CCLS Printable Handouts

Course Handouts

The Westin – Houston Memorial City 945 Gessner Road Houston, TX 77024

1

CONTACT LENS DISCOMFORT

A Global Perspective

JASON J. NICHOLS, OD, MPH, PHD, FAAO (DIPCL) UNIVERSITY OF HOUSTON COLLEGE OF OPTOMETRY

505 J. DAVIS ARMISTEAD BUILDING, HOUSTON, TX 77005 [email protected]

ABSTRACT Dry eye symptoms impact about one-half of contact lens wearers, and can ultimately lead to dropout and failure of continued lens wear. The goal of this course is to facilitate an understanding of contact lens discomfort to keep our patients happily in contact lenses. LEARNING OBJECTIVES: 1. To discuss recent activity in global thinking on contact lens discomfort (CLD), including the recent

completion of the Tear Film and Ocular Surface Society’s (TFOS) International Workshop on CLD. 2. To review concepts of definition and classification of CLD. 3. To review the epidemiology of CLD, including past and recent studies on patient-reported symptoms and

risk factors for CLD; I. To review the process of the TFOS International Workshop on CLD.

A. Historical look at other workshops—the TFOS Dry Eye Workshop (DEWS) and Meibomian Gland Dysfunction Workshop.

B. Process, objectives and timelines for current CLDW.

II. What is “Contact Lens Discomfort?”

A. Review of terminology, including that associated with the TFOS CLD Workshop.

B. Outline of the current definition of CLD.

C. Review of the current classification scheme for CLD. III. Epidemiology of CLD

A. Prevalence: Signs or Symptoms or Both?

B. Is it really dry eye? C. Factors associated with contact lens discomfort.

D. Prognosis

Ocular Surfaces: Sources of Contact Lens Discomfort Kelly K. Nichols, OD, MPH, PhD FERV Professor [email protected] Abstract: The impact of contact lenses on the ocular surface and the link between these interactions and contact lens discomfort are important considerations in contact lens practice. Evaluation of the ocular surface pre-fitting, as well as post-fit monitoring and management can improve contact lens outcomes. Objectives: Following completion of this course, the attendee will be able to: (1) Discuss current and previous literature that identifies ocular surface tissue alterations that may occur as a result of lens wear and (2) Identify diagnostic techniques that enable the clinician to detect ocular surface damage/ abnormalities that may lead to contact lens discomfort (CLD). Outline: 1) Review of involved tissues/diagnostic techniques

a) Cornea (1) Corneal fluorescein staining (2) TBUT (3) Stromal evaluation (4) Hypoxia (5) Link to contact lens discomfort (minimal association)

b) Conjunctiva/Lid (1) Bulbar conjunctival fluorescein/ lissamine green staining (2) Cytological conjunctival changes (3) Hyperemia (4) Palepbral “lid wiper” involvement (5) Meibomian gland involvement (6) Link to contact lens discomfort (moderate to high association)

c) Summary excerpt from the Contact lens Discomfort Workshop report: “In conclusion, some evidence is available to suggest a link between conjunctival and lid changes with CLD, with the strongest evidence being that related to meibomian gland and LWE changes. No convincing evidence of a link to CLD was unearthed with respect to any of the other forms of CL associated tissue changes.”

d) Brief comment on Contact Lens Interactions with the Tear Film i) Biophysical and the biochemical effects of contact lens wear on the tear film and

their influence on discomfort ii) Pre- and post-lens tear film iii) Protein, mucin, and lipid changes in CL wear iv) “Tear film stability (via evaporation) is recognized as a key factor in CLD”

Treatment and Management of Contact Lens Discomfort William L. Miller, OD, MS, PhD

The Tear Film and Ocular Surface Society (TFOS) just completed and published in Investigative

Ophthalmology and Visual Science (54:11) results from the International Workshop on Dry Eye Discomfort. This course will look at the treatment and management of this condition.

The treatment and management of contact lens-induced discomfort is often addressed through a variety of approaches by the individual practitioner. However, much of what is attempted is anecdotal with little support from evidenced-based medicine. This course will highlight what we know and don’t know about treating and managing this important issue influencing wearing time and ultimate contact lens wear in our patients. Specific topics to be addressed will include: I. Adjusting the Replacement Frequency II. Changing lens material III. The value of wetting agents a. external b. internal IV Lens factors a. edge shape b. base curve c. diameter d. back surface shape e. center thickness V. Lens Care systems VI. Nutrition VII. Punctal occlusion VIII Topical medication IX Environment X Blinking behaviour XI Neuromodulation.

Biologic Bandages: A Corneal “Rebirth”

Seema Nanda, OD

Cornea & Contact Lens Symposium

7th December 2013 Houston, TX

OUTLINE:

The Basics of Amniotic Membrane

The Amniotic Membrane

The amniotic membrane is the innermost lining of the placenta (amnion)

Amniotic membrane shares the same cell origin as the fetus

• Stem cell behavior

Structural similarity to all human tissue

The CRYOTEK™ Method

Patented and proprietary cryopreservation

Ensures key active components of the Extracellular Matrix (ECM) are retained

The only method that retains both:

The integrity of the tissue structure

The key active (ECM) components

Safe and effective

Supported by over 300 peer-reviewed articles

Over 100,000 implanted

Bio-Tissue Cryopreserved Amniotic Membrane is the ONLY AM granted wound healing indication by the FDA.

Technology Highlights

Impressive regenerative platform that possesses natural growth factors and optimal scaffolding properties within a complex extracellular matrix that are:

• Anti-inflammatory

• Anti-scarring

• Anti-angiogenic

Therapeutic actions:

• Promotes Stem Cell Expansion

• Suppresses pain

• Promotes cellular migration

• Expedites recovery

Inflammation & Healing

Inflammation is the Hallmark of All Ocular Surface Diseases

Inflammation’s Effect on Healing

� Inflammation: the first sign of wound healing & is also the hallmark symptom of all ocular surface diseases

� Uncontrolled inflammation leads to:

� Chronic pain and discomfort/irritation

� Delayed healing, more tissue damage

� Vision-threatening complication, e.g., scar/haze

� Effective control of inflammation is an important strategy to promote healing and minimize the risk of scar/haze

Different Outcomes of Tissue Injury

Passive vs. Active Therapies

• PROKERA® is an Active Therapy (Biologic Corneal Bandage)

• Controls inflammation

• Prevents additional damage

• Promotes and accelerates wound healing

• Prevents / reduces scar formation

PROKERA®: Biologic Corneal Bandage

� PROKERA® utilizes the proprietary CryoTek™ cryopreservation process that maintains the active extracellular matrix of the amniotic membrane which uniquely allows for regenerative healing.

� PROKERA® is the only FDA-cleared therapeutic device that both reduces inflammation and promotes scar less healing

� PROKERA® can be used for a wide number of ocular surface diseases with severity ranging from mild, moderate, to severe

PROKERA®: Biologic Corneal Bandage An Active Amniotic Membrane

PROKERA® Specifications

PROKERA® Insertion

Set patient expectations! Inform the patient they may experience some foreign body sensation

Apply topical anesthesia

Rinse the PROKERA® a with a sterile solution (saline, BSS etc…)

Hold the upper eyelid

Ask the patient to look down

Insert the PROKERA® into the superior fornix

Slide the PROKERA® under the lower eyelid

Post-Treatment Protocol

Tegaderm/Tapesorrhaphy

When to Remove PROKERA®

Determining when to remove PROKERA®

patient and case dependent

Follow your usual protocol for follow-up

Fluorescein staining can be used while PROKERA® remains on the eye to determine healing progression

Expect to see the amniotic membrane in PROKERA® to thin when:

Significant inflammation is present

There has been over exposure to air

PROKERA® Removal

Topical Anesthetic

Pull the lower eyelid

Lift the lower edge of PROKERA® using a Q-tip or forceps

Ask the patient to look down

Slide the PROKERA® out with gentle pressure on the upper eyelid

Case Study 1: Recurrent Corneal Erosion

Published Case Review

� Publication: Clinical Experimental Ophthalmology

� Publication Year: 2013

� Purpose: To evaluate the efficacy of placement of PROKERA® in treating recurrent corneal erosion

� Results: After debridement & placement of PROKERA® complete epithelialization was noted in ALL eyes in 4 – 7 day

� Recurrence rate: 1/11 eye

Case Study 2: Bacterial Keratitis

Published Case Review

Summary

11/11/2013

IOLs Competing withthe Contact Lens?

