57277 2 hours PH Therapeutic 58290 Pages 20 - 28 PS ...€¦ · passionate about education and has taught in a variety of settings including educating residents at the VA, students

PACIFIC UNIVERSITY COLLEGE OF OPTOMETRY 2018 VICTORIA CONFERENCE

July 12 – 15, 2018 Hotel Grand Pacific

Victoria, B.C. CANADA COPE EVENT #115672

Date Speaker Title COPE Verification

Thursday, July 12,

2018 Lee Carr, OD Judicious Management of Eye

Pain (2 hrs) 57277

PH 2 hours

Therapeutic

James Kundart, OD, MS

Epiretinal Membrane Update (1 hr)

58290 PS

1 hour Therapeutic

Beth Kinoshita, OD

Contact Lens Complications (2 hrs)

58273 CL 2 hours

Friday, July 13

Anthony DeWilde, OD Anti-VEGF and the Eye (1 hr)

46566 PS

1 hour Therapeutic

Lee Carr, OD Judicious Prescribing, Government Oversight of Controlled Substances (1 hr)

57981 EJ 1 hour

Anthony DeWilde, OD

An Optometrist’s Guide to Glaucoma Surgery (1 hr)

58005 GL

1 hour Therapeutic


Ehlers-Danlos Syndrome and the Eye (1 hr)

47567 SD

1 hour Therapeutic

Lee Carr, OD Assessing Diplopia (1 hr) 55718

GO 1 hour

Hours offered: 10 Total hours earned:

Name License #

Mailing Address ______

Please retain a copy of this stamped form as verification of hours earned. Please be advised that your individual state board makes the final determination of applicable hours. For more information, contact Pacific University College of Optometry,

2043 College Way . Forest Grove, OR 97116 . 503-352-2202

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PACIFIC UNIVERSITY COLLEGE OF OPTOMETRY 2018 VICTORIA CONFERENCE

July 12 – 15, 2018 Hotel Grand Pacific

Victoria, B.C. CANADA COPE EVENT #115672

Date Speaker Title COPE Verification

Saturday, July 14

Beth Kinoshita, OD Corneal Ecstasias (2 hours)

58271 AS

2 hours Therapeutic


Visual Consequences of Chiari Malformation (1 hour)

58291 NO

1 hour Therapeutic

Anthony DeWilde, OD

An Evidence Based Approach to Managing Unilateral Optic Nerve Edema ( 2 hours)

51336 SD

2 hours Therapeutic

Sunday, July 15


Macular Cherry Red Spots: Causes and Consequences (1 hr)

58293 PS

1 hour Therapeutic

Lee Carr, OD Recognizing Red Flag Headaches (1 hour)

58029 NO

1 hour Therapeutic

Beth Kinoshita, OD

Coatings and Treatments and Agents, oh My! (1 hr)

58270 CL 1 hour

Anthony DeWilde, OD

Rethinking Gonioscopy from Fundamentals to Future Developments (1 hr)

58004 GL

1 hour Therapeutic


Climate Change, Eclipses and The Eye (1 hour)

58295 PH

1 hour Therapeutic

Hrs offered: 10 Total hours earned:

Name License #

Mailing Address ______

Please retain a copy of this stamped form as verification of hours earned. Please be advised that your individual state board makes the final determination of applicable hours. For more information, contact Pacific University College of Optometry

2043 College Way . Forest Grove, OR 97116 . 503-352-2202 3 of 205

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Anthony DeWilde, OD, FAAO Director, Tele-Retinal Imaging Program Staff Optometrist, Kansas City Veteran’s Affairs Medical Center Anthony DeWilde, OD is a graduate of the University of Missouri – St. Louis College of Optometry. He completed the KCVAMC Optometry residency in 2008. Dr. DeWilde is an Adjunct Instructor for the University of Missouri College of Optometry. In addition to seeing patients in the general clinic, he also works with TeleRetinal Imaging Program for diabetic patients and provides patient care for the low vision rehabilitation clinic. Dr. DeWilde is passionate about education and has taught in a variety of settings including educating residents at the VA, students at University of Missouri – St. Louis, College of Optometry, and

optometrists at both state and national meetings. He is a Diplomate, American Board of Optometry.

Leland (Lee) Carr III, OD Assistant Dean and Professor, Northeastern State University Oklahoma College of Optometry Dr. Carr graduated from Michigan College of Optometry at Ferris State University. Immediately following graduation, Dr. Carr was employed by Dow Corning Ophthalmics, and subsequently established a solo private practice in East Lansing, Michigan. Dr. Carr's academic career began in 1982 when he began working as a part-time clinical faculty member at Ferris State. In 1984, he accepted a full-time appointment as an assistant professor at Northeastern State University Oklahoma's College of Optometry (NSUOCO) in Tahlequah, Oklahoma. In July 1993, Dr. Carr joined the faculty at Pacific University, where

was appointed dean in 1997. Dr. Carr was named Oregon Optometrist of the Year in 2000 and received the Oregon Optometric Physicians Association Award of Special Merit in 2001. From 2003 to 2004, Dr. Carr served as president of the Association of Schools and Colleges of Optometry. In 2006, Dr. Carr returned to NSUOCO where he is currently Assistant Dean and Professor of Optometry .

Dr. Carr served as president of the Oklahoma Association of Optometric Physicians (OAOP) from 2012 to 2013. He was inducted into the OAOP Hall of Fame, and in 2014 received the OAOP Award for Service. He was the winner of the 2015 AOA Distinguished Service Award,

James Kundart, OD, MEd, FAAO, FCOVD-A Professor, Pacific University College of Optometry Dr. Kundart received his BS in astronomy and astrophysics and BA in history from the Pennsylvania State University in 1993. He matriculated from Pacific University in 1999 with his doctorate in optometry, with distinction, and a master's of education, visual function in learning. He joined the faculty of the College of Optometry in 2005, where he teaches visual perception, ocular motility, nutritional optometry, and pediatric ocular disease.

Dr. Kundart was in private practice for five years in Easton, Pa., where he specialized in primary care and low vision for the working poor and special needs children. Dr. Kundart is a fellow in the American Academy of Optometry and an academic fellow in the College of Optometrists in Vision Development. He provides pediatric and binocular vision care to the Ocular Motility and Neuro-Optometry (OMNO) service in Portland, and runs the 3D Performance service in Beaverton.

Dr. Kundart was named Clinical Faculty of the Year three times and has served as the chair of the board of directors of Amigos Eye Care since 2010. He maintains the continuing education website for the College of Optometry, is founding editor-in-chief of the new online journal, Interprofessional Optometry, and is an active member of the Vision Performance Institute and Vision Science graduate program on campus.

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Born in McAdoo, Pa., Dr. Kundart and his wife Alicks have a young son and share their home with a collection of rescued pets, including a cat with low vision.

Beth T. Kinoshita, OD, FAAO Associate Professor, Pacific University College of Optometry Dr. Kinoshita is an associate professor and serves as the Director of the Pacific Eye Clinic in Forest Grove and as an instructor for the Patient Care and Contact Lens courses. She is a graduate of the Southern California College of Optometry at Marshall B. Ketchum and of the Contact Lens Residency Program at Pacific University College of Optometry. Dr. Kinoshita is a Fellow of the American Academy of Optometry (AAO) and a Diplomate in the Cornea, Contact Lens and Refractive Technologies Section of the AAO. She lectures and conducts research on topics related to contact lens complications and specialty contact lens fitting and design. She is a member of the Contact Lens Assessment in Youth (CLAY) study team. She

had practiced for three years in Phoenix, Arizona prior to joining the faculty at Pacific University in 2006.

Cathy Evans Schwartz, ABOC, FNAO Ms. Schwartz boasts over 40 years in the optical industry and started as Oregon’s first female Apprentice Optician. Over the years she has managed several optometric practices. She has owned and operated “Oswego Optique”, an optometric practice is Lake Oswego Oregon. Ms. Schwartz worked as an optician in Alaska where she traveled extensively to the bush to deliver eye care to native Alaskans.

Cathy Schwartz served as Director of ophthalmic services at Pacific University College of Optometry for 11 years. In that role, she taught Ophthalmic Dispensing Procedures to Optometry students and oversaw the operations of the school’s five optical dispensaries known as Pacific EyeTrends. She is certified ABOC by the ABO, is a member of the Optician’s Association of Oregon, and is a Fellow Member of the National Academy of Opticianry. She is currently serving as a Commissioner in the Commission of Opticianry Accreditation for Education Programs in the United States. She previously served on the Board of Directors of the National Academy of Opticianry. In 2011, she was honored by Vision Monday as one of the 35 most influential women in Optical.

Ms. Schwartz recently accepted the position of Operations Manager at Specs 20/20 Vision, in Portland, Oregon.

VICTORIA CONFERENCE STAFF

Carole Timpone, OD, FAAO, FNAP Moderator

Jeanne Oliver Director of External Relations

[email protected]

Miki Buckingham C.E. & Events Coordinator

[email protected]

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mailto:[email protected]

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Judicious& Practical

Management of Eye Pain

Leland Carr, O.D.

Oklahoma College of Optometry

Northeastern State [email protected]

Speaker Disclaimers

Corporate Compensation: None Investments/Interests: None

PAIN is very real to patients….

And they DON’T LIKE IT !!!

Many Ocular Conditions Hurt: Lid Laceration Chalzion Preseptal Cellulitis Conjunctival Laceration Corneal Abrasions Corneal Erosions Iritis/Iridocyclitis H.S.V. Keratitis Intense Adenoviral “Crud”

Bacterial Ulcers

Bullous Keratopathy

Traumatic Echymosis

Traumatic Hyphema

Orbital Fractures

Procedures:

Lid “Repairs”

Foreign Body Removals

Corneal Puncture Procedures

“Lump & Bump” Removals

Punctal Cautery

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Injuries

“Patients have a right to adequate pain treatment—failure to properly manage pain is professional negligence.”J Law Med Ethics. 2001; 29:28-51

Most Don’t Require Narcotics

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BASIC SCIENCE

PAIN

RELIEVERS

2 Main Mechanisms

INHIBIT PROSTAGLANDINS“peripheral pain relief”“central pain relief”

INTERRUPT C.N.S.NEUROTRANSMISSION“central pain relief”

Prostaglandins

Actions of Prostacyclin and Prostaglandins

Vasodilation Inhibit platelet aggregationBronchodilatation Increase glomerular filtrationRegulate renal automaticityGI tract contractionGI tract relaxationContract uterus (if pregnant) Inhibit lipolysis

Actions of Prostacyclin and Prostaglandins

Decrease gastric acid secretion

Increase gastric mucus secretion

Increase naturalneurotransmitters

Increase platelet activityand responsiveness

Hyperalgesia

spinal neurons

Pyrogenesis hypothalamus

The Classic “Big 3” of Pain Relief

#1: Acetaminophen#2: N.S.A.I.D.s#3: Narcotic Analgesics

Rapidly Growing in Popularity#1: Anti-depressant Medications

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Mechanism of Perceiving Pain

PAIN

Action of Anti-Depressants

PAIN

Actions of N.S.A.I.D.’s

Inhibit the production ofProstaglandins

(Inhibit the production of Prostacyclins)

Actions of acetaminophen

Inhibits cyclo-oxygenase 2 (COX-2) (+) pain reduction (+) fever reduction (-) delay in clotting time (+/-) anti-inflammatory effect

Activates the endogenous cannabinoidsystem in the brain

Inhibits sodium channels involved inneurotransmission

NARCOTIC AGENTS

1) True derivatives of Opium

Morphine Codeine

2) Synthetic derivatives of Morphine

3) Synthetic agents that resemble themorphine structure

4) Narcotic antagonists (used in treatingnarcotic overdose)

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Actions of Narcotics

Interfere with neurotransmission within the Central Nervous SystemCerebral HemispheresMedulla

Pain Management Pearls

Easier to “Treat” than to “Catch Up”

Beware: Pain building under treatment

Synergism—Topical + Systemic

Synergism—Caffeine + Systemic

Remember: Rx “with lots of water”!Gentler on stomach“Kinder” to kidneys

Treat PAIN not the INFLAMMATION

EXAMPLE Ibuprofen:MAX: 3200mg daily for InflammationMAX: 1600mg daily for Pain

General “Heads Up” information

Ask: “Sensitive to Aspirin?”

