converted to glaucoma.
Grading cup to disc ratio
  Optic Nerve Head Analysis

                                                                               Key
                                                                               parameters
   Disc edge is                                                                are Horizontal
 determined by                                                                 Integrated Rim
 the end of the                                                                Volume* and
RPE -shown by                                                                  Cup/Disc
   blue marker                                                                 ratios

  Yellow line on
      composite
        diagram                                                                Fundus image
       indicates                                                               for verification
individual radial                                                              of scan
  scan selected
  and displayed                                                                placement


*Comparison of three optical coherence tomography scanning areas for detection of glaucomatous damage.
     Wollstein G, Ishikawa H, Wang J, Beaton SA, Schuman JS. Am J Ophthalmol. 2005 Jan;139(1):39-43
xxx
CCT-Central Corneal Thickness
• Ultrasound Pachymetry (sound waves)
• Visante OCT Pachymetry (light waves)

• Ocular Hypertensive Treatment Study
 OHTS – CCT can suggest/determine risk
>588 microns (low risk)
=555-588 microns (mod. risk)
<555 microns (high risk)
Gonioscopy
Virtual Gonioscopy
Scanning Laser Polarimetry: GDx VCC
Retinal Nerve Fiber Layer
               GDx VCC Printout
    Normal                               Glaucoma

                      Fundus Image

                       Parameters

                      Thickness Map


                      Deviation Map


                      TSNIT Graph



Comparisons of each scan to the Normative Database
allows accurate and rapid interpretation in one exam
Correlation of the Deviation Map and Thickness
    Map with Visual Field Pattern Deviation
                 is shown below




 These are examples from normal to advanced glaucoma
 • A normal eye with normal thickness and deviation maps and normal visual field
 • An eye with focal Retinal Nerve Fiber Layer loss prior to visual field loss
 • A moderate glaucoma eye with superior RNFL loss and inferior visual field loss
 • An advanced glaucoma eye with advanced RNFL and visual field loss
Stratus OCT™   Cirrus™HD-OCT
Glaucoma – RNFL Thickness Analysis
 An OU analysis example (2)
         VISUAL FIELDS
• Helps to confirm a definitive diagnosis of
  glaucoma.
• Determines the degree of vision loss
  associated with glaucoma.
• Helps to monitor the progression of the
  disease and determine treatment
  strategies and if the medications and/or
  surgeries are working.
                                 Treatment
• Treatment – ultimate goal is to lower IOP by reducing
   the production of the fluid in the eye or increasing the
   outflow of the fluid (Aqueous)

• Medical Treatment
• Topical Glaucoma Drops
• Various Classes: reduce aqueous production or
  increase aqueous outflow
• Neuro-protection (now and future)
• Blood flow enhancers (future)
• Timoptic, Betimol, Betagan, Betoptis S, Azopt, Trusopt Travatan, TravatanZ,
  Lumigan, Xalatan, Alphagan, Alphagan-P, Cosopt, Combigan, Pilocarpine

• What about oral meds ? (Diamox, Neptazane)
Surgical
Treatment

• Laser treatment: The laser treats the tissue that
  the aqueous fluid drains through such that it
  opens or “cleans” it out increasing drainage
  ALT - Argon Laser Trabeculoplasty
  SLT - Selective Laser Trabeculoplasty

• Other Lasers
• Trabeculectomy - creates drainage canal
• Glaucoma valve – creates drainage canal
Glaucoma Management
• Once diagnosed patients should be monitored
    on a quarterly basis for IOP and yearly (at
    minimum) for changes in VF, optic nerve, nerve
    fiber layer damage and gonioscopy.
•   The more advanced the more often VF, and
    other testing should be performed.
•   Glaucoma suspects should be monitored yearly
    or on a 6 month basis depending on their
    findings and other health issues.
GLAUCOMA
QUESTIONS ?
MACULAR DEGENERATION
• Leading cause of severe irreversible central vision loss
    and legal blindness in individuals 60 and older in the US.
•   Predominantly Caucasian (Hispanics on the rise)
•   Approximately 30% of those over 75 have early AMD
•   23% of the remainder of those will develop it with
    in five years
•   By 2020 the incidence is estimated to rise by 70%
•   By 2036 all today’s numbers will double (Baby Boomers)
Macular Degeneration- Two Forms