Shehzad A. NarooBSc (Hons), MSc, PhD, FCOptom, FIACLE, FAAO, FBCLA, FEAOO

Senior Lecturer, Aston UniversityExaminer - College of Optometrists

Editor - Contact Lens and Anterior EyePresident – Int’l Assoc’ of CL Educators

Consultancy and grants

ConsultancyAlcon, J+J (TVCI), B+L, EyeSpy Products Ltd, College of Optometrists (UK), IACLE, BUCCLE, Contact Lens and Anterior Eye Journal, University of Canterbury, Al-Shifa Eye Trust

GrantsLenstec, Lensar, Refocus, Technology Strategy Board, Oculus, Oculentis, Bimrimgham Optical Group (Nidek UK)

Non-laser refractive surgery procedures

Intrastromal corneal ringImplantable contact lens / Phakic IOLClear lens extractionSurgery for presbyopia

Multifocal ablationsMonovisionScleral elongation bands (SEBs) /ScleroectomyMultifocal IOLsAccommodating IOLs

Intrastromal corneal ring

Biocompatible semi circular PMMAused to correct myopia l.00 - 4.50DS

Phakic IOL

Posterior phakic lensImplantable contact lensAnterior chamber depth of at least 2.8 mm requiredPeripheral iridotomyMyopia 3-20 DSHyperopia 4-14 DS

Anterior phakic lensIris claw lens

Posterior phakic IOLs/ Implantable CLs

video courtesy of Ioannis Pallikaris

11/11/2013

Anterior Phakic IOLs

video courtesy of IOLtech

Iris claw IOL

Clear lens extraction

Cataract surgeryPhacoemulsificationSmall incisions (3-4 mm)Combined with other procedures (AK)

Higher refractive errorsCareful biometryNot diseased lensesFoldable and multifocal intraocular lenses (IOLs)

Principles of Phacoemulsification

High speed ultrasonic hollow bored probe inside the eye allows emulsification of lensVibrating tip cuts nucleus into tiny particles and aspirates themClear back lining (posterior capsule) is preserved and acts as a support for the IOLAllows small self-sealing incisions (no sutures)Lower complication rate than older surgeryShorter recovery time (4 - 6 weeks)

Astigmatic Surgery

Only for corneal astigmatismPaired limbal relaxing incisionsAxis of positive cylinderGreater than 1.5D pre-op cylinder

Surgery for presbyopia

MonovisionLasers, IOLs and Thermokeratoplasty

Multifocal laser ablationsScleral elongation bands /ScleroectomyIOLs (Multifocal and accommodating)Surgery on the lens

Replacement of the lens with a flexible material within the capsule

11/11/2013

Ho:YAG laser (Holmium)

80-90% corneal depthMean temperature 55-60oc1 to 3 DS of hyperopiaWavelength of 2.1µmPrimary or surgically induced hyperopia

Conductive Keratoplasty (CK)

Radio wavesNon-contact75% corneal depthTip width of 90 µmDuration = 0.6sMean temperature 65oc

Scanning spot excimer laser

Power gradually becomes more plus (+)

towards lens center

Power becomes more positive towards lens center, plus a distinct

central zone of greater plus (+) power

2.4mm

5.5mm

8.0mm

CLs for presbyopia Scleral Surgery

Based on Schachar’s theoryPresbyopia = � distance between ciliary muscle and lens equator

Zonules slack and lens bows in relaxed position

Lens cannot bow further when ciliary muscle contracts

Scleral surgery –� lens/ciliary body distanceIncreasing the effective working distance of the ciliary muscle in eyes with presbyopia

11/11/2013

Scleroectomy / SEBs

Radial incisions

Allows ciliary body to shift outwards?

Silicone implants can be placed in cuts

Scleral expansion bands (SEBs)

Conventional theory

Helmholtz theoryPresbyopia = hardening of the lens

Lens growth and hypertrophy are minor factors

Confirmed by Glasser in enucleated eyes (Glasser et al. 1998, 2001)

Reduction in stretch mimics loss of accommodation with age

About PresVIEWTM

Scleral implant to improve and restore the natural accommodative process in the aging eye Implants reengineered 2006 to 2009- Two part interlocking design holds permanently in the sclera

PresVIEW : Strong Safety Profile

Outside of visual axis- Cornea shape & integrity unaffected- Crystalline lens remains intact

Low incidence of adverse eventsReversible - Implants can be easily removedNo foreign body sensation for patients19% reduction in IOP

Patients See Significant Improvement in Near VisionHow Has Your Near Vision without Glasses Changed Since The Procedure? (at 24 months, n=44)

NEC patient survey used in FDA pivotal study

Clear lens extraction

PhacoemulsificationSmall primary incisions (3 mm)Not diseased eyesElective procedure

High refractive errorsCombined with other proceduresCareful biometryNew designs of IOLs

11/11/2013

AMO Array IOL

Distance-dominant, effectively 3.5D add

Other mutlifocal designs

AcrySof ReSTOR by AlconGradually reducing diffractive steps (apodizing optics)

ReZoom by AMOCentre near design, similar to Array

Tecnis by AMOControls spherical aberration

Hinged optic allows forward movement in response to accommodationAs ciliary body contracts, vitreous cavity pressure rises & IOL optic moves forwardMovement causes �+ve power

Accommodating IOLs Accommodating IOLs

Our Results

Subjective amplitude of accommodation1CU: 2.2 ± 0.4D (range 1.5 to 3.0D)KH3500: 3.5 ± 1.5 D (range 1.5 to 6.4 D)

Objective amplitude of accommodation1CU: 0.72 ± 0.38DKH3500: 0.32 ± 0.29 D (Range 0.0 to 1.1D)Monofocal 0.2 � 0.1 D (Range: 0.0 to 0.4 D)

24+ months data with KH-35000.3 � 0.3 D; range: 0.00 to 1.0 D Inserted through a

3.8mm incision

11/11/2013

UBM video LENSAR�femtosecond�laser

Restore flexibility to the crystalline lensPermits sliding of fibers necessary for changes in lens shape during accommodation

Determine the ideal model of the lens that will assist in the development of treatment algorithms

Visual�axis�spared�to�limit�subjective�symptoms Appearance�at�1�week�post�operative

Results

A third of subjects showed an improvement in objective accommodation (measured with Grand Seiko autorefractor)

The Grand Seiko measures over a central diameter of ~2.2mm which may underestimate the outcomes

Over one half of subjects showed an improvement in subjective accommodation (push down method)Over 40% of subjects showed increase in near acuity

Personal opinions

CL should be used as a first optionRefractive surgery should be offered only to carefully selected patientsOptometrists to offer unbiased adviceOptometrists should be fully aware

1

2

3

4

5

6

7

8

9

10

11

12

13

14

15

16

17

18

19

20

21

22

23

24

25

26

27

28

29

30

31

32

33

34

35

36

The Corneal Stroma Is A Continuous, Self-Stabilizing Structure Without Independent Layers.

James V. Jester, Moritz Winkler and Donald J. Brown

Introduction

Motivation:

Based on the observation by Werner Kokott (1938) our goal has been to develop a "blueprint" of the corneal collagen fiber patterns to better understand the mechanisms controlling corneal shape and function.

Purpose:

Define the micro- to macrostructural and biomechanical details of the cornea to understand what controls corneal shape and how this may impact refractive surgery.

Classical Corneal Model:

Five (six?) layer structure for which collagen is the principal structural component. Collagen is thought to be organized in a basket weave pattern of orthogonally organized collagen fibers or lamellae.

Non-linear Optical High Resolution Macroscopy (NLO HRMac) of the Cornea

Basis of NLO HRMac

Uses femtosecond lasers to generate multiphoton tissue interactions leading to two photon excited fluorescence, second harmonic generated (SHG) signals and laser induced optical breakdown

SHG signals from the cornea detect longitudinally oriented collagen fibers only.

NLO HRMac

Serially acquired consecutive overlapping 3-D image stacks that are digitally combined into a single large-scale, high-resolution mosaic.

Images planes can span the entire width of the corneal cross-section at sub-micron resolution.

HRMac Quantification of Corneal Structure

Quantifying fiber interconnectivity.

Collagen fibers show a high degree of branching and anastamosis. Measurement of fiber branching patterns show a gradient that is highest in the anterior stroma that decreases logarithmically in the posterior stroma.

Collagen fiber interconnectivity also correlates with an axial gradient in corneal stiffness and compliance.

Species variations in fiber interconnectivity (rabbits versus human) suggest that fiber interconnectivity regulates corneal stiffness.

3-D characterization of fiber interconnectivity.

Three types of interacting fibers can be identified. bow spring fibers that connect to the anterior limiting lamina, densely intertwined anterior corneal fibers that show marked branching and anastomosis, and anchoring fibers that extend from the limbus to the central cornea.

Bow spring fibers in conjunction with densely intertwined fibers form a rigid anterior corneal region. Anchoring fibers form connections between distant parts of the cornea. Together these fibers stabilize corneal biomechanics and determine corneal shape.

Bow spring fibers and densely intertwined fibers are absent in the anterior cornea of Keratoconus buttons.

Stromal collagen architecture is a continuum.

Interconnections of collagen fibers connect fibers from the anterior stroma to the posterior stroma and form a continuum. Fiber are not arranged as independent structures.

The posterior stroma is similarly connected to the anterior stroma and does not form a distinct layer.

Conclusions

The classical "basket weave" model of corneal structure is not correct. Rather the human cornea is a continuous, self-stabilizing structure showing interconnection between the anterior and posterior cornea.

Implications for refractive surgery.

Anterior cornea likely has stabilizing function.

Refractive procedures weaken corneal biomechanics by removing some of the stabilizing components.

Removal of anterior layers do not destabilize the cornea due to the interconnectivity to posterior layers until some critical threshold is reached.

Corneal Anatomical Pearls

Recently it was reported that a new corneal layer had been discovered by researchers at the University of Nottingham, UK. This observation was published in the September issue of Ophthalmology.1 In the same issue of this journal a dissenting view of this observation was presented.2

Dua et al1 reported that using the Big Bubble (BB) technique they were able to separate the 5 to 8 most posterior lamellae from the rest of the stroma and that these posterior lamellae were acellular. The thickness of this postulated layer was on average 10 microns and contained the same collagenous components as the rest of the stroma. Dua and co-workers felt that this new observation ‘will have considerable impact on posterior corneal surgery’

The authors of the alternative interpretation2 pointed out that this posterior portion of the stroma is not acellular and showed pictures of keratocytes within 5 microns of the posterior limiting lamina (eponymous name – Descemets’ membrane). A review of literature shows that it has been known for 150 years that there is a difference between anterior and posterior stroma with regards to its biomechanical properties. Furthermore, many surgeons have for years avoided the BB procedure in posterior corneal surgery because corneal microperforation can easily occur. Trefination with blunt dissection is a safer alternative. The extensive and intricate interwoven layout of anterior lamellae as opposed to the more simple layering of posterior lamellae on top of each other explains the biomechanical change the stroma undergoes from anterior to posterior. Indeed, over the past couple of decades my own dissections of human cadaver corneas confirm this mechanical difference. A current textbook on ocular anatomy has for years contained text and images pointing out the differences between anterior and posterior stromal architecture,3

Therefore, the BB technique, which is after all a highly non-physiological approach, has not demonstrated anything we did not already know. In addition, the proposed corneal layer does not contain anything we do not find in the rest of the stroma. The dissenting view article2 acknowledges Dua et al’s1 work as novel in demonstrating the biomechanical property of the extreme posterior stroma but it was argued that their work has not isolated a new corneal layer. However, future research will determine the final outcome of this difference of opinion among scientists, An additional guest editorial in the same issue of Ophthalmology made the point that that science is self correcting but

not self congratulating.4 The latter is a reference to the fact that Dua et al1 proposed that we call this ‘new’ corneal structure ‘Dua’s layer’. Historically it is not the discoverer that adds his or her name to the anatomical nomenclature but subsequent followers may wish to promote such an acknowledgement. A classic example of this more respectful approach is Sir William Bowman, who 1847 proposed that the layer he was first to describe and sandwiched between the epithelium and the stroma be called the anterior elastic lamina. However, modern morphologists are trying to get away from the confusing anatomy of eponyms and replace these names with a more descriptive terminology. This is not a new idea but a 150 year old effort, which most recently was published in 1998 as Terminologica Anatomica.5

In summary, my last count of the layers forming the cornea ended with 5 layers and that is what I will teach my students!