Ask: “Sensitive to N.S.A.I.’s?”

Ask: “History of Ulcers?”

Ask: “Any Kidney Disease?”

Ask: “Any Liver Disease?”

Longterm Diabetes?

Longterm Hypertension?

Considering RXing Narcotics?

Ask: “Any history of alcoholism, addiction, compulsion, or drug dependency?”

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Analgesics containing ACETAMINOPHEN

Hard on the Liver

Generally well-tolerated….

Not much anti-inflammatory action

Actions: Peripheral & Central?

Aspirin and other N.S.A.I.D. products

Hard on G.I. Tract mucosa

Hard on Kidney microcirculation

Can Trigger Asthma Attacks

Often cause fluid retention

Occasionally cause major fluid retention

Occasionally interfere with anti-diabeticagents----facilitating HYPOglycemia

Aspirin & other N.S.A.I.D.’s are Blood-Thinning Agents Be careful with patients taking

Coumadin, vitamin E, bilberry extract, ginkgo biloba, ginseng, etc.

And Conditions Where You Don’t Want to Encourage Bleeding!

HYPHEMA Retrobulbar Hemorrhage Ocular/Periocular Surgery

General Pointers for Pain: Go CENTRAL and Go PERIPHERAL

Ibuprofen + Acetaminophen Naproxen + Acetaminophen Aspirin + Acetaminophen

Go SYSTEMIC and Go TOPICAL Don’t forget ANESTHETICS for short-term

use Don’t use ANESTHETICS for long-term use

!!!!

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Judicious use of

narcoticanalgesics

Which of the following is NOT required to be on a prescription you write for a controlled substance? Your Office Address Your Office/Personal Telephone # Your DEA # Your State License #

What evaluation is required, and must be documented, in order for you to prescribe a controlled substance?

Uncorrected visual acuities Blood pressure & Pulse rate Allergies to medications Complete medical status evaluation

When writing for a controlled substance, how many total Rx’s can you write for on a single prescription blank?

One Two Three Five

When writing for a controlled substance, the maximum duration of therapy permitted for single Rx is ??

48 hours 72 hours 5 days 30 days Varies by state

When writing for a controlled substance, how many refills may be authorized on a single Rx ??

None One Two Five

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Which of the following conditions cannot be ethically treated with controlled substances Rx-ed by an optometrist? Corneal abrasion Hyphema Chalazion incision & currettage Abcessed tooth

Which of the following constitutes unethical conduct under state law in virtually every state allowing for RX-ing Controlled Substances by OD’s?

Indiscriminately prescribing, administering, or dispensing a controlled substance

Prescribing in excess of the amount of drugconsidered “good optometric practice”

Prescribing “without medical need” to prescribe

Refilling an Rx for a controlled substancewithout re examining the patient first

Rx-ing controlled substance to immediatefamily member

For some patients, narcotic analgesics are the analgesic of choice

Moderate to Severe Pain Treatment Plan includes Sedation Patient is allergic to NSAID’s Patient is allergic to acetaminophen Patient is using blood-thinners Patient is using anti-seizure medication Patient has peptic/duodenal ulcer disease Patient has renal disease Patient has hepatic disease

Managing Pain in Addictsor High-risk Patients

Try to manage without Rx-ing a controlledsubstance

Obtain & Document a Worthwhile Consult Patient’s Primary Care Provider Pharmacist Patient’s mental health provider of choice “Questions regarding TREATMENT are

permissible even without specificauthorization by the patient” (HIPPA)

“DRUG ABUSE”

“Use of the drug is other than what theprescribing physician intended.”“recreational use”, or In larger amounts, orMore frequently, orFor different indications, orBy different route of

administration

Drug “Diversion”

USER of the drug, USE of the drug, Or both USER and USE of the drug…..

…..IS OTHER THAN THE DRUG WASINTENDED FOR

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“Drug Addiction” NOT the same as “Drug Dependence” “Drug Addiction”

PreoccupationLoss of ControlObsessive-Compulsive Behavior Pattern

“Based in psychological or physical need” (OLD)

“Based in neurochemical and physiologic need” (NEW)

“Drug Dependence”

IS same as “Physiologic Dependence” “Physiologic Dependence”

Homeostasis requires presence of thedrug

Risk & Physiology BOTH influenced by:DOSEDURATIONPOTENCY

“Tolerance”

“Reduction, over time, in Drug’s effect”Therapeutic EffectSide-Effects

Schedule Drugs

I NO accepted

medical use II

High Abusepotential

Severe DependencyLiability

III Less Abuse risk

than II Less Dependency

risk than II IV

Less than III V

Less than IV

Federal & State Oversight

U.S. Department of JusticeDrug Enforcement Agency (DEA)

Local/regional Bureau of Narcotics &Dangerous Drugs Control (OBN)

Pharmacists have a legal obligation toensure the drugs they dispense are forlegitimate medical purposes

Characteristics of PractitionersInvestigated by the DEA#1: Duped by Patient-initiated Fraud#2: Dated in their Knowledge of current

Pharmacology and/or Therapy#3: “Impaired Physician”#4: Knowingly Rx-ing improperly for purposes of

Personal Gain#1-money#2-sex#3-other drugs

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D.E.A.’s “Watch Out!!!”s

Rx is for condition outside legitimate scopeof practice

Rx is inconsistent with the patient’scondition

Rx is inconsistent with patient’s medicaland/or medications history

Practitioner’s “practice pattern” is heavy onRx’s for controlled substances

Rx is for personal use Rx is for immediate family member Rx is for pet Rx is given without documentation of:

--physical exam--medical history

More than one Rx for the same medication, for thesame patient, is issued or presented on a single day Even if different dose is specified

“Doctor Bewares”

Who is At-Risk for Addiction?

15-30% of general adult population (+) history of substance abuse (any sort) (+) family history of substance abuse

(any sort) 20-50% of institutionalized individuals 45-55% of patients under treatment for

psychiatric/psychological disorders Also noteable: (+) Attention-deficit

Disorder diagnosis

“Bewares” (cont.)

NEW PATIENTS“I’m from out of town…..”“I lost my prescription

No Appointment/Late PM Appointment After-hours Call-in Appointment Sketchy Version of Medical History and

Previous Providers Noticible “disconnect” between symptoms

and objective findings

“Bewares” (cont.)

“I’m in a hurry…..” “OTC’s never work for me…..” “I have a low tolerance for pain…..” Patient insists on brand name (“No

generic”) Threats (or Praises!)

“I’ll get it from a smarter/better Dr.”“….a more caring Dr…..”“I’ll sue if I’m not satisified.”

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“Doctor’s Big Beware!”

An Initial “NO” is changed to a “YES.” “I’d rather write than fight…….”

Don’t Give a Narcotic “Just Because You Can”………

Moderate to Severe Pain Real Value: Gentler Systemically Real Value: Provide Sedation Real Risk: More Abuse Potential

Considerations in Selecting an Analgesic

SAFETY

Inherent side-effects

Allergic considerations

Interactions with other medications

Interactions with systemic conditions

EFFICACY

Relief of Pain

Relief of Fever

Relief of Cough

EASE OF UTILIZATION

Frequency of Dosing

Impact on Meal Schedules, etc.

Impact on Diet, etc.

COST

Availability of generics

Tramadol HCL (ULTRAM)

Rx: 1-2(50mg) 4 times daily Centrally-acting, NON-narcotic Not an NSAID Does work on opioid receptors Overdose+Alcohol=Respiratory Collapse Safe for Geriatric Patients Carbamazepine users: Less Pain Relief

LORTAB and VICODIN

2.5mg and 5.0 mg HYDROCODONE,respectively

500mg acetaminophen Rx: 1 tablet every 4-6 hours as needed Schedule III controlled substance

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LORTAB ELIXER

2.5mg HYDROCODONE Ethyl Alcohol 7% Rx: 15ml every 4 hours as needed for pain Schedule III controlled substance

VICOPROFEN

7.5 mg HYDROCODONE 200 mg Ibuprofen Rx: 1 tablet every 4-6 hours Schedule III controlled substance Potency can be enhanced dramatically

Add 1 200mg Ibuprofen tabletAdd 1 500mg Acetaminophen tablet

DARVON FDA recall 2011

Schedule IV controlled substance 65mg Propoxyphene Rx: 65mg every 4 hours as needed for pain MILD analgesic GOOD sedative WARNING: Do NOT Rx to suicidal or

addiction-prone patients!

DARVOCET-N FDA recall 2011

100mg Propoxyphene 650mg Acetaminophen Schedule IV controlled substance Rx: 1 tablet every 4 hours (1 every 6 hours

if over age 65) NOT really more potent than DARVON Better anti-fever effect than DARVON

PERCOCET

5mg Oxycodone 325mg Acetaminophen Schedule II controlled substance Rx: 1 tablet every 6 hours For “moderate to severe pain” Good anti-pyretic action

PERCODAN

4.5mg Oxycodone .38mg Oxycodone Terephthalate 325mg Aspirin Schedule II controlled substance Rx: 1 tablet every 6 hours For “moderate to severe pain”

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DEMEROL

50mg Meperidine Schedule II controlled substance Rx: 1-3(50mg) tablets every 4 hours Numerous Drug Interactions!