   • Non-neovascular, dry or atrophic
         macular degeneration

    • Neovascular, wet or exudative
         macular degeneration
              Dry or Atrophic
         Macular Degeneration-AMD
• The retina is 10 layers thick. The last layer is called the RPE - Retinal
   Pigment Epithelium

• The RPE is responsible for providing nourishment to the retinal visual cells
   and maintains the retinal environment

• If the RPE is sick or damaged the retina degenerates
• AMD is characterized by abnormalities in the retinal pigment epithelium
   (RPE) with drusen formation

• Drusen are tiny white or yellow accumulations in Bruch’s membrane, a
   membrane between the final layer of the retina (RPE) and its blood supply
   in the choriocapillaris.
              Wet or Exudative
            Macular Degeneration
• The wet form of AMD is defined by the
    appearance of “new” blood vessel growth,
    neovascularization, originating in the layer below
    the retina called the choricapillaris.
•   These new blood vessels are abnormal and leak
    fluid and blood into the subretinal space causing
    disruption of the RPE with subsequent fibrosis
    and scarring
•   The damage to the RPE is irreversible
Macula
###
                 RNFL

                 RGC




          Rods & Cones

Retinal          RPE

Anatomy
      Cirrus HD-OCT Healthy Macula

                               NFL   ILM     GCL                       IPL     INL       OPL       ONL




                                      ELM       IS     IS/OS      OS         RPE        Choroid


NFL: Nerve Fiber Layer               OPL: Outer Plexiform Layer                    IS/OS: Junction of inner and outer
ILM: Inner Limiting Membrane         ONL: Outer Nuclear Layer                              photoreceptor segments
GCL: Ganglion Cell Layer             ELM: External limiting membrane               OS: Photoreceptor Outer Segment
IPL: Inner Plexiform Layer           IS: Photoreceptor Inner Segment               RPE: Retinal Pigment Epithelium
INL: Inner Nuclear Layer
DIAGNOSIS
• Primarily observation
• Patients must be seen yearly for eye
  health exams
• Retinal evaluation with various lenses and
  photographic devices
• OCT/HRT scans (Stratus,Cirrus,HRT-II,III)
• Fluorescein Angiography (RSFA)
• Macular pigment optical density
DRUSEN
Drusen and RPE Changes
Drusen and RPE Changes
SOFT DRUSEN
FLOURESCEIN ANGIOGRAPHY- RSFA
xx
DRUSEN
DRUSEN WITH PROGRESSIVE
RPE DISRUPTION/DROPOUT
RSFA OF DRUSEN AND
   RPE CHANGES
  EXUDATIVE OR WET
MACULAR DEGENERATION
WET AMD
    RSFA OF WET
MACULAR DEGENERATION
  WET OR EXUDATIVE
MACULAR DEGENERATION
   EXTENSIVE WET
MACULAR DEGENERATION
Macular Pigment
RISK FACTORS
                                                Diets high in antioxidants
                                                and lutein have been shown
•   Age                                         to have a positive effect on
•   Smoking                                     controlling the formation and
•   Family History                              advancement of dry AMD
•   Exposure to UV (sunlight)
•   Females
•   Caucasian
•   Hyperopia
•   HTN
•   Diabetes
•   Cardiovascular Risk Factors
•   High Fat Intake
•   Diets with foods that have a high glycemic index, refined sugars
    starchy foods “the white stuff”
Atrophic and Exudative
Macular Degeneration
Patient Education
• The leading cause of blindness in people over 60
• To avoid: don’t smoke, UV protection, diet high
    in lutein/antioxidants
•   Carrots vs. broccoli, peas and spinach
•   Dry accounts for 90%, Wet 10%
•   “New abnormal blood vessels” – CNV
    membranes, grow at a rate of 20 microns/day
•   Wet AMD patients prompted to seek exam when
    membranes are on avg. 3300 microns
            Lutein Concentration
                 mcg/100g
•   Kale          39,550    •   Yellow corn   764
•   Turnip Gr.     12,825   •   Asparagus     710
•   Spinach       12,198    •   Green Beans   640
•   Mustard Gr.     9,900   •   Artichokes    464
•   Collard Gr.     8,932   •   Red Cabbage   329
•   Green Peas      2,477   •   Tomatoes      123
•   Brussel Sprouts 1,819   •   White Onion     5
•   Broccoli        1,403
Injections for Exudative AMD
• Block Vascular Endothelial Growth Factor – Anti-VEGF
  drugs stop the growth of neovascularization in and
  beneath the retina restoring vision in many cases. Prior
  to 2005 these drugs were not available and most with
  wet macular degeneration lost significant vision if laser
  treatment was not an option.