References 1. Dua HS, Faraj LA, Said DG, Gray T, Lowe J. Human Corneal Anatomy

Redefined. A Novel Pre-Descemet’s Layer (Dua’s Layer). Ophthalmology,120 (9), 1778 – 1785, 2013.

2. Jester JV, Murphy, CJ, Winkler M, Bergmanson JPG, Brown D, Steiner RF, Mannis MJ. Lessons in Corneal Structure and Mechanics to Guide the Corneal Surgeon. Ophthalmology, 120 (9), 1715 – 1717, 2013.

3. Bergmanson JPG. Clinical Ocular Anatomy and Physiology. 20th Edition. Texas Eye Research and Technology Center, Houston, Texas, 2013.

4. Schwab I. Who’s on First. Ophthalmology, 120 (9), 1718 – 1719, 2013. 5. Terminologica Anatomica. Federative Committee on Anatomical Terminology

(FCAT). Stuttgart, Thieme, 1998.

1

DAILY DISPOSABLES

A Daily Dose of Good Vision & Comfort

JASON J. NICHOLS, OD, MPH, PHD, FAAO (DIPCL) UNIVERSITY OF HOUSTON COLLEGE OF OPTOMETRY

505 J. DAVIS ARMISTEAD BUILDING, HOUSTON, TX 77005 (713) 743-2471

[email protected]

ABSTRACT Daily disposable lenses have been available for over 15 years and have been associated with widespread use in various worldwide markets. The purpose of this talk is the review the benefits associated with daily replacement contact lenses and to discuss perceived barriers to this modality’s continued growth. LEARNING OBJECTIVES:

1. To review market trends in various contact lens modalities and replacement schedules, 2. To discuss the documented benefits associated with daily replacement schedules for

soft contact lenses (e.g., ocular health, convenience, compliance, comfort) 3. To discuss perceived barriers to continued adoption of daily replacement contact lenses,

and practice tips for overcoming these barriers. I. Market Overview

A. Key terminology

B. Trends 1. Materials

2. Modalities 3. Replacement Schedules

C. Contact Lens Options

II. Benefits of Disposability A. Contact Lens, Tear Film, Ocular Surface Interactions

B. Deposition

C. Vision

Nichols, JJ. Daily disposables.

2

D. Ocular Health 1. Allergies

2. Dry Eye 3. Inflammatory Complications

4. Infectious Complications

E. Compliance III. Daily Replacement Adoption

A. Major Barriers 1. Patient Perception

2. Practitioner Perception

3. Economics

B. Opportunity for Growth

1. Doctor-Patient Discussions

2. Special Populations

Surface Wettability- Key to Dropouts? William L. Miller, OD, MS, PhD

The surface of the contact lens and its influence on contact lens comfort is often debated.

Certainly large areas of surface dryness whether from surface deposition or material properties will make a lens less comfortable and will affect visual performance. Deposition and the lack of adequate surface wettability will increase surface friction which can lead to contact lens-induced papillary conjunctivitis and lid wiper epitheliopathy respectively. In all, the importance of surface wettability to successful contact lens wear has been demonstrated in several peer reviewed studies. Its absence is also a key component to contact lens dropouts. I. The creation of a wettable surface II. Relation of contact lens surface wetting and comfort a. friction III. Observation of the contact lens surface IV. Issues that decrease contact lens surface wetting V. Treating and managing surface dryness a. contact lens materials (daily disposable) b. tear supplements c. resoaking

Daily Disposable Contact Lenses and Dry Eyes William D. Townsend, O.D., F.A.A.O. Course Description Daily disposable lenses are often beneficial for individuals who wish to wear contact lenses but have issues with ocular dryness. Between 50% and 80% of contact lens patients report some degree of ocular dryness. Daily disposable lenses (DDL) are may be an alternative for these individuals. Non-contact lens wearers with severe dry eye may benefit daily disposable lenses as a means of protecting the ocular surface and facilitating healing of compromised ocular surface. This presentation addresses the use of DDL for these purposes.

Myopia Control with Contact Lenses

Katherine Bickle, OD, MSPost-Doctoral Clinical and Research Fellow

The Ocular Surface Institute (TOSI)University of Houston College of Optometry

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 2 Financial Disclosures

No financial interests to disclose

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 3 Etiology of Myopia

Myopia

Genetics Environmental

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Potential Factors Impacting Myopia Development

• Refractive Error• Parents’ refractive error

• 1 myopic parent: 2.17x risk

• 2 myopic parents: 5.40 x risk

• Patient’s current refractive error • +0.75 D or less hyperopia with young

school-aged children

• Time spent outdoors • Non-myopes: 11.65 ± 6.97 hours/week

• Future myopes: 7.98 ± 6.54 hours/week

Jones et al., 2007, Zadnik et al., 1999

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 5 Rise in the Prevalence of Myopia

1971-1972 1994-2004

Myopic Individuals 12-54 (%) 25% 41.6%

African Americans (%) 13.0% 33.5%

Caucasians (%) 26.3% 43.0%

< 2.00 D Myopia (%) 13.4% 17.5%

-2.00 to -7.90 D Myopia (%) 11.4% 22.4%

> -7.90 D Myopia (%) 0.2% 1.6%

Vitale, Sperduto, & Ferris, 2009

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 6 The Prevalence of Myopia

• Ethnicity* • Asians – 18.5%

• Hispanics – 13.2%

• African Americans – 6.6%

• Caucasians – 4.4%

• Gender*• Females – 11.5%

• Males – 7.1%

* Data collected from 5-17-year-old subjects enrolled in the Collaborative longitudinal Evaluation of Ethnicity and Refractive Error (CLEERE) Study Group

Kleinstein et al, 2003, Fredrick, 2002

• Countries/Continents• United States – 30-40%• Europe – 30-40%• Asia – 70-90%• Africa – 10-20%

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Rate of Myopia Progression

Donovan et al., 2012, Walline, Rah, & Jones, 2004.

*Data represents a summary of 20 compiled published journal articles

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 8 Rate of Myopia Progression

• Ethnicities*• European ethnicities: -0.55 D after 1 year • Asians: -0.82 D after 1 year

• Gender*• Females: -0.80 D after 1 year • Males: -0.71 D after 1 year

• Final myopic state reached• Females: 15 years old • Males: 16 years old

*Data represents a summary of 20 compiled published journal articles Donovan et al., 2012, Walline, Rah, & Jones, 2004.

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 9 Public Health Considerations

Myopia increases the risk for:

• Retinal holes and tears • Glaucoma • Cataracts • Retinal and vitreal detachments

• Lattice degeneration

• Lacquer cracks

• Myopic macular degeneration

Saw et al., 2005

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Clinically Significant

• An 8-year-old patient presents with a refractive error of -1.00 DS OU

Percentage of myopic reduction

Patient’s final refractive error

0% -5.00 D

25% -4.00 D

50% -3.00 D

75% -2.00 D

100% -1.00 D

*Estimate of myopia progression of -0.50 D per year from ages 8-16

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 11 Myopia Control Treatment Options

• Topical Agents • Atropine • Pirenzepine

• Spectacles• Bifocals• PAL’s• Undercorrection

• Contact Lenses• Alignment fit GP’s • Corneal reshaping lenses• Soft multifocal lenses

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 12 Corneal Reshaping Studies

• Ongoing Study

• Stabilization of Myopia by Accelerated Reshaping Technique (SMART) Study

0

10

20

30

40

50

60

70

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Soft Multifocal Contact Lens Studies

0

10

20

30

40

50

60

70

80

90

Sankaridurg (2011) Walline (2013) Anstice (2010) Holden (2010) Aller (2006)

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 14 Myopia Control Treatment Options

• Most effective• Atropine (76 to 96%)

• Least effective • Undercorrection (-16 to -22%)• Gas permeable contact lenses (-5 to -8%)

• Overall best treatment options • Soft bifocal contact lenses (34 to 79%)• Corneal reshaping contact lenses (36 to 58%)

% = reflects the percentage of reduction of myopia progression when compared to a control group

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 15 Peripheral Optical Profile

Myope corrected with spectacles or single vision soft contact lenses

Image obtained from Dr. Jeffrey J. Walline

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Peripheral Myopic Defocus

Myope corrected with center distance soft bifocal contact lenses or corneal reshaping lenses

Peripheral myopic defocus

Peripheral myopic defocus

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 17 Peripheral System at Distance and Near

At distance At near

Berntsen & Kramer, 2013

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 18 Do Children Accommodate with Bifocal CL’s?