Phenothiazines and other tranquilizers Methicillin Phenytoin (Dilantin) Heparin

TYLENOL WITH CODEINE Tylenol-2

300mg Acetaminophen 15mg Codeine

Tylenol-3 300mg Acetaminophen 30mg Codeine

Tylenol-4 300mg Acetaminophen 60mg Codeine

TYLENOL-3

Schedule 3 controlled substance Rx: 1 tablet every 4 hours Moderately sedating Excellent anti-cough effects Low-risk of physical dependency Analgesic Effect? “Similar to that of

aspirin”

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Epiretinal Membrane

UpdateVictoria Conference 2018

James Kundart OD MEd FAAO FCOVD-A

Pacific University College of Optometry

Financial Disclosure: Nothing to Disclose

Images from Cirrus OCT

Learning Objectives

1. How is epiretinal membrane (ERM) best diagnosed?

2. How is ERM differentially diagnosed from central serousretinopathy and cystoid macular edema?

3. Which ERM cases can be monitored, and which will need surgical intervention?

4. What are the expected outcomes of macular peel microsurgery for ERM?

5. Which symptoms are expected to remain after successfulsurgery, and will need optical treatment?

Case Study #1, First Visit: Macular Cube OCT, 2014

BCVA 20/60 OD, OS


Case Study #1: Macular Cube OCT 2014

BP 175/113BMI 23


Case Study #1: 10-2 Matrix Visual Fields 2014

Images from Humphey Matrix

Case Study #1, Second Visit: Macular Cube OCT 2015


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Case Study #15-Line Raster

OCT 2015

BP 166/84BMI 23

BCVA 20/50 OD, OS


Case Study #1, Third Visit: Macular Cube OCT Spring 2016

BCVA 20/60 OD and OS Images from Cirrus OCT

Case Study #1: Macular Cube OCT Spring 2016


Case Study #1: 5-Line Raster Macular OCT Spring 2016


Case Study #1:Macular Cube OCT Summer 2016


Case Study #1: Corneal Topography and 10-2 Matrix Visual Fields 2016

Images from Medmont Topographer and Humphrey Matrix

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Case Study #1: Before ERM Peel/Vitrectomy5-Line Raster OCRT 2017

BCVA 20/70 OD, OS


Case Study #1, Last Visit: 10-2 Matrix Visual Fields

BCVA 20/50 OD, OS

BP 130/88 BMI 22

Images from Humphrey Matrix

Where ERM Comes From: Coats’ Disease Pre-Op

• “(a) Color fundus photographof the right eye of a 38-year-old man with epiretinal membrane alongsupertemporal arcade

• (b) Ultra-wide-field color photograph showing exudationand telangiectatic vessels in temporal periphery.”

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5678313/

Where ERM Comes From: Coats’ Disease Post-Op (Peel/Vitrectomy)


Where ERM Comes From: Eales Disease


Where ERM Comes From: Eales Disease


• (a) Fundus photograph and (b) fluorescein angiogram of a 22-year-old male with Eales disease Stage 3A and best-corrected visual acuity 0.1 showing fibrovascular proliferation at the disc

• (c) spectral domain optical coherence tomography showed cystoid macular edema

• (j) spectral domain optical coherence tomography showed epiretinal membrane and macular edema

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ERM DDx: Prevenitng Cystoid Macular Edema (CME) with NSAIDs Post-Cataract Surgery


ERM DDx: Cystoid Macular Edema (CME)Do Steroids Help?

• Optical coherence tomography images of cystoid macular edema (CME)

• Top: Preoperative and postoperative findings of definite CME

• Middle: Preoperative and postoperative findings of probable CME

• Bottom: Preoperative and postoperative (cataract surgery) findings of possible CME


Where ERM Comes From: Latanoprost, CME, and ERM

• A. Optical coherence tomography of right eye before latanoprost administration No pathology is detected

• B. Seven months after treatment with preservative free latanoprost optical coherence tomography in right eye revealed cystoid macular edema with well-defined, intraretinal cystic areas of low reflectivity in the macula with serous retinal detachment

• C. Two months after latanoprost discontinuation optical coherence tomography demonstrated complete resolution of cystoid macular edema

• A subtle epiretinal membrane is noted

ERM DDx: Does Latanoprost Cause CME?(after cataract surgery OD)

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5360021/pdf/13104_2017_Article_2448.pdf

ERM DDx: Microcystic Macular Edema

http://iovs.arvojournals.org/article.aspx?articleid=2190200


• An example of a normal retina compared with the retina of a patient with MME. (A) A normal retina from a healthy control subject

• The pseudocolored surface image is the infrared surface photo; the vertical stacked gray image an OCT B-scan

• (B) Optical coherence tomography image taken from a 76-year-old woman with a 3-year history of ARMD, for which she received regular injections with ranibizumab and bevacizumab

• At time of imaging, her best corrected VA OS was 0.7


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• Representative OCT images of patients with MME from the clinical spectrum are shown

• The infrared surface photo and OCT image are presented to the left and the manually segmented INL to the right

• (A) Microcystic macular edema in the right eye of a 70-year-old male patient with a history of proliferative diabetic retinopathytreated with panretinal photocoagulation (VA OD 0.3)

• (B) Optical coherence tomography image showing MME 8 months after occlusion of the vena temporalis superior OD in a 66-year-old female patient (VA OD 0.7)

• Microcystic macular edema was located in the temporalsuperior quadrant of the inner 3-mm EDTRS grid

• However, INL thickening extended to the periphery. In addition,hyperreflective spots were observed in all inner retinal layers



• (D) Microcystic macular edema in a 58-year-old female patient with a newly diagnosed pucker in the right eye (VA OD 0.2)

• Again, there were multiple hyperreflective spots in the inner retinal layers

• (E) Microcystic macular edema 3 months after vitrectomy, in a 71-year-old female patient with a retinal detachment in the left eye (VA OS 0.05)



• Microcystic macular edema in a patient with multiple sclerosis and a history of optic neuritis and branch retinal vein occlusion in the right eye

• This 55-year-old female patient was diagnosed with clinical definite MS in 1992

• Magnetic resonance imaging showed multiple periventricular brain lesions, and spinal T2 hyperintense lesions

• In 2001, she experienced one episode of optic neuritisOD; coincidentally, an occlusion of the vena temporalissuperior was found (VA 0.4)

ERM DDx: Microcystic Macular EdemaPropensity for the Nasal/Temporal Quadrants


• Most frequently, MMEwas observed in patientswith ARMD (27.1%) followed by patientswith precedingophthalmic surgery(20.3%) or presence ofan epiretinal membrane(18.8%)

Last ERM DDx: Case Study #2

• A 62-year-old male first reported to our clinic with a chief concern was a largerimage size OS

• The patient had no history of eye surgery of any sort

• There was a history of blunt trauma to the right nasal canthus almost 40 years previously

• The patient reported that he was generally healthy with a history of hay fever

https://journals.lww.com/optvissci/Abstract/2018/03000/Retinal_Nerve_Fiber_Layer_Thickness_in_Various.11.aspx

Case Study #2: Optic Nerve Head OCT


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Case Study #2: Optic Nerve and RNFL


Case Study #2: Optic Nerve Head OCTCompare OD to OS


Case Study #2: Optic Nerve OCT


Case Study #2: Retinal Nerve Fiber Layer OCT


Case Study #2: Nerve Fiber Layer Analysis


Case Study #2: Optic Nerve OCT Summary


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Case Study #2: Matrix N-30-5 Screener is Unremarkable

• Why did we run afrequency-doubling visualfield screening?

• There are two reasons:both related to cranialnerves

• Which two nerves were wechecking with hisscreening field?

Images from Humphrey Matrix

Case Study #2: 24-2 SITA Standard Visual Fields

Case Study #2: Pachymetry with Ant Seg OCT


Case Study #2: Assessment & Initial Plan

http://opticaldiagnostics.com/info/aniseikonia.htmlhttp://cdn.iofferphoto.com/img3/item/568/007/701/o_xalatan-

eye-drops-latanoprost-0-005-anti-glaucoma-3932.jpg

Case Study #2, Second Visit: Contact Lens Telescope and New discovery

https://www.flonase.com/allergies/is-flonase-a-nasal-steroid-spray/

http://gogadgetplus.blogspot.com/2014/02/terminator-telescopic-contact-lens.html

Case Study #2: Macular OCT OD and OS


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Case Study #2, Visit 1: Macular OCT OU


Case Study #2, Second Visit: Macular OCT OD


Case Study #2, Visit 2: Macular OCT OS




Case Study #2: What’s Your Diagnosis OS?


Case Study #2: Macular OCT 5-Line Raster


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Case Study #2 Dx: Central Serous Retinopathy (CSR) OS




Summary: Epiretinal Membrane

• Epiretinal membrane can be associatedwith:

• Systemic hypertension• Eye disease, like Coats’ and Eales• Cystoid Macular Edema

• It should be differentially diagnosed fromcentral serous retinopathy

• Aniseikonia is a presenting and residual symptom, uniquely treated by optometry

https://www.ncbi.nlm.nih.gov/pubmed/25012933

Questions? Thank You!

James Kundart OD MEd FAAO FCOVD-A

Professor, Pacific University College of

Optometry3D Performance Clinic,

Beaverton, [email protected]

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Soft Contact Lens Complications

Beth Kinoshita, OD, FAAO 2043 College Way

Forest Grove, OR 97116 503-352-3140

[email protected]

Course Description This course will review soft contact lens complications and their treatment options as well as basic anatomy and physiology. Diagnosis, management and current research will be discussed.

Course Learning Objectives After participating in this course, the participant should be able to:

• Understand treatment and management of common soft contact lens associatedcomplications

• Describe basic corneal physiology and its relationship to soft contact lens complications• Describe current research in the area of complications• Be familiar with the relationship of lens modality and replacement schedules to

complications rates• Be familiar with the signs and symptoms of serious and significance complications and

their incidence rates

Course Outline • Interactions with a contact lens

o Lids and Lasheso Conjunctivao Limbuso Cornea

• Meibomian Glandso Secrete meibum

Upper lid: ~36 glands Lower lid: ~26 glands

o Obstruction causes stasiso Meibomian gland structure changes with ageo Arita et al studied the relationship between CL wear & M-gland function

Results• MG atrophy was statistically higher in CL wearers• MG atrophy correlated significantly with duration of lens wear

o Meibomian Gland Dysfunction Early Stage Moderate Stage

• Minimal to moderate ocular discomfort• Vascularization to lid margin• Plugging• Meibum is thicker, turbid

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mailto:[email protected]

Severe Stage• Ocular discomfort• Irregular and vascularized lid margin• Meibum is thick and opaque

o Treatment Warm Compresses Lid Hygiene Artificial Tears / ointment qPM Therapeutics?