• Lucentis $1500 to $ 2500 per injection

• Avastin $70 to $400 per injection
AMD/Cataracts and
Carbohydrate Consumption
• Carbohydrates – high glycemic index
• American Journal of Clinical Nutrition –
  followed 1036 women over 10 years.
  Carbohydrate intake directly correlated to
  incidence of early AMD.
• Dietary glycemic index was also linked
  with higher incidence of cataracts.
AMD/Cataracts and
Carbohydrate Consumption

• Annals of Internal Medicine – Study
  demonstrated women with early AMD
  were twice as likely to suffer a stroke vs.
  those who didn’t have AMD.
• This finding was noted after factoring out
  smokers, Diabetics, and HTN patients.
  MACULAR
DEGENERATION

QUESTIONS ?
DIABETIC EYE DISEASE
• DIABETES IS THE LEADING CAUSE OF NEW BLINDNESS
    IN THE US AGES 25-74.
•   Accounts for 5800 new cases a year of legal blindness.
•   Approximately 25% of diabetics have some degree of
    retinopathy.
•   A significant increased risk of cataracts and glaucoma is
    seen in patients with both Type I and Type II diabetes.
•   At minimum, a diabetic should be seen yearly for a full
    eye health exam.
DIABETIC EYE DISEASE
• The prevalence of retinopathy increases with the
    duration of diabetes and in those with uncontrolled blood
    sugar.
•   Patients are usually spared of diabetic retinopathy for
    3-5 years following the onset of the disease.
•   Diabetic retinopathy is broadly classified as
    nonproliferative and proliferative diabetic retinopathy –
    NPDR, PDR.
•   NPDR – bleeding and exudates (by-products) present in
    the retina
•   PDR – the growth of “new and abnormal” blood vessels
    or neovascularization
DIABETIC EYE DISEASE
• Macular Edema – diabetic cystoid macular
    edema (DCME) can occur in any stage of
    retinopathy and results in decreased visual
    acuity.
•   Retinal treatment other than diet, oral meds and
    insulin is considered when patients have NPDR
    with clinically significant DCME to avoid
    permanent vision loss and progression to PDR
TREATMENT
• Control of blood sugar is always paramount; daily
  evaluation as well as regular Hemaglobin A1C.
• Laser Treatment:
  Macular Grid - for Diabetic Cystoid Macular Edema
  (DCME)

  Pan-Retinal Laser Photocoagulation –
  or “PRP” to prevent or treat PDR which is characterized
  by the growth and extension of new blood vessels in the
  retina and vitreous.
NONPROLIFERATIVE DIABETIC
RETINOPATHY - NPDR
NPDR
NPDR
NPDR
NONPROLIFERATIVE DIABETIC
RETINOPATHY WITH MACULAR EDEMA
AND COTTON WOOL SPOTS (CWS)
PROLIFERATIVE DIABETIC
     RETINOPATHY
PROLIFERATIVE DIABETIC RETINOPATHY
  WITH PRE-RETINAL HEMORRHAGE
PROLIFERATIVE DIABETIC RETINOPATHY
 WITH NEOVASCULARIZATION OF THE
               DISC
          TERMED “NVD”
PDR WITH NEOVASCULARIZATION IN THE
       RETINA TERMED “NVE”
  NEOVASCULARIZATION ELSEWHERE
PAN-RETINAL PHOTOCOAGULATION

          “PRP”
RETINAL FIBROSIS
RETINAL FIBROSIS
RETINAL FIBROSIS WITH SUBSEQUENT
       RETINAL DETACHMENT
RETINAL DETACHMENT
PATIENT MANAGEMENT
• Diabetics should be examined yearly at
    minimum.
•   Visit schedule should be adjusted when patients
    are suspect for progression of retinopathy and
    or Diabetic Cystoid Macular Edema (DCME).
•   Photodocumentation, IOP checks, retinal
    imaging (OCT, HRT), and gonioscopy should all
    be considered based on the patients clinical
    presentation.
•   Education should include other ocular
    complications; glaucoma and cataracts.
DIABETIC EYE DISEASE

    QUESTIONS ?