• Anstice and Phillips measured accommodation in two situations, and, yes, they do accommodate• 1. One eye wearing dual-focus lens and one eye

wearing single vision distance correction lens• Accommodative response = 2.07 D

• 2. One eye wearing dual-focus lens and one eye wearing single vision near correction lens (+2.50 D more than distance correction)• Accommodative response = 1.78 D

Anstice & Phillips, 2011

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Contact Lens Safety

Stapleton et al., 2008

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 20 Orthokeratology Safety

Conclusion: Overnight corneal reshaping contact lenses and other overnight contact lens modalities show similar risks of microbial keratitis

Children Adults Overall

N 677 640 1317

Cases 2 0 2

Years at risk 1435 1164 2599

Rescaledincidence rate (95% CI)

13.9 (1.7 to 50.4) 0 (0 to 31.7) 7.7 (0.9 to 27.8)

*Rescaled rate is per 10,000 patient-years

Bullimore, Sinnott, & Jones-Jordan, 2013

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 21 Benefits of Contact Lens Wear

• Pediatric Refractive Error Profile (PREP) survey

• Largest improvement with contact lens wear vs. spectacles

• Appearance

• Recreational activities

• Satisfaction with correction

Rah et al., 2010 (Adolescent and Child Health Initiative to Encourage Vision Empowerment (ACHIEVE) Study)

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Center Distance Soft Bifocal Contact Lenses

Brand Proclear Multifocal “D” and XR “D”

BiofinityMultifocal

Acuvue Oasysfor Presbyopia

MiSight

Material Omafilcon A Comfilcon A Senofilcon A Omafilcon A

Power ranges +20.00 to -20.00 D +6.00 to -8.00 D +6.00 to -9.00 D -0.25 to -6.00 D

Add powers +1.00 to +4.00 D in 0.50 D steps

+1.00 to +2.50 D in 0.50 D steps

Low, Mid, and High

Replacement Monthly Monthly Bi-weekly Daily disposable

Not currentlyavailable in

the US

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 23 Evaluating the Literature

• Subjects’ demographics• Age • Ethnicity

• Primary outcome measures and their significance• Axial length• Vitreous chamber depth• Refractive error change from baseline

• Study length

• Number of subjects

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 24 Dual-Focus Soft Contact Lenses

+2.00 D

3.36 mmDist

0.71 mm0.98 mm0.76 mm1.67 mm


___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Dual-Focus Soft Contact Lenses

Soft bifocal contact lens

group

Single vision contact lens

group

-0.44 D -0.69 D


Spherical equivalent refractive error change at 10 months

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 26 Axial Length and Change in Spherical Equivalent Refractive Error

Sankaridurg et al., 2011

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 27 Multifocal Contact Lens Myopia Control

A 2-year-study using a commercially available center distance soft multifocal contact lens

Walline et al., 2013

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Bifocal Lenses in Nearsighted Kids (BLINK) Study

• Eligibility criteria• 8-11 years old

• Spherical equivalent non-cycloplegic subjective refraction between -1.00 D to -4.00 D with less than 1.00 DC

• Study Design• 5-visit study with each visit separated by 5-7 days

• Subjects wore Proclear Spherical, Proclear Multifocal +2.00 D, +3.00 D, and +4.00 D add lenses for 5-7 days each

Bickle & Walline, AAO 2013

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 29 BLINK Results

• Subjective Responses• Glare or Starbursts

• Reduced with +4.00 D add lenses compared to

spherical lenses

• Ghost Images and Overall Opinion of Vision• Reduced with +3.00 D and +4.00 D add lenses

compared to spherical lenses

• Objective Responses• Low Contrast Distance Visual Acuity

• Reduced with +3.00 D and +4.00 D add lenses compared to spherical lenses

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 30 BLINK Conclusions

• Multifocal contact lenses with a +3.00 D or +4.00 D add power may not be well tolerated by myopic children

• Practitioners fitting soft multifocal CL for myopia control should consider the possible compromise in overall vision

• May be difficult for children to convey symptoms

• Reductions in low contrast VA and contrast sensitivity may be issue (dim lighting situations, cloudy days, spotting objects that blend in with their background)

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Corneal Reshaping Guidelines

• FDA approval• Refractive error: - 5.00 D to -6.00 D

• Cylinder: -1.50 DC to -1.75 DC

• No age restriction

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 32 Change in Axial Length and Vitreous Chamber Depth

Axial Length Vitreous chamber depth

Cho, Cheung, & Edwards, 2005

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 33 Impact of Refractive Error

Cho, Cheung, & Edwards, 2005

Orthokeratology subjects Spectacle-wearing subjects

Orthokeratology subjects with higher baseline refractive error experienced a smaller increase in vitreous chamber depth than

subjects with lower baseline refractive error

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Retardation of Myopia in Orthokeratology (ROMIO) Study

Group Ages 7-8

Ages 9-10

Ortho-k 20% 9%

SV spectacles 65% 13%

% of subjects who progressed >1.00 D

Cho & Cheung, 2013

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 35 Factors to Consider with Corneal Reshaping Lenses

Santodomingo-Rubido et al., 2013

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 36 Patient Management and Education

• All treatment options discussed are used off-label for myopia control as there are no FDA approved treatments for myopia control

• Choose the most appropriate treatment option • Consider the impact on the patient’s vision, ocular

health, and quality of life

• Set realistic expectations for the patient and patient’s parent(s)

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Soft Multifocal Contact Lenses vs. Corneal Reshaping

Soft MultifocalContact Lenses

Corneal Reshaping Lenses

Rx less than -2.00 D or greater than -5.00 D

X

Rx between -2.00 D to -5.00 D X X

Flatter keratometry values X

Low contrast vision, glare, halos X

No correction required throughout the day

X

Up to -0.75 DC X X

-0.75 DC to -1.50 DC X

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 38

Thank you!

Katherine Bickle

[email protected]

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

��

��

Advances in Diagnosis and Therapy of Tear Dysfunction

30th Annual Cornea, Contact Lens and Contemporary Vision Care Symposium

Stephen C. Pflugfelder, M.D. Professor, James and Margaret Elkins Chair

Department of Ophthalmology Baylor College of Medicine

Classification of Tear Dysfunction

��

SS ATD Non SS ATD

Altered Distribution Decreased Clearance

Conjunctivochalasis Lagophthalmos

Nodular Degeneration Pterygium/Pingueculum

MGD

Loss of Reflex Tearing

Behen A et al. Cornea 2006

Aqueous Deficient

Aqueous Sufficient

Tear Instability

Tear Dysfunction Alters Tear Composition

Lacrimal Gland Disease

Increased Osmolarity

MMP-3, MMP-9 Inflammatory Cytokines

Tomlinson et al 2006 Sullivan et al 2011 Solomon et al 2001

Chotikavanich et al 2009 Enriquez-de-Salamanca 2010

Reduced Growth Factors

Anti-microbial Factors Solomon et al 2001 Ohashi et al 2003

Lam et al 2009 Rao et al 2010

Meibomian Gland Disease

Delayed Clearance D l d

Conjunctivochalasis onjj tunctiivoch lhalas

Approach to Treating Tear Dysfunction

Aqueous Deficient Aqueous Sufficient

MGD Altered Distribution

Schirmer Test OCT

��Mild

CE Disease

Artificial Tears Osmoprotectants

PUFA Supplements (n-3, n-6 EFA) Punctal plugs

�

��Moderate to Severe

CE Disease Level 1 Tx +

Anti-inflammatories Serum/albumin

Punctal Occlusion Contact Lenses (PROSE)�

PUFA Anti-

inflammatories

Treat Chalasis

Pinguecula Pterygium

Salzmann’s nodules Exposure�

D fi i t A S ff

DEWS Report Ocular Surface 2007 MG Workshop IOVS 2011

��

��

Essential Information for Diagnostic Classification

•  Tear instability •  Tear production and meniscus height

(volume) •  Severity of corneal and conjunctival

epithelial disease/ocular Surface Inflammation

•  Presence of distribution problems: –  Conjunctivochalasis –  Basement membrane disease –  Nodular degeneration –  Pterygium/Pingueculum

Tear��

•  Invasive – Fluorescein TBUT

•  Noninvasive quantitative – Static topography (SRI) (Liu Z et al.

Ophthalmology 1999; 106: 939-43) – Kinetic topography

•  Tear Stability Analysis System – TSAS (Gumus K et al. Invest Ophthalmol Vis Sci 2010)

•  Oculus Keratograph

Tomey Tear Stability Analysis System (TSAS)

•  Software captures images of 11 central rings each second for up to 10 consecutive seconds and analyzes ring width at intersections with 256 radial lines (2816 points) Rings widths are converted to waveforms

•  The time until deviation from ideal crosses a defined threshold, as well as the sum of devations at each second is calculated

Gumus et al. IOVS 2011; 52:456-61�

••

••

TSAS

Gumus et al. IOVS 2011; 52:456-61�

��

��

Oculus Keratograph 5�

•  Noninvasively measures tear break-up location and time in reflected Placido rings (Best N et al. Cont Lens Ant Eye 2012)

•  Data is presented in a color-coded map

Lipid Interferometer •  White light interferometry can measure

thickness and spreading pattern of tear lipid layer (Yokoi et al. Arch Ophthalmol 1996; Goto E, Tseng SCG Arch Ophthalmol 2003)

•  Oculus Keratograph 5 – Qualitative analysis •  The LipiView interferometer

(TearScience®) captures and records the colored tear interference pattern at 32 frames per second –  thickness and quality of lipid layer are

analyzed by system software to identify LTD

Lipiview Interferometer Assessment of Tear Production/Volume

•  Traditional tests –  Schirmer test –  Cotton thread test

•  Tear Meniscus Dimensions (Tear volume) –  Anterior segment OCT –  Keratograph 5