• Omega-3 – Fish Oil, Flax Seed Oil• Doxycycline

o 50-100mg QD PO• Azithromycin Ophthalmic Solution

o Off-Label Use• Lipiflow® Thermal Pulsation

o CL Wear and Discomfort Further studies necessary to determine how MGD and CL wear is

correlated• Cannot state that CL wear causes MGD• Cannot state that MGD alone would cause CL discomfort

• Dry Eye Diseaseo Nearly 40% of Americans experience Dry Eyes in the USo Approximately 8% of women ages 45 to 84 have a clinical diagnosis of Dry Eyeo Evaporative Dry Eye

Lipid Layero Aqueous Deficient Dry Eye

Aqueous Layero Contact lens dropout

Dryness cited as a reason for discontinued wear in 50% of wearero “Successful” wearers report similar comfort issueso Contact lenses split the tear film into two sections

Pre-lens and Pre-cornealo Considerations

Allergies, age, sex, medicationso Ocular surface disease

Subjective• FBS, burning, gritty, itchy, light sensitivity, tearing

Objective• Hyperemia, chemosis. lid Involvement, corneal involvement

Moderate to severe DES may be a relative contraindication to CL wearo Dry Eye Questionnaire (DEQ – 5)

Validated questionnaire – 5 questions Distinguishes between patients with and without dry eye and between dry

eye patients with and without Sjogren’s Syndrome (SS)o CL parameter changes / Lens Care Producto Lid interventions

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Warm compresses, lid massage, hygiene Punctal occlusion

o Ophthalmic Artificial Tears Steroid Cyclosporine ophthalmic emulsion

o Oral Doxycycline 50mg Omega-3 – Fish Oil, Flax Seed Oil

o Supplements o Management of associated disease o Scleral Contact Lenses

• Mucin Balls o Mucin Balls: Objective

Small discrete particles of mucin, proteins, and lipids The immovable “deposits” that appear trapped against the corneal surface

o Mucin Balls: Subjective Cause no discomfort, vision loss or ocular health concerns Differential Diagnosis

• Microcysts, epithelial vacuoles, dimple veiling o Mucin Balls at 1 & 3 Months o 70% of subjects exhibited mucin balls on some occasions with silicone hydrogel

lenses o < 5% of subjects exhibited significant numbers o No effect on symptoms, vision or biomicroscopy o Not related to age, gender or prescription o Higher incidence found if:

steep cornea 30 day EW vs. 6 day EW no use of rewetting drops

• Contact Lens Papillary Conjunctivitis o Remove SCL

Lids, Lashes, Lacrimal • Blepharitis • Papillae - lid eversion

o Contact Lens Papillary Conjunctivitis (CLPC) or Giant Papillary Conjunctivitis (GPC)

o CLPC: Subjective Mucus discharge in the nasal corner of the eye upon awakening Itching immediately after lens removal Decreased wearing time

o CLPC: Stages Stage 1 - Pre-Clinical Stage 2 - Early Clinical Stage 3 - Moderate Stage 4 - Severe

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o Antigen on a CL → Immune response → vascular changes → basophil and mastcell accumulate → release of eosinophil chemotactic factor – A → attractseosinophils → histamine release → itch, erythema, edema

o CLPC: Treatment Rule out mechanical GPC Manage contact lens deposits

• More frequent lens replacemento Daily disposable

• Enzyme cleaners Change to a preservative-free lens care system Artificial tears Pharmacologic intervention

• mast cell stabilizer Topical steroids Hydra-PEG Consider GPs

• Contact Lens Acute Red Eye (CLARE)o Appears as a response to endotoxins from gram-negative bacteria on lenso Resolution is rapid and complete, with no known association with propensity to

MKo CLARE: Objective

Bulbar Hyperemia, infiltration, none to mild VA reduction Uncommon

o CLARE: Treatment D/C CL Wear Lubricants & Cycloplege Steroids?

• severe symptoms• significant infiltration

Re-establish successful DW first Recurrence possible

• Contact Lens-Induced Superior Limbic Keratoconjunctivitis (CLSLK)o AKA thimerosal keratoconjunctivitis or thimerosal keratopathy

Strong association with lens care products that contained the preservativethimerosal

• Discontinued in LCP in the mid-1980s• All CL manufacturers have discontinued use of noxious

preservatives – No more CLSLK!o Not to be confused with Theodore’s SLK (unrelated to CL wear)o CLSLK: Subjective

Increased lens awareness, burning, itching. light sensitivity Vision loss

• Severe cases where extensive pannus is presento CLSLK: Objective

Injection in superior bulbar conjunctiva Infiltrates

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Pannus Corneal & conjunctival staining

• Superior 1/3 of cornea Haze

• V-Shaped pattern (apex towards the pupil) Sub-epithelial opacities Superior limbal edema, hypertrophy, staining and injection Pseudo-dendrite (no terminal bulbs)

o CLSLK: Objective Bilateral with symmetry Variable onset

• 2 months to 2 years o Thimerosal hypersensitivity o Clinical studies linked thimerosal to CLSLK o Mechanical effects may play a role o CLSLK: Treatment

Discontinue SCL wear Eliminate thimerosal exposure Lens parameters

• New CL • Minimal thickness • High Dk? • More frequent lens replacement

o GP wear has no additional benefits Pharmaceutical agents Scraping the affected epithelium

o Resolution can be slow o Differential

SLK without CL wear = Theodore’s SLK • Over 40 years old • More in females • Linked to thyroid disease

• Limbal Epithelial Hypertrophy (LEH): Objective o Asymptomatic o Observed in some long term extended wear HEMA wearers o Appears as a possible precursor to corneal neovascularization o Must be viewed with Nafl

Not detectable with white light alone o White Light vs. Cobalt Blue Light o LEH: Treatment

The condition resolves in 3 to 5 days after discontinuing lens wear Decrease wearing time from EW to DW Keratometry

• Suspect a steep fitting lens • Superior Epithelial Arcuate Lesion

o Epithelial Splitting: Subjective

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Patients relatively asymptomatic Usually found during routine CL examination

o Epithelial Splitting: Objective Linear breaks seen in the superior corneal epithelium of soft lens wearers In most cases the epithelium is eroded down to the basement membrane Usually unilateral, located beneath the upper lid Normal corneal epithelium separates the lesion from the limbus Lesion 0.5 mm wide and 2-5 mm in length Little or no injection of the superior bulbar conjunctiva

o Epithelial Splitting Etiology

• Relatively stiff lens materials• Relatively thick lenses• Relatively high levels of lens dehydration resulting in stiffening of

the lens materialo SEAL: Treatment

Initial therapy• D/C CL wear• lubricants• topical antibiotics?

Long term management• change base curve

o Change OADo Change material

• Inferior Arcuate Corneal Stainingo Coarse punctate epithelial disruption in the inferior corneao Seen in patients with clean, well-fitted wet lenses, in DW and EWo Appears independent of water content or lens thickness, occurs with hyperopic as

well as myopic lenseso Toxicity to debris accumulation under lenso Modulus dependent?o Lens Removal Abrasion

• Solution Sensitivity and Ocular Inflammationo Solution related non-keratitiso Palpebral hyperemiao Treatment Options

Hydrogen Peroxide PuriLens System Daily Disposable Continuous Wear

o Solution Study Compared the overall comfort of SCL

• MPS vs. Hydrogen Peroxideo Chemical Properties

Tonicity pH

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Buffers Viscosity Agents (lubricants)

• Hyaluronic acid, sodium hyaluronate Surfactants Stabilizers Preservatives

• Keep the solution sterile • Disinfect the CL

o Solution Recalls o SCL Care Products

Private Labels • All changed the formula of their private label multi-purpose

solution at least 2 times in the past 5 years. • No change in packaging

Patent number o Staining Protocol o IER Study vs Andrasko Study

Andrasko Grid: % Corneal Staining at Two Hours Institute for Eye Research Matrix Study: Corneal Staining % of patients IER Matrix Grid vs. Andrasko Grid

• Preservative-Associated Transient Hyperfluorescence (PATH) o Preservatives

Aldox / Polyquad • Opti-Free Express / RepleniSH, PureMoist

Alexidine • RevitaLens (Alexidine & Polyquad)

PHMB • Aquify (PHMB & EDTA) • Biotrue (PHMB & Polyquad) • Complete Easy Rub (PHMB & EDTA) • RevitaLens Ocutec (PHMB & EDTA)

Dymed • Renu Fresh / Sensitive

o Staining is thought to be binding of the Nafl to preservatives on the epithelium o Preservatives have different peaks incidence of binding

PolyQuad and Aldox – 30 minutes PHMB – 2 hours

o Noted after lens application o Diffuse corneal staining o Epithelium unaffected o Generally bilateral o Asymptomatic o Non-pathological o Resolution is 6-8 hours post lens removal o PATH vs. SICS

• Microcysts

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o Microcysts: Subjective Vision – asymptomatic Comfort – asymptomatic

• If symptomatic consider concurrent pathology

o Microcysts: Objective Small (~15-50 microns) translucent or grey Irregular-shaped or ovoid inter-epithelial cysts Form near the basement layer and move toward the anterior surface Do not stain until they break through the surface epithelium Set observation arm and illumination arm at least 450 apart. 2mm wide beam focused at the cornea Lateral margin of the pupil

• Background is split between the iris and pupil Reversed illumination

• Distribution of light within the microcyst is opposite to the lightdistribution of the background.

o Consist of accumulated cellular debriso Chronic metabolic stresso Response to high levels of cornea hypoxiao Does not affect vision and does not appear to have any direct clinical

consequenceso Number correlates with length of lens wear and lens Dk/to Microcyst Time Course

Onset is slow usually after 2 months of lens wear Number increase and decrease in cycles On the average, it takes 3 months to clear after cessation of lens wear

o Microcysts: Treatment Decrease wearing time, i.e. EW to DW Change to higher Dk/t material

• Hydrogel to GP?o Microcysts: Differential Diagnosis

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• Vascularizationo Limbal Hyperemia

Increase in blood flow at the limbal arcades resulting in dilation anddistention of limbal the blood vessels.

o Neovascularizationo Lipid Leakageo Corneal Vascularization Etiology

Hypoxia Theory Vasostimulation Theory

o Oxygen Permeability Dk 125

o Water Content and Dk in SiHy An increase Dk is generally linked with a decrease in water content

o Documentation of Vascularization Location Depth

• Superficial• Deep

Degree of penetration Severity

o Corneal Vascularization: Treatment Discontinue lens wear if needed Treat any underlying external pathology Minimize physiologic insult

• A higher Dk lens material• Minimize mechanical pressure• Avoid preserved lens care products

• Other signs of hypoxiao Vertical striaeo Folds in Descemets

• Oxygen Transmissibility Required• Corneal Edema

o Epithelial Vacuoles 10% of non-lens wearers Unknown etiology 5-30 microns, spherical fluid or gas filled vacuoles in the periphery Unreversed illumination Occur in areas overlying a corneal opacity in aphakic patients

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Generally asymptomatic Prognosis

• Epithelium has a high turnover rateo Epithelial Bullae

Low prevalence in CL wearers Indicates the presence of chronic epithelial edema 5-30 microns, irregular shaped (typically oval) that may coalesce in the

central cornea Unreversed illumination Fluid filled formations Generally asymptomatic Prognosis

• Identify the cause• In severe cases the bullae may break through the epithelial surface

– ouch!• Cornea – Keratitis - Involves multiple layers of the cornea as well as multiple structures

o Infiltrative Keratitiso Contact Lens Peripheral Ulcer (CLPU)o Microbial Keratitis

Bacterial Protozoa Fungal Viral

o What is an Infiltrate? A focal accumulation of cells or tissue within the anterior stroma Physiological factors Response to:

• Reaction to topical or systemic meds• Preserved lens care solutions• Immune reaction (debris entrapment)• Bacterial infection• Viral infection Staph hypersensitivity• Corneal hypoxia• Dystrophy• Exposure

• Infiltrative Keratitiso Infiltrative Keratitis: Subjective

Inflammatory reaction of cornea, mild to moderate irritation, redness,occasional discharge

o IK: Objective Anterior stromal infiltration, with or without epithelial involvement, A/C

reaction rare, can be bilateral, no lid edema, moderate redness, VA may ormay not be affected

o Etiology - multifactorial FB entrapment, mechanical trauma, bacterial toxins MPS reaction

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• SICS o Risk factor

CL wear (DW or EW) o DDx: Viral KC, CLARE, CLPU o Infiltrative Keratitis: Treatment

D/C CL wear temporarily Steroids if moderate symptoms or VA

• i.e. Lotemax QID X 5-7 days +/- taper • Resolution quick vs. Viral KC

Ocular lubricants Rarely scars vs. CLPU (Bull’s eye scar) Recurrence possible - esp. if toxic reaction Switch to Single Use lenses or Preservative Free system if in DW

• Contact Lens Peripheral Ulcer (CLPU) o Compared with microbial keratitis:

Peripheral location. regularity of lesion, absence of photophobia, no visual involvement, no AC reaction, rapid resolution (2 to 3 days)

o CLPU: Subjective Discomfort

• moderate to severe, FB sensation, slight irritation, asymptomatic Redness - slight Tearing

o CLPU: Objective Infiltrate, no lid edema, moderate redness, unilateral, no A/C reaction,

peripheral or mid-peripheral o Inflammatory reaction to G+ Exotoxins o Toxins released by S. aureus colonizing on lens surface o Bacteria rare in cultures of corneal scraping o CLPU: Treatment

Anti-infective agent • 4th generation

Cycloplege Steroids after re-epithelialization? Monitor closely

• Microbial Keratitis o Focal defect or excavation of the sub-epithelial corneal surface o Produced by sloughing of necrotic inflammatory tissue (loss of stromal substance) o Often interchanged with “corneal ulcer”

May have an infection without loss of tissue May have an ulcer without bacterial infection

o Microbial invasion & infection Bacteria (Pseudomonas, Serratia, Staph, Strep) Protozoan (Acanthamoeba) Fungal (Aspergillus, Candida, Fusarium) Viral

o Non-infectious ulcers

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Immune reaction Hypersensitivity reaction

o Microbial Keratitis: Subjective Symptoms may be mild to severe Patient may experience

• Pain, photophobia, tearing, blepharospasm, red eye, floaters, AMlid crusting, purulent discharge

o Must have an acute inflammatory infiltrate of the epithelium and stroma in thepresence of an infectious microorganisms

o Infection of the corneal surface cannot occur without initial bacterial attachmentor binding to epithelial cells

o The normal cornea binds few, if any, bacteria Spontaneous infection is rare

o Microbial Keratitis with Traditional EWo Microbial Keratitis: Objective

Infiltrate• Central or paracentral, sometimes peripheral, large, irregular, focal

>1mm, satellite lesions common, anterior stromal to full thickness,corneal edema, full thickness epithelial loss, anterior chamberreaction, lid edema, severe bulbar & limbal redness, unilateral,hypopyon

o Risk Factors Trauma, surface disease, smoking, age, high ametropia, lens replacement,

years of wear, CL material, CL case care, water exposure, illness,extended wear

o Extended Wear 1989 Schein & Poggio (N Engl J Med) data suggest MK: 1999 Cheng (Lancet) – Planned Replacement What about Silicone Hydrogels? 2005 Schein, McNally et al. (Ophthalmology)

• The incidence of loss of visual acuity due to MK among users ofSiHy contact lenses was low

2005 Morgan, Efron, et al (Br. J. of Ophth.) 2007 Keay, Stapleton, et al (Eye & CL)

• Principal risk factor of MK is EW 2008 Stapleton et al. - Microbial keratitis - Annualized incidence / 10,000

o CLAY – Contact Lens Assessment in Youth Driving Assumption

• In the future, more children will use SCL for medical (myopiacontrol, blood sugar monitor) and cosmetic reasons.

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o Study serious and significant events o Study risk factors for events that interrupt lens wear o In children and young teens

Age as a Risk Factor for Infiltrative Events Survey Development

• SCLs complications ARE related to age o 15 to 25 years most at risk

• What characterizes the behaviors in this group of SCL wearers? CLRS – Contact Lens Risk Survey

• 15 to 25 year olds are… o more likely to nap in lenses o more likely to sleep in their lenses in different situations o water exposure

Rinsing lenses, showering in lenses, wwimming in lenses

Surprisingly, across all ages… • overnight wear was reported equally • hand washing before application and removal was consistent • Lens case care was consistent

Survey • The CDC asked the CLAY study group to collaborate to distribute

a survey o CLRS o CDC healthy habits questions

• On-line survey o Convenience sample of 1,141 CL wearer

93% SCL, 7% GP 20-76 years old

• Results o 99% reported at least one risk factor for a serious infection

due to poor hygiene behaviors, sleeping in CL (50%), napping (87%), topping off (55%), showering (85%) swimming (61%)

o 30% sought medical help for a red/painful eye o Water Exposure

o What We Fear Acanthamoeba keratitis (Joslin. Am J Ophthalmol 2007)

o Protozoa Keratitis Appear dendritic or patchy stromal infiltrates Symptoms disproportionate to signs Risk factors

• CL wear – 90% of cases • 3 per 100,000 / year vs. 1 per 1,000,000 • Injuries from vegetative matter • Hot tub exposure

Treatment

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• Brolene 1% q1h, Neosporin q1h, Chlorhexadine 0.02% q1h, andoral itraconazole 100-200mg

• PKPo Bacterial keratitis

Pseudomonas (P. aeruginosa 70% of CL wearers, S. Aureus 50% of non-CL wearers)

• One of the most common isolates in CL related MK• Liquefactive necrosis

o Perforation in 48 hours• Semi-opaque ground glass appearance

Intact epithelium• Corynebacterium diphtheriae, Listeria, Haemophilus

Treatment• Culture (1:2:3 rule), broad spectrum antibiotic

o Fungal Keratitis Large white infiltrate with fluffy or branching margins Significant edema Fusarium

• Found in soil, vegetation & water “Recent” outbreaks

• Associated risks High risk of loss of BCVA Treatment (No Steroids)

• Natamycin 5% and/or Amphotericin B 0.3-0.5% (toxic) q1haround the clock, oral Itracanozol 200-400mg loading dosefollowed by 100-200mg QD, and cycloplege

o Viral Keratitis Simplex (HSV-1)

• Case-control study found no association between HSV keratitisand CL wear

• HEDS study determined that there was no association between CLwear and HSV recurrence

• Retrospective study found increased risk of recurrence in 21 CLwearers compared to 96 non CL wearers

o Treatment Options Progressively worsens without treatment D/C CL wear immediately Corneal scrapings & antimicrobial therapy Which therapeutics? Referral to cornea specialist if in visual axis

o Wearing Modality & Material Daily Disposable

• Benefitso Convenience, no CL storage caseo Decrease deposit formation

• Decrease in incidence severity of MK

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Silicone Hydrogel • Benefits

o Increase oxygen permeability • Equal risk but wearing SiHy for longer periods of overnight wear

(continuous wear) o Other factors contributing to complications

o Summary of CL Associated Serious & Significant Events Rare Absolute risk has remained constant for DW and EW SCL Occurrence

• 1 in 10,000 for GP • 3-4 in 10,000 for DW SCL • 10-20 in 10,000 for EW SCL

Vision loss with CL related MK • 0.3 to 3.6 in 10,000

Sterile keratitis – 1% to 7% of SCL wearers ♦Principle risk factor for MK is overnight wear♦

• Cornea - Endothelium o Endothelial Bedewing, endothelial blebs, polymegathism, pleomorphism

• Put it into Practice o Evidence based care o Identifying those patients at higher risk

15-25 year olds, extended wear, living environment, stress level o Customize prescribing habits to decrease risk o Customize patient education to decrease risk

• Practitioner Resources o Grading Scales

• Patient Resources

o Association of Contact Lens Educators o Food and Drug Administration o Institute for Eye Research (Brien Holden Vision Institute) o Industry

• Patient Resources o Center for Disease Control o https://www.cdc.gov/visionhealth/home/index.html

• Targeted Education

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https://www.cdc.gov/visionhealth/home/index.html

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ANTI-VEGF AND THE EYE

ANTHONY DEWILDE, OD

FINANCIAL DISCLOSURE

KMK Update

GOALS

Understand AMD, Diabetic Retinopathy, RVO

Evidence regarding Anti-VEGF

Develop referral strategy

ANTI-VEGF

Vascular Endothelial Growth Factor

Embryonic Development

Collateral Development

New Vessels

ANTI-VEGF

1994 - VEGF increased with hypoxia

2000’s - anti-VEGF can treat certain tumors

2006 - anti-VEGF (ranibizumab) for wet AMD

Macular Degeneration

Retinal Vein Occlusions

Diabetic Retinopathy

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MACULAR DEGENERATION

Threats to Vision

Atrophy

Neovascularization

Atrophy

NeovascularizationMACULAR DEGENERATION

Four potential findings

Sensory detachment

Pigment epithelium detachment (PED)

Sub-Retinal hemorrhage

Sub-RPE hemorrhage

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MACULAR DEGENERATION

Historically treated with

Nothing

Laser

Visudyne

STUDIES

MARINA/ANCHOR

VIEW

CATT/GEFAL

Treat and Extend

STUDIES

90% maintain acuity with treatment

Only 50% untreated maintain

STUDIES

41% gained 3 lines of acuity with treatment

Only 6% untreated gained

STUDIES

33-42% achieve 20/40 or better treated

Only 6% untreated reach 20/40

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STUDIES

Avastin = Lucentis = Eylea

Fewer injections with Eylea

11 vs 16 at 2 years

TREAT AND EXTEND

Treat every month for 3 months

If stable, extend out

TREAT AND EXTEND

90% had stability at 2 years

45% had 20/40 acuity

Ophthalmology 2015;122:1212-1219

TREAT AND EXTEND

Fewer injections (13 versus 17) - over 2 years

Fewer Visits

Less $$

PATIENT

80 YO WM

AMD OU

S/P PCIOL OU

PATIENT

2007

20/50 OD

20/20 OS

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PATIENT

2009

20/50 OD

20/40 OS

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PATIENT

Start Lucentis OS

Stable PED w/o net OD

PATIENT

Between 2009 - 2014 was sent to local specialist

Lucentis OD x 16, OS x 22

Eylea OS x 3

20/400 OD

20/25 OS

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AMD - SUMMARY

Lucentis and Eylea similar

May be able to give Eylea less frequently

Lucentis and Avastin similar

AMD - SUMMARY

Still developing exit strategy

PRN vs Treat and Extend

AMD - SUMMARY

25-40% had 20/40 acuity with Anti-VEGF

90% had stable vision

Good safety profile

AMD REFERRAL

If Wet AMD

Does acuity matter?