•  Tear Dynamics –  Fluorescein clearance test –  Tear osmolarity

li (T

��

��

Tear Meniscus Assessment Tear Meniscus Assessment

•  Noninvasive methods to quantify the TM •  Photography 1

•  Video recording 2

•  Reflective meniscometry 3

•  OCT 4

•  Tear interference imaging by Tearscope 5

•  Optical pachimetry 6

•  Strip meniscometry 6 1 Mainstone et al. Curr Eye Res 1996; 2 Glasson MJ et al. Invest Ophthalmol Vis Sci 2003;

3 Yokoi N et al. 1999; 4 Wang et al. Invest Ophthalmol Vis Sci 2006; 5 Uchida A et al. 2007; 6 Dogru M et al. Invest Ophthalmol Vis Sci 2006

yy

Anterior Segment OCT

��

Cornea�

Lower Lid Margin�

Tear Meniscus Assessment Tear Meniscus Assessment �  A significant correlation was found between the OCT

upper and lower TMH measurements and •  slit-lamp TMH •  strip meniscometry •  vital staining scores •  Schirmer test

1 Ibrahim OM et al. Ophthalmology 2010; 117: 1923-9.

�  TMH < 0.30 mm 1 •  sensitivity: 67% •  specificity: 81%

��

�

Tear Dysfunction Conditions Tear Meniscus Height�

•  ATD but not MGD was significantly lower than control group (Tung C et al. Am J Ophthalmol 2013, in press)

Tear Volume vs FL staining

0

100

200

300

400

500

0 10 20

SSATD

Corneal staining

R = -0.35 p = 0.04

TMH

(µm

)

0

100

200

300

400

500

600

700

0 10 20

R = +0.4 p = 0.05

R = -0.35 p = 0.04

Corneal staining

MGD

ATD TMH

(µm

)

Tung et al. AJO 2013

� Conjunctivochalasis with Age

��

Gumus et al. AJO 2012

Lab on a Chip Tear Osmometer (TearLab)

Measures osmolarity by Na+ ion conductivity in 50nl sample collected from the inferior tear meniscus on microchip

�

��

��

TearLab Osmometer��

The most sensitive threshold between normal and mild or moderate subjects was 308 mOsm/L; whereas 315 mOsm/L had the greatest

specificity

Distribution of tear osmolarities in Survey of 314 consecutive subjects classified as normal or mild, moderate or severe Dry Eye based on DEWS composite severity score (Lemp et al. AJO 2011)

TearLab Osmometer�•  Inter-eye variability in osmolarity was

noted in dry eye and �� with disease severity (r2 =0.32)

•  Range of three consecutive osmolarity measurements is typically 10-15 mOsm/L, but may be as high as 35 mOsm/L - mean of 3 consecutive readings on both eyes was recommended for clinical trials enrolling < 50 subjects (Khanal S, Millar T BJO 2012)

Lemp et al. AJO 2011

Among 6 tests, Osmolarity showed greatest correlation with composite disease severity score (Sullivan et al. IOVS 2010)

Szalai et al. found no difference in mean tear osmolarity between non-Sjögren syndrome (SS) ATD, SS ATD and normal subjects and no correlation between tear osmolarity and any clinical test.

(Cornea 2012)

Ocular Surface Disease •  Dye staining is the current standard

– Time and concentration dependent – Difficult to grade (complicates multicenter

clinical trials) •  Topographic assessment of corneal

smoothness (�� •  Conjuntival Goblet Cell density •  Inflammatory mediators (in conjunctival

cells or tears)

��

��

NEI Grading Scheme for Ocular Surface Dye Staining

��

��

Lemp MA. CLAO J 1995; 21:221-232

iPod/iPhone Photo/Video •  Commercially

available adaptors for eyepiece –  Eyephotodoc.com

•  iPhone apps (Procamera)

•  Visually or software grade staining

�� !�� "�!��

��

��

Impression Cytology •  Technique used for decades

–  Evaluate conjunctival epithelial morphology –  Measure goblet cell density and expression of

differentiation and inflammatory genes

Sjögren Syndrome TB Conjunctiva

MUC5AC TB Conjunctiva

mmatory y geng estiation and inflamm

EyePrim® Cell Collector •  Manufactured by

Opiatech (www.opiatech.com)

•  Supor 450 membrane with high affinity for conjunctival epithelium

•  Applied with uniform pressure to ocular surface with a plunger

•  Membranes can be stained or protein or RNA can be extracted from adherent cells for molecular assays

EyePrim® Sample Collection

��

��

mRNA IL6

Controls Patients0

1000

2000

3000

4000

N=9 N=20

P=0.002

copi

es

IL-6 Transcripts

Comparison of number of IL-6 transcripts in TB conjunctiva measured by Q-Real-time PCR

RPS InflammaDry Detector •  InflammaDry is a rapid point of care

semiquantitative immunoassay to detect elevated levels (>40ng/mL) of the MMP-9 protein in tear fluid

•  Single use, disposable assay that can be performed by a technician without additional equipment

•  Approved in Europe and Canada; pending approval in US

MMP-9 and Tear Dysfunction •  MMP-9 is an “inflammatory protease” produced by stressed

epithelium and inflammatory cells

–  8-fold greater expression found in conjuntival epithelium of tear dysfunction patients (Chotikavanich et al. IOVS 2009)

–  Tear concentration and activity � in ATD and MGD (Afonso et al. IOVS 2009, Sobrin et al. IOVS 2000, Chotikavanich et al. IOVS 2009)

–  Tear MMP-9 activity found to correlate with a number of Clinical Parameters

•  OSDI Symptom severity score (p<0.001) •  Corneal FL staining (p<0.001) •  Conjunctival LG staining (p<0.001) •  TBUT (p<0.001)

r2 = 0.56, P<0.001

0 2 4 6 8

10 12 14 16

0 100 200 300 400 500 600 700

Cor

neal

Sta

inin

g

Tear MMP-9 activity (ng/ml)

Tear MMP-9 Activity Shows Linear Increase with DEWS Categorical Disease Severity

Chotikavanich et al. IOVS 2009

��

� �

Distribution Problems

•  Conjunctivochalasis •  Basement membrane disease •  Pterygum, pingueculum

ase

Pre Post

Cauterization Restores Tear Meniscus

Summary •  Variety of new diagnostic

technologies to: –  Image the tear film –  Sample ocular surface cells –  Evaluate tear composition

•  Addition of certain tests appears to improve ability to identify and classify tear dysfunction

•  May prove valuable in selection of appropriate therapy

ABCs: Allergy, Blepharitis, and Conjunctivitis Kelly K. Nichols, OD, MPH, PhD FERV Professor [email protected] Abstract: There are many masquerading conditions under the umbrella category of ocular surface disease. While the recent focus has been on dry eye and MGD, new advances in technology make differentiating between the ABCs even easier. New diagnostics and therapeutics are reviewed. Objectives: Following completion of this course, the attendee will be able to: (1) review symptomology for each condition; (2) discuss new diagnostics for allergy, blepharitis, and conjunctivitis; (3) contrast and compare therapeutics for allergy, blepharitis, and conjunctivitis. Outline: 1) Review of Allergy

a) Introduction i) Prevalence ii) Seasonality, pollen counts, geography

(1) The “office” environment (2) The outdoor environment

iii) Systemic associations (1) Rhinitis, asthma

b) Diagnosis and management i) Symptomatology—listen! ii) Contact lens considerations—wearing and replacement schedule and solutions iii) Review oral and nasal concurrent medications

(1) Dryness iv) Severity dictates therapeutic approach and referral

(1) New algorithm 2) Review of Blepharitis “inflammation of the eyelid”

a) Introduction i) Prevalence ii) Anterior vs Posterior Blepharitis iii) Is posterior blepharitis = meibomian gland dysfunction (MGD)?

(1) MGD definition b) Diagnosis and management

i) Symptomatology—morning vs evening ii) Contact lens considerations—wearing and replacement schedule and solutions iii) Therapeutics (steroids, antibiotics)

iv) Lid hygiene—wipes, warming, and more

3) Review of Conjunctivitis

a) Introduction i) Types and prevalence ii) Incorrect diagnosis common

(1) Bacterial (2) Viral (3) Allergic

iii) Systemic associations (1) Systemic allergy? History of recent illness? Time of year and other factors

b) Diagnosis and management—“the red eye exam” i) Symptomatology—listen! ii) Contact lens considerations—D/C? iii) AdenoPlus®

(1) First and only CLIA-waived point-of-care diagnostic test that aids in the rapid differential diagnosis of acute conjunctivitis.

(2) Addition of IgE in 2014 iv) Severity and differential diagnosis dictates therapeutic approach

(1) Antibiotics/ antivirals

UHCO Award Lecture A. J Bron 30th Annual Corne, Contact lens and Contemporary Vision care Symposium

Spreading of the Tears and Staining of the Ocular Surface

-Remarkable Events and Mechanisms- The purpose of this lecture is to introduce some ideas about spreading of the tears and the mechnaisms by which dyes used in clinical practice, are taken up at the surface of the eye The tears occupy two compartments at the surface of the open eye. The first lies in the fornices and the spaces behind the lids and the second is the preocular tears, comprising the tear menisci and the tear film. The precorneal tear film is about 3μm thick and its thickness over the conjunctiva is less certain. Most of the aqueous component is derived from the lacrimal glands, a little from the conjunctiva and gel mucin is added from the conjunctival goblet cells Evaporation is strongly retarded by the tear film lipid layer (TFLL), derived from the meibomian glands and water lost by evaporation and drainage is continuously replaced by newly formed tears. We usually say that fresh tears are regularly mixed and distributed by blinking but our recent studies show that eye movements play an essential role. The TFLL is extremely stable. If the lipid layer is observed during blinking, by interferometry, it can be seen that despite rapid compression and expansion with each blink, successive interference patterns closely resemble each other, although they eventually degrade over a series of blinks. It appears that the force of the downstroke is sufficient to strip the TFLL from the aqueous subphase but that cohesion between the lipid molecules allows it to retain its gross structure and remain as a sheet. Then, after a series of blinks, the pattern changes abruptly as the lipid layer mixes with with the reservoirs of meibomian oil at the lid margin and the TFLL is refreshed. If the TFLL is now observed during a series of horizontal saccades to either side, in the absence of blinking, again the pattern is only slightly changed when the eye returns to the primary position but degrade in a stepwise fashion if saccades are repeated in the blink interval. Here it appears that, since little force is applied to the TFLL during each saccade it remains attached to the aqueous layer during the movement and they move together as a fluid shell What happens if we study the effect of saccades on the fluorescein-stained tear film? What we see is that dark arcs form in the stained film, close to the region of the lid margin, when the eye is deviated to one side or the other. If, after blinking to clear the arcs, the subject looks down for a few moments and then returns to the primary position, two, striking, dark, horizontal bands are seen acros the tear film. We have found that both arcs and bands are caused by meniscus-induced tear film thinnnig which imprints the film as the cornea comes into relation with the menisci at the lid margin. What is remarkable is that, in the absence of blinking the arcs or bands may barely change in appearance, indicating that we are looking imprints imposed upon a fluid gel and not upon a simple aqueous layer. Exceptions to this rule do occur, however. These experiments also show that as the cornea moves under the lids it is coated and re-coated with a gel layer much as paint is applied by a roller. This indicates that eye movements are as important as the blink in spreading and distributing the tears.

UHCO Award Lecture A. J Bron 30th Annual Corne, Contact lens and Contemporary Vision care Symposium

Now how about the mechanism of staining of the ocular surface with dyes used in clinical practice? Water-soluble dyes are generally excluded from the surface epithelium by the tight junctions and surface glycocalyx of the most superficial layer of cells. A proportion of normal corneas, however, do show a time-dependent fluorescein uptake, giving rise to a limited degree punctate staining. We hypothesise that this is due to a graded loss of the glycocalyx barrier, as cells prepare for shedding, which permits entry into these pre-shed cells. Shed cells take up dye. The term ‘punctate erosion’ is often used to describe the punctae uptake of dye at the ocular surface that is a feature of pathological staining., However, there is little evidence of the ‘micropooling’ that this implies and the term may be a misnomer. It is more likely that the initial event involves dye entry into cells with a defective glycocalyx and in addition, diffusion across defective tight junctions which would normally seal the surface. Transcellular spread of dye from cell to cell seems unlikely in the surface layer, because there is a lack of connectivity between these cells via gap junctions. Different dye staining characteristics probably reflect differences in molecular size and other physical properties, coupled with differences in visibility under the conditions of illumination. This is most relevant to the rapid epithelial spread of fluorescein from sites of punctate staining, compared to the apparent confinement of dyes such as lissamine green. We assume that fluorescein, with the lowest molecular weight, spreads initially in the intercellular space and which then gives them access to all cells by transcellular diffusion. Solution-Induced Corneal Staining (SICS), related to the use of certain contact lens care solutions, may have a different basis, involving the non-pathological uptake of cationic preservatives, such as biguanides, into epithelial membranes and secondary binding of the fluorescein anion. It is transient and may not imply corneal toxicity. Conclusions. i. Both blinking and eye movements are important for distributing the tears. ii. Pathological punctate staining by instilled dyes is likley due to entry acroos a defective glycocalyx. Spread of fluorescein dye probably reflects dye entry across defective tight junctions and intercellular diffusion.

AMD & Sunlight – What Does the Evidence Tell Us Today?

Jan P. G. Bergmanson, OD, PhD, PhD hc, DSc, FCOptom, FAAO

Texas Eye Research and Technology Center

University of Houston College of Optometry In the unprotected eye, such as the aphakic eye, the retina is very vulnerable to ultraviolet radiation (UVR) injury but in the intact eye less than 5% of the UVR will reach the retina. The question whether this small proportion of transmittance is sufficient to be damaging in a lifetime UVR dose has remained unclear. Some epidemiological studies have resulted in conclusions suggesting that age-related macular degeneration (AMD) is the result of excessive sunlight exposure but other investigations have indicated that there is no association between exposure to sunlight and AMD.

This presentation reports on a study that reviewed all relevant epidemiological publications in this field. The meta-analysis employed in this publication has the potential to change the way we look at sun exposure as a risk factor for AMD.

Fourteen studies qualified for this meta-analysis and the cumulative data clearly indicated that persons with higher sunlight exposure had a significantly higher risk of developing AMD. The odds ratio (OR) significantly decreased for increasing gross domestic product (GDP) per capita but latitude was not proven as a risk factor.

The Sui et al (2013) study did not forward new data but by a sophisticated statistical analysis of existing data they succeeded in adding new insights, which points at sunlight as a significant risk factor for AMD. Further epidemiological studies are needed and we must develop a better appreciation for what wavebands in the sun spectrum are causative of AMD. However, in the meantime the practice of evidence based medicine is highly suggestive of the need to filter out UVR to reduce the risk for AMD.

Reference:

Sui GY, Liu GC, Liu GY, Gao YY, Deng Y, Wang WY, Tong SH Wang L. Is the sunlight exposure a risk factor for age-related macular degeneration? A systematic review and meta-analysis. Brit J Ophthalmol, 97, 389 – 394, 2013.

Quantifying Solar Ultraviolet Radiation Behind Eyewear The human eye is exposed to toxic Ultraviolet Radiation (UVR) from natural sunlight and man-made light sources and related diseases can occur in a number of tissues within the eye, ranging from the corneal surface to the retina. While the cornea and crystalline lens provide inherent UVR protection, the anterior ocular surface and the stem cell bearing limbal region are exposed to toxic levels of UVR from relatively short term solar exposure. Shading headwear and UVR-blocking spectacles and sunglasses greatly reduce direct solar UVR exposure but may not provide protection from diffuse ambient and surface reflected/scattered light. Also, if the squint mechanism is reduced due to the reduction of direct visible light the ocular surface may be exposed to significant levels of diffuse ambient and reflected UVR. In addition, laterally incident radiation that is focused across the cornea onto the limbus, a phenomenon known as peripheral light focusing, can increase the dose at the nasal limbus by a factor of 20. UVR-blocking contact lenses, that cover the limbus, will therefore provide high levels of protection from all sources of ocularly incident UVR but the overall protection provided by non-contact eyewear is a function of frame and lens design. When recommending non-contact UVR blocking eyewear clinicians rely on protection factor metrics that are based on lens transmission but they have no way of assessing the UVR protection efficacy of frame design. There is therefore a requirement for scientifically rigorous, clinically applicable protection factor metrics that are not simply based on the transmittance of the eyewear in question but also on the protection afforded from the total UVR field that the wearer is exposed to and the length of that exposure. To quantify the overall protection factor of eyewear the UVR levels at the ocular surface, behind the lenses, need to be quantified for a broad range of natural daylight scenarios. A sensor array that provides this sort of data has been designed and constructed and field testing is underway. Data from this research will quantify the overall protection factor of specific eyewear designs and provide calibration data for eyewear UVR protection models that can fully inform clinicians and the public.

The Intelligent Filter

-Pete Hanlin, LDO, ABOMEssilor of America

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 2 THE ELECTROMAGNETIC SPECTRUM

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 3 THE ELECTROMAGNETIC SPECTRUM

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

VISIBLE LIGHT

A healthy human retina responds to light with wavelengths between approximately 380-720nm.

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 5 ULTRAVIOLET LIGHT

Light waves shorter than 380nm (down to 10nm) are classified as Ultraviolet, or UV light…ht…

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 6 ULTRAVIOLET LIGHT

All UV is not created equal- shorter wavelengths have the greatest potential for damage...

Contribution to total UV burden Es(ʎ) = spectral distribution

Damage potentialS(ʎ) = relative spectral function efficiency

0.0001

0.001

0.01

0.1

1

10

100

1000

Es (ʎ

)

280 300 320 340 360 380

Wavelength(nm)

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

UV AWARENESS

Over 90% of Americans know UV damages skin…

An 18 month old shows no evidence of UV damage under both visible and UV illumination…

A 4 year old already shows freckling (nose) under UV illumination…

A 64 year old has evidence of damage under visible and UV illumination…

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 8 UV AWARENESS

<10% of Americans know UV damages the eye…Healthy ocular structures undamaged by UV…

Cornea Crystalline Lens Retina

…UV contributes to pterygium, cataract, and ARMD damage

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 9 ACTIVE PROTECTION- TRANSMISSION

Crown Glass (1.523) (UVT= 91%)

– does not block UVCR-39 (and other 1.50 materials) (UVT= 45%)

– must be treated to block UVA & UVB– 1.50 Transitions® lenses block UVA & UVB

Many lens substrates inherently block UVA & UVB (UVT= <1%)

– Polycarbonate– Trivex– Mid-Index (1.56)– ALL High Index (>1.60)

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

ACTIVE PROTECTION- TRANSMISSION

Polarized lenses block glare while preserving contrast-making them a safer sunwear solution…

Non-polarized lenses must be very dark to reduce glare levels.

Polarized lenses selectively block glare AND preserve contrast.

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 11

20/100

20/80

20/63

20/50

20/40

20/32

20/25

20/20

20/15

20/10

1.0 10.0 100.0

Contrast

Snel

len

VA

Tinted ARPolarized AR

Polarized applications - driving


Polarized lenses increase contrast perception & decrease reaction times.

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 12

0

800

1000

1200

1400

1600

1800

2000

1.0 10.0 100.0Contrast

reac

tion

time

(ms)

Tinted ARPolarized AR


Polarized applications - drivingPolarized lenses increase contrast perception & decrease reaction times.