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VEIN OCCLUSIONS

Threats to vision in BRVO

Macular edema

Macular ischemia

Proliferative (mostly V-Heme)

VEIN OCCLUSIONS

Threats to vision in CRVO

Macular edema

Macular ischemia

Proliferative (mostly NVG)

VEIN OCCLUSIONS

BRVO historically treated

If NV, treat with sector PRP

If edema, wait 3 months - then laser

VEIN OCCLUSIONS

CRVO historically treated

If NVG, treat with PRP

If edema, no treatment

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VEIN OCCLUSIONS

Intravitreal steroids improved vision

Complications

Cataract

Glaucoma

STUDIES

BRAVO/CRUISE/RETAIN

GALILEO/COPERNICUS

STUDIES- BRVO

61% gained 3 lines with Lucentis

Only 29% with laser did

STUDIES- BRVO

68% achieved 20/40 or better with Lucentis

Only 42% with laser reached 20/40

STUDIES - CRVO

48% gained 3 lines of acuity with Lucentis

Only 17% gained when left untreated

STUDIES - CRVO

47% achieved 20/40 with Lucentis

Only 21% when left untreated

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STUDIES - CRVO

Lucentis and Eylea are similar

DEVELOPMENT OF NV

Development of NV @ 2 years

6% Eylea

9% Sham

In CVOS this was 35% in control group (all ischemic)

Reduced to 22% with PRP

DEVELOPMENT OF NV

Does anti-VEGF eliminate NV or temporize it?

COPERNICUS

Development of NV year 1

0% Eylea

7% Sham

Development of NV year 2

6% Eylea

8% Sham + PRN

BRVO - CASE

46 YO WM

New to Eye Clinic

Uncontrolled HTN

Borderline Diabetes Mellitus

H/O CVA, MI

BRVO - CASE

“Seems like letters are there and then missing in and out of vision”

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BRVO - CASE

BCVA

20/25 OD

20/40 OS

Anterior Segment Unremarkable

BRVO - CASE

ONH - 0.1 OU - Healthy

++Tortuous Vessels OU

Sup BRVO OD - Paramacular Heme

Old BRVO OS - Collaterals

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Bi-Nasal??

BRVO - CASE

Referral to University of Kansas

Macular Atrophy OS

Mild edema - anti-VEGF

Prognosis?

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BRVO - CASE 2

81 YO WM

Routine Eye Examination

No vision complaints

BRVO - CASE 2

BCVA 20/25 OD & OS


IOP 18/17

BRVO - CASE 2

BRVO OD

20/25 acuity

Refer?

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VEIN OCCLUSION - SUMMARY

BRVO, CRVO improve on Eylea

BRVO, CRVO improve on Lucentis

Longterm outcome of CRVO shows guarded prognosis


Laser photocoagulation still viable treatment option for BRVO


Most benefit show in first year or two

Benefit lessens over time


Very little NV on anti-VEGF treatment

Does this effect last?

VEIN OCCLUSION REFERRAL

BRVO - if central edema/reduced acuity

If no referral, monitor closely for NV or edema

VEIN OCCLUSION REFERRAL

CRVO - if central edema/reduced acuity

If no referral, monitor monthly for 6 months - gonioscopy

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DIABETIC RETINOPATHY

Threats to Vision

Macular Edema

Macular Ischemia

Proliferative

NVG

V-Heme

Traction RD

DIABETIC MACULAR EDEMA

Treatable Threats to Vision

Macular Edema

NV

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Treatable Threats to Vision

Macular Edema

NV


Historically treated with

Laser

Focal

Grid

Intravitreal steroids


Treatment Criteria (CSME)

Retinal thickening within 500 microns of fovea

Exudate within 500 microns of fovea w/ adj thickening

>1 disc area of thickening within 1 disc diameter


Treatment Criteria - Anti-VEGF

Central retinal thickening

<20/30

STUDIES

BOLT

RESTORE

RISE/RIDE

DRCR

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STUDIES

100% lost < 3 lines with Avastin

Compared to 86% with laser

STUDIES

40% gained > 3 lines with Lucentis

Compared to 22% with laser (deferred Lucentis)

STUDIES

60% achieved 20/40 with Lucentis

Compared to 42% with laser (deferred Lucentis)

STUDIES

At 5 years Lucentis + Laser

75% achieved 20/40

DRCR

1% rate of endophthalmitis

0.06% per injection rate (out of 3176 injections)

STUDIES

Could Eylea be given less frequently?

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VISTA/VIVID

2 Year Results

Aflibercept (Monthly or Bi-monthly) vs. Laser


VISTA/VIVID

Gain 3 lines

Monthly 38%

Bi-monthly 33%

Laser 13%

VISTA/VIVID

Average injections

Monthly - 22

Bi-monthly - 14

DME - SUMMARY

Lucentis and Avastin effective for DME

60-75% reading acuity at 5 years

Can be combined with laser

DME - SUMMARY

Aflibercept may be given less often

When can we stop?

CASE

68 year old Hispanic Male

IDDM (A1c = 7.8%)

Hypertension

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CASE

Insulin

Metformin

Metoprolol

CASE

F/U for NPDR

BCVA

20/25 OD

20/30 OS

CASE

IOP 18/18

Entrance tests unremarkable

No NVI

Mild Nuclear Sclerosis OU

CASE

CASE CASE

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CASE CASE

CASE

Diagnosis

NPDR OU

No CSME OD

CSME OS

CASE

Treatment

Prompt referral to retinal specialist

Under treatment with IVI Avastin

CASE

Prognosis?

CASE

62 YO WM

Follow up for DM

Mild blur OU

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CASE


BCVA 20/30 OD, 20/25 OS

IOP 18/18

P + RXN NO APD

CASE

CASE CASE

CASE CASE

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CASE

Posterior Segment

PDR OU

High risk OD - Shallow traction RD

Borderline CSME

CASE

Plan

PRP

Avastin — Why?

CASE CASE

Worsening of CSME

10% of patients with PRP (Argon laser)

CASE

Can anti-VEGF help PDR?

ANTI-VEGF FOR PDR

Similar visual acuity at 2 years

JAMA 2015;314(20):2137-2146.

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ANTI-VEGF FOR PDR

Visual Field score

Anti-VEGF -23 dB

PRP -422 dB

ANTI-VEGF FOR PDR

Develop Macular Edema

Anti-VEGF = 9%

PRP = 28%

ANTI-VEGF

Benefits

Improvement of acuity!

Safe

Tolerable

ANTI-VEGF

Complications

Patient perception

Endophthalmitis

Systemic

Cost

ANTI-VEGF

Complications

Frequency of visits and injections!!

ANTI-VEGF

Future developments

PRN dosing

Treat and Extend

Trap-Eye

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ANTI-VEGF

Future developments

Eye drop?

Implant (similar to Ozurdex)

REFERRAL

Neovascular AMD - Prompt

REFERRAL

BRVO - if central edema/reduced acuity

If no referral, monitor closely for NV and edema

REFERRAL

CRVO - if central edema/reduced acuity

If no referral, monitor monthly for 6 months - gonioscopy

REFERRAL

Central Diabetic Macular Edema - 20/30 or worse

Meets CSME criteria

FUTURE OF ANTI-VEGF

Longer lasting medication

Fewer injections

Vitreous inserts (similar to Ozurdex)

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THANK YOU!

[email protected]

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Judicious Prescribing

TEST YOUR KNOWLEDGE

GOVERNMENT OVERSIGHTof

CONTROLLED SUBSTANCES

Disclaimers• No current contractual arrangements with anyvendors of ophthalmic or pharmaceuticalsupplies

• No known “conflicts ofinterest”

INSTRUCTIONS:Rules of the Game………..

From the Choices Given, select the best ANSWER(S) for each question.

SAMPLE: As of today, who do you consider is responsible for the “Opioid Epidemic” in the United States?

A. Congress

B. Pharmaceutical Industry

C. D.E.A.

D. Organized Crime

E. Local Law Enforcement

F. Donald Trump

The Opioid “Crises” in America

#1: Post Civil War (late 1800’s)

#2: Post World War I (1913‐1920)

#3: Vietnam War era

‐ shortened by manyalternative choices

‐ stoked by targeted effortsagainst other “favorites”

#4: 2008‐present

‐ stoked by anti‐methamphetaminecampaigns

Which statement regarding Addiction to Opioid Narcotics is TRUE?

A. Most addicts are of lower socio‐economic status.

B. Most addicts are persons of color.

C. Most addicts lack college‐level education.

D. Most addicts are male.

E. Most addicts deny they have an addiction.

Which statement regarding Addiction to Opioid Narcotics is TRUE?

A. Risk is greater for Alcoholics

B. Risk is greater for Chronic Pain Patients

C. Risk is greater for Cigarette Smokers

D. Risk is greater for patientsbeing treated for Anxiety

E. Risk is greater for patientsbeing treated for Depression

F. Risk is greater for Migraine sufferers

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Who established the very first Schedule of narcotics in the U.S.?

A. President Truman

B. Food & Drug Administration

C. U.S. Congress

D. U.S. Dept of Justice

In what Year was the first Scheduling of drugs developed and published?

A. 1878

B. 1912

C. 1927

D. 1970

Which statement is FALSE?

IN THE UNITED STATES, PRIOR TOWORLD WAR 1:

A. All narcotics were legal

B. Narcotics were regularlyavailable at doctors officesand pharmacies

C. Accepted uses included “pain relief”and “for the cure of illness”

D. Addicts accounted for greatest amount of use ofthese products

What is the basis for assigning a Scheduled substance as I, II, III, IV, or

V?A. Potential for Abuse

B. Accepted medical use fortreatment in the UnitedStates

C. Degree of Dependence thedrug may cause

D. All of the above are to beconsidered

Hydrocodone‐containing products (H.C.P.’s) are currently classified by the D.E.A. as belonging to which Schedule?

A. Schedule 1

B. Schedule 2

C. Schedule 3

D. Schedule 4

E. Schedule 5

Were any states able to maintain O.D. prescribing rights by keeping Hydrocodone‐containing Products

as Schedule 3?

• Oklahoma and West Virginia

• Idaho

• California and Oregon

• The Answer is “NO”

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Oxycodone‐containing products (O.C.P.’s) are currently classified by the D.E.A. as belonging to which Schedule?

A. Schedule 1

B. Schedule 2

C. Schedule 3

D. Schedule 4

E. Schedule 5

What is the non‐narcotic analgesic contained in Percocet?