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

0

2

4

6

8

10

12

14

16

18

20

280 330 380 430 480 530 580 630 680 730 780Wavelength (nm)

Refle

ctio

n (%

)

Standard ARUV Optimized AR

ACTIVE PROTECTION- REFLECTION

Most AR surfaces cancel visible reflections- but intensifyUV reflections…

…standard AR is not recommended for sunwear applications!

UV Visible Light

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 14 ACTIVE PROTECTION- REFLECTION

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 15 AVOIDING UV EXPOSURE

If the patient cannot/will not avoid exposure, at least limit exposure during times of peak UVB intensity…p g p y

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

AVOIDING UV EXPOSURE

The NOAA “UV Index” indicates daily radiation levels for an area.

A person who only burns on occasion will likely burn after 35-50 minutes of unprotected exposure on a day with a UV Index 10.

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 17

HIGH ENERGY VISIBLE (HEV) LIGHT

400 450 500 550 600 650 700Violet Blue Cyan Green Yellow Orange RedViolet Blue Cyan Green Yellow Orange Red

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 18

*Based on in-vitro tests on swine retinal cells

EYE HEALTH RESEARCH

Paris Vision Institute - One of the most important research centers on eye diseasesIn 2008, Essilor partnered with Paris Vision Institute on an eye health research program

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

*Based on in-vitro tests on swine retinal cells

EYE HEALTH RESEARCH

First in-vitro tests in the ophthalmic industry– Visible light spectrum split into 10 nanometer bands– Each band focused on retinal cells*– Specific bands induced maximum retinal cell death

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 20 DISCOVERY OF SPECIFIC BAND OF HARMFUL BLUE-VIOLET LIGHT

PEAK TOXICITY OCCURRED AT 435NM (BLUE-VIOLET LIGHT)

415-455nm wavelengths were found to have the highest toxicity for RPE.

TOXIC415-455NM

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 21

AMD

Normal VisionNormal Vision

AMD Vision

Blue-Violet light ranges from 415-455nmCumulative exposure can lead to retinal cell deathExposure to Blue-Violet light is a risk factor for AMD– AMD is the leading cause of severe vision

loss and legal blindness in adults over 60– There is no cure for AMD today

BLUE-VIOLET LIGHT

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

BLUE-TURQUOISE LIGHT

COLOR PERCEPTION, ACUITY

SLEEP/WAKE CYCLEMEMORY & MOOD

COGNITIVE PERFORMANCEPUPILLARY CONSTRICTION

Blue-Turquoise light ranges from 465-495nmBlue-Turquoise light is essential for:– Pupillary Constriction Reflex

• Retina’s natural protection against light overexposure– “Human biological clock” synchronization

• Allows the right functioning of the sleep/ wake cycle, mood, etc.– Visual acuity & color perception

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 23 BLUE-TURQUOISE LIGHT

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 24 BLUE-VIOLET LIGHT SOURCESSOUURCES

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

SUNLIGHT

Widely modified by the atmosphere– Season– Time of day– Geographic location– Gaze direction

Blue Light proportion of daylight varies between 25% and 30%– Blue-violet light is about 10%

On a cloudy day, up to 80% of the sun’s UV rays can pass through the clouds

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 26 ARTIFICIAL LIGHT

Compact fluorescent lamps– Contain 25% Blue-Violet Light

LEDs– Contain 35% harmful Blue

Light– The cooler the white LED, the

higher the blue proportionBy 2020, 90% of all light sources will be LED

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 27

Blue Toxicity Index:Sunlight (noon) = 1.00Compact Fluorescent Light = 1.35Light Emitting Diode = 1.80Incandescent Lightbulb = 0.21

LIGHT TOXICITY

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Yellow-tinted lenses block all blue light– Blue-violet & Blue-aqua

Neutral Grey lenses block full spectrum

HEV PROTECTION- TRANSMISSION

Kodak/VSP UNITY®Blu-Tech™ (in mass)Hoya ReCharge AR™ (coating)Essilor Crizal® Preventia™ (coating)Nikon SeeCoat Blue™ (coating)Zeiss® Gunnar™ (in mass)

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 29 HEV PROTECTION- TRANSMISSION

No-Glare Lenses

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 30 HEV PROTECTION- TRANSMISSION

This graph shows the front-side reflection of Visible Light– 20% Blue-Violet light deflected– Blue-Turquoise transmitted– Rest of visible light transmitted

No-Glare Lenses

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Protection from Blue-Violet light– New No-Glare lens treatment– Features Light Scan™– Selectively deflects harmful Blue-Violet

light by 20%– In recent lab tests, Crizal Prevencia

lenses reduced retinal cell death by 25%*

– No other No-Glare lens on the market offers selective protection against harmful Blue-Violet light

*Results from in-vitro tests on swine retinal cells

HEV PROTECTION- TRANSMISSION

No-Glare Lenses

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 32 DANGERS OF LIGHT TO THE EYE

UV HEV

CATARACT NORMAL AMD

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 33

CATARACT POPULATION AMD POPULATION

Source: http://www.nei.nih.gov/eyedata

AMD & Cataract cases expected to DOUBLEin the next 20 years

CATARACT & AMD IN THE US

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

SUMMARY

Polarized lenses selectively filter glare– Provides higher level of contrast / quicker reaction times

AR/UV stack reduce UV reflections to the cornea– E-SPF measures protection level

Blue / Blue-Violet Filters reduce HEV exposure– Not all blue light is bad- some is essential

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 35

THANK YOU

Pete Hanlin, LDO, ABOMEssilor of [email protected]

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Problem Solving the Scleral Lens Patient: Therapeutic

and Lens ManagementNorman E. Leach, OD, MS, FAAO

Texas Eye Research and Technology Center University of Houston College of Optometry

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 2

I have no financial interest in any of the products mentioned in this presentation.

TERTC has received grants from the following companies over the last 2 years:

- Alcon- AMO- Bausch & Lomb- Cooper Vision

Disclosures

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 3 Scleral Lens Indications� Vision Improvement

- High Refractive Errors- Irregular Corneal Surface� Ectasia

- Keratoconus- Pellucid Marginal Degeneration

� Corneal Trauma� Corneal Surgery

- Keratoplasty- Refractive Surgery

� Corneal Infection- Post HSV and HZV

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Scleral Lens Indications� Corneal Protection

- Ocular Surface Disease- Exposure Keratitis- Trichiasis- Entropion- Graft vs Host Disease (GVHD)- Stevens-Johnson Syndrome- Ocular Pemphigoid- Neurotrophic Keratitis

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 5 Scleral Lens Indications� Corneal Protection

- Symblepharon- Severe Dry Eye

- Sjogren’s Syndrome- Filamentary Keratitis

� Cosmetics and Sports- Active water sports, vigorous sports

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 6

� Vault the cornea- Masks irregular astigmatism� Often results in improved visual acuity

Why Scleral Lenses?

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

� Reduction of lens interaction with the cornea

� Continuous hydration to a cornea with inflammation or desiccation

� Provides mechanical protection from eyelid

� Little to no adaptation

Scleral Lens Advantages

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 8

� Increased chair time� Lens handling for some patients

- Provide increased time for I&R training- Provide written instructions

� If air bubbles become trapped under lens corneal desiccation may occur locally in area of bubble

� Increased cost of lenses� Solutions

Scleral Lens Disadvantages

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 9 Scleral Lens Nomenclature

(after Gromacki CL Spectrum 2011)

Corneo-scleral 12.5 – 13.5mmSemi-scleral 13.6 – 14.9mmMini-scleral 15.0 – 18.0mmScleral (Texas Size!) 18.1mm +

It’s all about where you want the lens to sit

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

� Corneal Lens – supported entirely by the cornea

� Corneo-Scleral Lens – supported by both cornea and sclera

� Mini-Scleral Lens – supported mostly by the sclera- Up to 6mm larger than HVID

� Scleral Lens – supported entirely by the sclera- More than 6mm larger than HVID

- *the Scleral Lens Education Society and the CLMA, 2013

C l L t d ti l b thL

Scleral Lens Nomenclature*

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 11 What are you looking for….

Achieve

� Central Corneal Vault (Clearance)

� Movement

� Limbal Vault

� Edge Clearance

Avoid

� Bubbles and touch

� Adherence

� Chafing

� Conjunctival vessel blanching

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 12 Scleral Contact Lens Fit Aims� Vault the cornea

- Green all over with no bubbles

� Land gently on sclera- No blanching

� Lens must move- 0.5 to 1.0 mm

� Look for NaFl flow beneath CL- Especially the periphery

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

The Optimal FitLens/Ocular Surface

Relationship Corneal vault

Peripheral Tightness & Lens Movement

(10-15% blanching OK)

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 14 The five most dreaded words you can say to your contact lens

patients.

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 15 The Red Eye

Should I stay or should I Go?

There are times to keep apatient in contact lenses and times when they are better off without them.

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

The Red Eye

Should I stay or should I Go?

Microbial keratitis? It’s time to go!

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 17 Therapeutics for MK

� Fourth generation fluoroquinolones are the antibiotics of choice

– Vigamox (moxifloxacin) 0.5% Alcon– Zymar (gatifloxacin) 0.3% Allergan– Quixin (levofloxacin) 0.5% Vistakon– Iquix (levofloxacin) 1.5% Vistakon– Zymaxid (gatifloxacin) 0.5% Allergan– Besivance (besifloxacin) 0.6% B+L– Moxeza (moxifloxacin) 0.5% Alcon

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 18 Conditions We Manage while Wearing CL’s

� Allergy

� Abrasion

� Inflammation

� Foreign body

� Dry eye disease

� Blepharitis

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Rationale for Abstaining from Contact Lenses

� Toxicity issues

� Type of infection/inflammation

� Absorption by the lens material

� Lens material degradation

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 20 The Red Eye

General Rule for topical drug therapy

Best accomplished while CL’s are not worn.