A. Aspirin

B. Codeine

C. Acetaminophen

D. Ibuprofen

On an annual basis, Abuse of this painkiller is associated with greatest number of cases of cirrhosis, and ultimately, with the largest

number of liver transplants?

A. Morphine

B. Oxycodone

C. Hydrocodone

D. Codeine

E. Acetaminophen

Which of these Analgesics are overused the most frequently, according to the C.D.C.?

• ACETAMINOPHEN

• IBUPROFEN

• ASPIRIN

• HYDROCODONE

• TOPIRAMATE

• GABAPENTIN (NEURONTIN)

• DULOXETINE (CYMBALTA)

Which factor is NOT credited for the Federal Government’s decision to take a role in the oversight of narcotics use

in the United States?A. The Prohibition Movement

B. Return of injured W.W.1veterans to the U.S.

C. Lobbying by women’sorganizations

D. Recommendations of theAmerican Medical Association

Which statement regarding the Harrison Narcotics Act of 1914

is TRUE?

A. Established the FederalBureau of Narcotics

B. Established the DrugEnforcement Agency

C. Banned physicians from prescribing a specific list of narcotic substances

D. It allowed for physicians to prescribe narcotics to known addicts

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In what YEAR was the Drug Enforcement Agency established?

A. 1918

B. 1948

C. 1964

D. 1973

The D.E.A. is currently an agency within which U.S. governmental department?

A. Food & Drug Administration

B. Department of Health & HumanServices

C. U.S. Department of Justice

D. Federal Bureau of Investigation

What was the initial purpose and charge given to the D.E.A.?

A. To establish a new listingof controlled substances

B. To monitor the prescribingpatterns of licensed physicians

C. To reduce the supply of illegaldrugs entering the U.S.

D. To investigate the abuse ofprescription narcotics in the U.S.

What is the approximate current level of funding for the D.E.A. as authorized

by Congress and the President?A. $250 million per year

B. $806 million per year

C. $1 billion per year

D. $2 billion per year

What is the Average Number of physicians investigated by D.E.A. each

year?

A. 50

B. 100

C. 900

D. 1,500

Who holds legal authority to add or transfer a drug between Schedules, if he/she finds the substance has “a

potential for abuse or greater abuse”A. President of the United States

B. Surgeon General of the U.S.

C. U.S. Attorney General

D. Administrator of the D.E.A.

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Which is TRUE regarding the ability of the Administrator of the D.E.A. to initiate

Scheduling (or Rescheduling) of a Controlled Substance?

A. Can do it on her/his own authority

B. “ “ “ at the request of the Secretary of the Dept. of Health and Human Services

C. “ “ “ at the request of any interested party

D. All of the above are TRUE

When did Hydrocodone‐containing Products (H.C.P.’s) become Schedule II?

A. January 1, 2013

B. December 31, 2013

C. October 6, 2014

D. December 31, 2014

Which H.C.P. is still classified as a Schedule III controlled substance?

A. Tylenol‐3

B. Percocet

C. Vicodin

D. None of the above

By what legal authority did the D.E.A. act to reclassify H.C.P.’s?

A. Harrison Narcotics Act of 1914

B. Safe Prescribing Act of 2013

C. Controlled Substances Act of 1970

D. By Congressional Endorsement

Who initiated the Petition to the D.E.A. that resulted in the reclassification of H.C.P.’s from Schedule III to II in 2014?

A. President Obama

B. Atty General Eric Holder

C. Assistant Secretary of Healthand Human Services, Kathleen Sibelius

D. F.B.I. Director,Robert Mueller

Who originally Petitioned the D.E.A. to reclassify H.C.P.’s to Schedule II?

A. President G.H. Bush

B. President G.W. Bush

C. Health and Human ServicesDirector, Kathleen Sibelius

D. An unnamed interested 3rd

party

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When?

A. 2003

B. 2008

C. 2010

D. 2013

What Action did the D.E.A. take?

A. Ignored the Petition, until legal action was taken by the Petitioner

B. Delegated the decision to Congress

C. Called upon the Dept of Health & Human Services to study the issue and come back with a recommendation to the D.E.A.

D. Decided to keep H.C.P.’s as Schedule III

What eventually lead to further Action?

A. Law Enforcement concerns

B. Public Concern

C. Lobbying

D. Food and Drug AdministrationSafety and Innovation Act of2012

Parallel Processes Take Place

• F.D.A. holds public meeting (“Drug Safety and Risk Management Advisory Committee”)– Call for public comments

– 29 members• National Institute on Drug Abuse

• Center for Disease Control

• Additional “medical and scientific professionals with expertise on the subject of opioid abuse”

• January 24‐25, 2013 meetings

• VOTE: 19 to 10 to recommend upscheduling H.C.P.’s

F.D.A. advises H.H.S.H.H.S. advises D.E.A.

D.E.A. accepts the recommendation

Meanwhile:

Senator Joe Manchia, III, (West Virginia) introduces the “Safe Prescribing Act of 2013” (S.B. 621) to amend the Controlled Substances Act of 1970 so as to make H.C.P.’s all Schedule II

‐‐Notable Co‐sponsors: Diane Feinstein, Jay Rockefeller, Charles Schumer, Marco Rubio, Thomas (Tom) Harkin

Which statement regarding the prescribing of Controlled Substances bycredentialed OD’s in ALASKA is TRUE?

A. AK. OD’s can prescribe Schedule III drugs

B. AK. OD’s can prescribe Schedule II drugs

C. The ONLY Schedule II drug that AK. OD’s can legally prescribe are those which contain hydrocodone

D. Both #A and #B are correct answers

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What is the maximum duration of treatment for which an O.D. in the U.S. can prescribe an H.C.P. product via a

single Rx?

A. 3 days

B. 5 days

C. 21 days

D. Not limitedby Law orBoard Rules

E. Varies by state

Which statement regarding Refills for H.C.P.’s is TRUE in all states?

A. Cannot be ordered via phonecall

B. Cannot be ordered via FAX

C. Cannot be written for uponthe initial (or on an earlier)Rx

D. Must be hand‐carried by thepatient to the dispensingPharmacist

E. These are all TRUE statements!

The Oklahoma Optometry Board of Examiners in Optometry considers which of the following to represent Unprofessional

Conduct?A. Prescribing H.C.P.’s for purposes other than for

generally accepted treatment of ocular abnormalities

B. Rx‐ing H.C.P’s for personal useC. Rx‐ing H.C.P. for use by an immediate family

memberD. Issuing H.C.P. refills without a physical re‐

examination of the patientE. All of the above are considered Unprofessional

Conduct by our Board!

Under states’ law, which of the following OD prescriptions for OxyContin would be

considered evidence of gross incompetence?

A. 1 tab q4‐6 hours for pain

B. 1 tab PRN as needed for corneal pain

C. 1‐2 tabs 4x daily for 4 days

D. 2 tabs per day for back pain

Synopsis of the Literature

STUDIES

On

ADDICTION & DEPENDENCE

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Predisposing Factors for Health Care Providers

Ease of access (availability) Family History of substance abuse Certain Personality Traits “Type A” Egotistical Grandiosity Overachievers

STRESS Home Work

“Thrill‐seeking” SELF‐TREATMENT MENTALITY Pain Sleep patterns Emotional /mood disorders

Chronic fatigue Social/Economic Status

High‐risk‐taker Types3x Greater Risk for Drug Abuse

• PERSONAL LIFE risk‐takers

• PROFESSIONAL LIFE risk‐takers

– Anesthesiologists

– E.R. Physicians

– OB/GYN Physicians

– “leading edge” Practitioners

20,000 US Physicians (10%)Estimated to have substance abuse

issues at any given time

#1: Alcohol

#2: Sedatives

#3: Opioid Analgesics

#4: “Street Drugs”

#5: Rx “uppers”

Current Lifetime Risks (USA)

• Alcoholism – 13.5%

– Males ‐‐‐ 24%

– Females ‐‐‐ 5%

• Prescription Drug Abuse/Dependency –6.2%

– Males ‐‐‐ 8%

– Females ‐‐‐ 6%Notice: The Data for Health Care Professionals is virtually identical as that for the General Population

NEARLY 1 IN 5 DEVELOP PROBLEMS WITH ALCOHOL AND/OR OTHER DRUGS DURING THEIR LIFETIME

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Drug’s “Addiction Potency”

• Varies by substance

– Generally: Category 1>2>3>4>5

• Varies from Individual user to Individual user

– Differing personal preferences

– Differing pharmacophysiology

• Alcohol is one of the very most addictive

WHY?

• Availability

• Cost

• Efficacy

• Easy to use longterm (risks increase withduration)

All Drug Addictions arise from repeated and frequent use

• Usually take weeks to years to develop

Elements of Addiction(American Society for Addictive Medicine)

1. Impaired Control over Use

2. Preoccupation with Use

3. Continued Use—despite knowing aboutadverse consequences‐ Personal

‐ Legal

4. Distortion of Thinking

Diagnostic & Statistical Manual

1. Preoccupation/Anticipation‐ cravings

‐ focus on obtaining the substance

2. Binge/Intoxication‐ use of substance in excess

‐ taking more than the “least, effective dose”

3. Withdrawal/Negative Effects‐ development of tolerance

‐ symptoms when blood levels drop

‐ decreased motivation for normal life activities

Current concept of ADDICTION

• A chronic, relapsing, brain disease…..

• With BIOGENTIC basis

• With PSYCHOSOCIAL basis

– Emotional dysfunction

– Abnormal social interactions

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Principle Predisposing Factors for Addiction

#1: Genetics#2: Psychological Factors

Addiction has its basis in NEUROBIOLOGY‐ Neurotransmitter Cascade‐Mesolimbic System (“Reward Circuit”)‐ Prefrontal Cortex (“Craving Centers”)‐ Nucleus Accumbas‐ Basolateral Amygdela‐ Hippocanthus (“learning & memory centers”)

Functional MRI studies

the “Addicted Brain” demonstrates changes in terms of Activity and Metabolism:

Activity/Metabolism Hyperactivity/Metabolism in the Prefrontal Cortex region

Also: Activity/Metabolism Hypoactivity in response to “naturally stimulating rewards”

‐ food

‐ social interactions

‐ sex

Contributing to the hard‐wiring of the addiction:

“Euphoric Reward” of drug usually decreases over time as the “Allostatic Load” increases

damage done

neurochemical changes

neurotransmission changes

DEPRESSION following drug use increases

‐ can be amplified by external stresses and changes!!!

Anyone you know……………………?

Characteristics of the Impaired Physician

• Tenacious Denial of a problem

• Denial by Family, Friends, Colleagues, Patients

• Delusional sense of self confidence

• Steady, sequential, progressive deterioration in every facet of life

– Family

– Community

– Finances

– Legal

– Spiritual & Emotional Health

– Physical Health

– Professional Performance

JOB PERFORMANCE AND IMAGE TEND TO BE PROTECTED AT THE EXPENSE OF EVERY OTHER LIFE DIMENSION!