Why?

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 21 The Red EyeBAC Toxicity is the most common, but not the only

concern� BAC rule: Count the zeros- 0.0…..?

- None or one - no good- Two – borderline- Three – okay

• Azasite = 0.003%

0.01%

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

� Patient has no viable spectacles

� Patient has no corrective alternatives- Keratoconus/PMD- Post-Surgical- Trauma- Post-infection/ulcer scarring- Dry Eye Disease

� Occupational and/or sports requirements

Contact Lenses may be the most Viable Option

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 23 Caveats

� Rule #1: Use unpreserved or self preserved whenever possible

� Rule #2: Utilize QD (once daily) or bid gtts

� Rule #3: Stay away from BAC

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 24 Keep things simpleDon’t overload the cornea

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Therapeutic Management of CLPC� Mast cell stabilizer and histamine

inhibitor- (Pataday 0.2%, Patanol 0.1%,

Alcon; Zaditor 0.025%, Novartis)

� Mast cell stabilizer- (Crolom 4%, B&L)

� Antihistamine- Lastacaft (alcaftadine, 1gtt qd OU)

� Mild steroids- (Loteprednol – 0.2%, Alrex,

0.5%, Lotemax)

� Steroids- (Pred Forte 1%, Allergan; FML

0.1%, Allergan)

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 26 Blepharitis is the most common cause of evaporative

dry eye� 5 million people over the age of 50 suffer

from dry eye

� Twice as common in women

(Dry Eye Workshop, Ocular Surface, 2007)

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 27 Incidence of Blepharitis� Ophthalmologists: 37%

� Optometrists: 47%

(Lemp and Nichols. The Ocular Surface Supplement, 2009)

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Lemp and Nichols (2009)The Ocular Surface Journal

Supplement:“…blepharitis today is a poorly defined

condition about which there is considerable misunderstanding.”

Probably due to multiple names for the same condition and outdated terminology.

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 29 Clinical Signs and Symptoms

� Generally mild and may include one or more symptom- intermittent blur- gritty and burning eyes- sticky eyelids in the morning- bulbar and limbal conjunctival hyperemia

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 30 Contact Lens Wearers� Typically handles lids and lenses 2x/day

� Often have mild to moderate blepharitis

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Phlyctenulosis

� Seasonal / allergy

� Nodules (PMNs) and lymphocytes

� Vascularization

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 32 Phlyctenulosis – Tx Options� Pataday or Patanol

(antihistamine & mast cell stabilizer)

� Lotamax 0.5%

� Prednisolone 1% or fluorometholone (FML) 0.1% qid– 8x/day, taper

� Zylet (0.5% loteprednol 0.3% tobramycin

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 33 Phlyctenulosis – Tx Options� Naphcon-A (vasoconstrictor &

antihistamine

� NSAID (Livostin, Acular, Voltaren) qid

� Topical antibiotic- Polytrim bacitracin, erythromycin

� Tear supplements/lid wipes

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Ophthalmic Combinations

� Offer the convenience of having both an anti-infective and anti-inflammatory in a single bottle

� Steroids are generally used in combination with anti-infectives for quick relief of acute episodes of conjunctivitis/blepharitis

� Treatment is generally limited to the extent of the acute episode– Monitor IOP

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 35 When do you Rx Combo Agents?

� Ocular/adnexa inflammations that may compromise ability to resist microbial invasion– Treat inflammation– Corneal epithelial edema or disruption

present?– Keep 2o infections out

� Clinical Ex: Ocular rosacea;superficial burn

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 36 Ocular Damage Caused by Uncontrolled Inflammation

Corneal Scarring & Neovascularization

Subepithelial Fibrosis

Corneal Perforation

Photos courtesy of University of Pittsburgh, Visual Services

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

When do you Rx Combo Agents?

� Inflammation and bacterial infection co-existing� Discharge?� Infiltrates?

� Clinical Ex: blepharitis; marginal corneal infiltrates; meibomian gland disfunction

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 38 Clinical Treatment of Inflammation

with Risk of Infection� Non-Otherwise-Specified (NOS)

Conjunctivitis

� Non-Infectious Keratitis

� Blepharitis

� Scleritis/Episcleritis

� UveitisAcute atopic conjunctivitis with itching, mucous, and

chemosis

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 39 Antibiotics in Combo Agents

� Tobramycin

� Polymyxin B

� Neomycin (high incidence of sensitivity)

� Sodium Sulfacetamide

� Bacitracin

� Gentamicin

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Steroids in Combo Agents� Dexamethosone

� Fluorometholone

� Prednisolone acetate

� Prednisolone sodium phosphate

� Hydrocortisone

� Loteprednol etabonate

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 41 Combo Suspensions and SolutionsGeneric Name / Concentration Trade Name PreparationDexamethosone 0.1%Neomycin 0.35%Polymyxin B sulfate 10,000 units/ml

Methadex-Major Maxitrol-Alcon Poly-Dex-OcuSoft Generics

Ophthalmic Suspension5ml

Dexamethosone 0.1%Tobramycin 0.3%

TobraDex-AlconGenerics

Ophthalmic Suspension2.5ml, 5ml

Fluorometholone 0.1%Sodium sulfacetamide 10%

FML-S-Allergan Ophthalmic Suspension5ml, 10ml

Prednisolone acetate 1%Gentamicin sulfate 0.3%

Pred-G-Allergan Ophthalmic Suspension2ml, 5ml, 10ml

Hydrocortisone 1%Neomycin 0.35%Polymyxin B sulfate 10,000 units

Generics Ophthalmic Suspension7.5ml

Loteprednol etabonate 0.5%Tobramycin 0.3%

Zylet-B&L Ophthalmic Suspension2.5ml, 5ml, 10ml

Prednisolone acetate 0.5%Neomycin 0.35%Polymyxin B sulfate 10,000 units/ml

Poly-Pred-Allergan Ophthalmic Suspension5ml, 10ml

Prednisolone acetate 0.2%, 0.5%Sodium sulfacetamide 10%

Blephamide-Allergan Metimyd-Schering

Ophthalmic Suspension5ml, 10ml

Prednisolone sodium phosphate 0.25%Sodium sulfacetamide 10%

Vasocidin-Novartis Generics

Ophthalmic Solution5ml, 10ml

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 42 Combo OintmentsGeneric Name / Concentration Trade Name PreparationDexamethosone 0.1%Neomycin 3.5 mg/gPolymyxin B sulfate 10,000 units/g

AK-Trol-Akorn Maxitrol-Alcon Poly-Dex-OcuSoft Generics

Ophthalmic Ointment3.5g

Dexamethosone 0.1%Tobramycin 0.3%

TobraDex -Alcon Ophthalmic Ointment3.5g

Prednisolone acetate 0.6%Gentamicin 0.3%

Pred-G-Allergan Ophthalmic Ointment3.5g

Hydrocortisone 1%Neomycin 3.5 mg/gPolymyxin B sulfate 10,000 units/gBacitracin zinc 400 units/g

AK Spore HCGenerics

Ophthalmic Ointment3.5g

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

� 16-year history with TobraDex, and the agent shows an outstanding safety record, with a reported rate of adverse events at less than 0.0001%

� Generic available with suspension; not ointment

TobraDex®

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 44

� Both have 0.3%

� Dexamethasone 0.1% vs Loteprednol etabonate 0.5%

TobraDex® vs Zylet

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 45

� Endotoxin-induced uveitis in rodents� Neutrophil inhibition at 24

hours� Dexamethasone

� 0.01% - 0.1%

� Loteprednol� 0.3% - 3.0%

TobraDex® vs Zylet

Phillips K, et al. Submitted for presentation at annual meeting of the Association for Research in Vision and Ophthalmology. Fort Lauderdale, FL; May 2005.

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

TobraDex® ST

TobraDex®ST(tobramycin/dexamethasoneophthalmic suspension)0.3%/0.05%

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 47 Episcleritis� Episcleritis is a descriptive diagnosis in

patients with localized or diffuse episcleralinflammation.

� Young adults- Most common in fourth or fifth decade of life.- Women affected in 2/3 of cases

� Self limiting

� Often recurrent

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 48 Pathophysiology

� Inflammation of superficial episcleral tissure with vascular dilation.

� Two types:� Simple:

� Sectoral or rarely diffuse redness� Resolves spontaneously in 1 to 2 weeks

� Nodular episcleritis:� Localized nodule with surrounding injection� Longer to resolve than simple� Recurrence can cause sclera to become translucent

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Simple Episcleritis

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 50 Nodular Episcleritis

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 51 Etiology

� Episcleritis: � 2/3 of cases are of unknown etiology� 1/3 can have associated systemic condition such as:

� Rheumatoid arthritis� Systemic lupus erythematosus� Atopy� Rosacea� Thyroid disease

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Clinical Signs� Localized or diffuse episcleral edema and

vasodilatation.

� Underlying sclera is Not edematous.

� Vasoconstriction with topical phenylephrine.

� Localized mobile nodule in nodular episcleritis.

� Anterior uveitis and corneal involvement rare.

� Vision unaffected.

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 53 Symptoms� Acute onset of localized or diffuse

hyperemia.

� Can be unilateral or bilateral.

� Overlying conjunctiva often inflamed.

� Mild discomfort or pain.

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

Slide 54 Treatment� Self limiting within 2 to 3 weeks� Mild: Artificial tears QID, cold compresses� Moderate to severe

- Mild topical steroid QID- Frequent short pulsed is optimal- Recheck every 2 weeks until resolved

then taper

� Oral NSAIDS as alternative- Ibuprofen 200 – 600mg PO TID

� Topical NSAIDS- Unsuccessful

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

for your attention!

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

___________________________________

CCLS Printable Handouts

Documents

Transcript of CCLS Printable Handouts