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Clues around Home

• Withdrawal from family, friends, community

• Emotional Lability

• Increased aggression, agitation, overt conflicts

• Deterioration of personal appearance &hygiene

• Increase in medical disorders

• Increased accidents and injuries

• Financial troubles

• Legal troubles

Clues around Work

Tardiness Increased Absences Increased Secrecy, less Communication, less Discussion

Worsening handwriting Poor charting Errors in Rx writing Decreased Productivity Increased Conflicts Increased Irritability and Aggression Overt Intoxication “smell of alcohol”

IS THIS Someone you know?

Helping the Impaired Physician is usually difficult; NOT

impossible!

Options for action are varied

The only choice that is wrong is to do absolutely nothing!!!

There is help (and hope) for the “Impaired Physician”

IMPAIRED PHYSICIAN PROGRAMS

• Championed by the A.M.A.

• All 50 state’s Medical Boards offer programs

• Virtually all state’s Optometry Boards havedeveloped programs

– THE OKLAHOMA BOARD OF OPTOMETRY HAS AN EFFECTIVE PROGRAM FOR OPTOMETRIC PHYSICIANS WHO NEED HELP

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Optometrist's Guide to Glaucoma Surgery

Anthony DeWilde, OD FAAO

I have no financial disclosures

How glaucoma surgery works

Who to refer/When to refer

Expected outcomes

Glaucoma can be a visually debilitating disease.

Cannot be reversed.

My role is to maintain quality of life by:

Minimizing disease with least cost, burden, and side effects

Outcomes:

Surgery = Medicine

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Complications:

Surgery >>> Medicine

Progressive glaucoma despite medication

Cannot tolerate medication

Moderate/advanced disease

Surgeon's role

Lower IOP

Minimize risk

Optometrist's role

Help maintain visual function

Co-manage

Surgery does NOT

Improve vision (not LASIK)

Cure glaucoma

Young

African American

Uveitic Glaucoma

Rubeotic Glaucoma

Prior failed glaucoma surgery

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webeye.ophth.uiowa.edu

Virgin eyes

Older

POAG

White

IOP <18

IOP <21

No HVF or ONH progression

Additional Medication?

Conjunctival flap

Make scleral flap

Remove section of TM

Create Iridectomy*

Suture

Goal

Create a non-healing fistula

Allow direct access from AC to subconj

Bypass TM and Schlemm's canal

http://www.ngsglaucoma.com/images/trab.jpg

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Remove TM

New passage

Filtering bleb

Functional Bleb

Cystic

Diffuse

Good IOP

Non painful

Improvements

Guarded/Partial Thickness

Anti-metabolites

Suture Manipulation

http://emedicine.medscape.com/article/1844332-overview

Mitomycin C

5 Fluorurocil (5 FU)

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http://www.glaucoma-surgery.org/trab_closing_one.htmlt/mobile/namratagupta96780/trabeculectomy-trabeculotomy-goniotomy-and

Hypotony

Leak

Flat A/C

Infection

Pain

ps://www.reviewofophthalmology.com/article/filtering-surgery-late-complicatio

20 Year Follow Up

Complete Success

13% failure first year

1.6% per year after


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20 Year Follow Up

Qualified Success

7% failure first year

0.3% per year after

At 20 years 15% were blind

Other complications

Expulsive Hemorrhage

Phthisis

Endophthalmitis

TVT study

Similar IOP post-op

Similar number post-op meds

Failure Trab (47%)**

Failure Tube (30%)

TVT study

All eyes had prior surgery

2-% of patients lost 3 lines

1% per year risk of endophthalmitis

Am J Ophthalmol. 2012 May;153(5):789-803.e2.

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Ahmed

Baerveldt

Mean IOP

Ahmed - 16 mmHg

Baerveldt - 14 mmHg

Am J Ophthalmol. 2017 Apr;176:118-126

Post-Op Meds

Ahmed - 2

Baerveldt - 1

Failure

Ahmed - 51%

Baerveldt - 34%

Complications

Ahmed - 52%

Baerveldt - 62%

Complications Success

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ww.acvci.com/eyecare-services-list/glaucoma-care/glaucoma-surgery-express-mi

Advantage

Lower rate of Hypotony

No Iridectomy

Standard trabecular opening

Define "success"

3 Trials

No complications (i.e. Hypotony)

IOP 6-18 mmHg

IOP <21 mmHg with or without med

Complications

Hypotonous maculopathy

ExPRESS - 4%

Trabeculectomy - 6%

Success

IOP 6-18 mmHg

(Qualified success) - 54%

Success

IOP <21 mmHg with or without meds

ExPRESS - 94%

1/4 were on meds

J Ophthalmol. 2015;2015:720109

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Microinvasive Glaucoma Surgery

iStent

Trabectome

Cypass

Xen Gel Stent

Only FDA approved MIGS surgerieswww.drdylanjoseph.com/istent-exciting-technology-for-the-treatment-of-your-gla

glaukos.com

Advantages

Minimally invasive

No cutting conjunctiva

Less risk (infection, hypotony)

Can perform trab or tube later

Disadvantages

Has to be combined with CE

Not for Advanced Glaucoma

Not for Secondary Glaucomas

Success

Reduce medication (1.6 to 0.4)

Reduce IOP (range 22% - 40%)

J Cataract Refract Surg. 2012; 38(8): 1339-1345.

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Complication

Hyphema (transient) - 3-70%

Malposition - up to 16% iStent Inject

http://gusgazzard.com/trabectome/trabectome-ab-interno-surgery-condon/

Advantages

Minimally invasive

No cutting conjunctiva

Less risk (infection, hypotony)

Disadvantages

Not for Advanced Glaucoma

Not for Secondary Glaucomas

Less effective if IOP is already low

Success

Reduce medication (1.2 to 0.4)

Reduce IOP (range 18% - 40%)

J Cataract Refract Surg; 34(7). 1096-1103.

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Complication

Hyphema (transient) - 60-78%

PAS - up to 25%

https://www.myalconstore.com/glaucoma-surgery/cypass-micro-stent/

https://www.myalconstore.com/glaucoma-surgery/cypass-micro-stent/ https://www.myalconstore.com/glaucoma-surgery/cypass-micro-stent/

Ophthalmology 2016;123:2103- 2112

Success

IOP reduction 20% at 2 years

77% CyPass

60% CE

Ophthalmology 2016;123:2103- 2112

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Success

IOP between 6-18

65% CyPass

44% CE

Success

Average number of meds

CyPass 1.4 pre-op -> 0.2

CE 1.3 pre-op -> 0.7

Complication

Iritis - 9%

Hyphema (transient) - 3%

(IOP < 6%) - 3%

MIGS.org

MIGS.org

65 patients

75% had > 20% reduction in IOP

Avg reduction 9 mmHg

Meds decreased from 3.5 to 1.7

Ophthalmology 2016;123:2103- 2112

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[email protected]

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James Kundart OD MEd FAAO FCOVD‐A 6/18/2018

1

Ehlers-Danlos Syndromeand the Eye

2018 VICTORIA CONFERENCEJAMES KUNDART OD MED FAAO FCOVD-A

PACIFIC UNIVERSITY COLLEGE OF OPTOMETRYFINANCIAL DISCLOSURE: NOTHING TO DISCLOSE

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3504533/figure/F1/

Learning Objectives

1. Why doesn’t Ehlers-Danlos Syndrome(EDS) present more often with high myopia, keratoconus, and lacquer cracks in Bruch’s membrane?

2. What are the most common presenting symptoms of EDS?

3. What are the most common clinical signs of EDS, including subtle ones?

4. How are these EDS problems best treated by the primary-care optometrist?

Connective Tissue Disorders and Optometry

The eye and adnexa areboth made ofconnective tissue, fromlid tissue, sclera and cornea to the zonulesand extra-ocular muscletendons

Refractive error, binocularity, and eyedisease are all impactedby connective tissueproblems

https://www.pressrelease.com/news/ehlers-danlos-society-receives-transformational-gift-for-119892

Connective Tissue Disordersin Primary Eye Care

Ehlers-Danlos Syndrome Pseudoxanthoma

Elasticum Osteogenesis Imperfecta Marfan Syndrome Stickler Syndrome Others

https://en.wikipedia.org/wiki/Angioid_streaks

Ehlers-Danlos Syndromes (EDS)

This connective tissue disorder comes in several types with slightly differentsystemic and ocular signs

Hyperextensible joints, bruising, and poor-woundhealing are a well-known feature of many types of EDS (especially the most common Types, II and III)

“As of 2017, 13 Ehlers–Danlos syndromes had been characterized, with a significant overlap in features” https://sites.google.com/site/ehlerd

anlosfordummies/the-history-of-eds

2017 Genetic Classification of EDS

Hypermobile Classical Vascular Kyphoscoliosis Arthrochalasia Dermatospraxis

Brittle CorneaSyndrome

Classical-like Spndylosplastic Musculocontractural Myopathic Periodontal Cardiac-Vascular

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Most Common: HypermobileEhlers-Danlos Syndrome

“Characterized primarily by joint hypermobility affecting both large and small joints, which may lead to recurrent joint dislocations and subluxations (partial dislocation)

In general, people with thistype have soft, smooth and velvety skin with easy bruising and chronic pain of the muscles and/or bones”https://www.pressrelease.com/ne

ws/ehlers-danlos-society-receives-transformational-gift-for-119892

Classical-TypeEhlers-Danlos Syndrome

Associated with extremely elastic (stretchy), smooth skin that is fragile and bruises easily, wide, atrophic scars (flat or depressed scars), and joint hypermobility

Molluscoid pseudotumors(calcified hematomas overpressure points such as the elbow) and spheroids (fat-containing cysts on forearms and shins) are also frequently seen

https://rarediseases.info.nih.gov/diseases/6322/ehlers-danlos-syndromes

Vascular-Type Ehlers-Danlos Syndrome

”Characterized by thin, translucent skin that is extremely fragile and bruises easily

Characteristic facial features including large eyes, a thin nose, and lobeless ears

Joint hypermobility is present, but generally confined to the small joints(fingers, toes)”

https://rarediseases.info.nih.gov/diseases/6322/ehlers-danlos-syndromes

Kyphoscoliosis-TypeEhlers-Danlos Syndrome

”Associated with severe hypotonia at birth, delayed motor development, progressive scoliosis (present from birth), and scleral fragility

Affected people may also have easy bruising; fragile arteries that are prone to rupture; unusually small corneas; and osteopenia (low bone density)”

https://www.scoliosisassociates.com/conditions/ehlers-danlos-syndrome/

Brittle Cornea Variant of Ehlers-Danlos Syndrome (RARE)

Brittle CorneaSyndrome (BCS) is“characterized bythin cornea, earlyonset progressivekeratoglobus andblue sclerae”

Like blue sclera, this is rare in ambulatory patients

http://www.cityeye.com.au/patient-information/

Brittle Cornea Syndrome:Presentation and Ant Seg OCT


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Systemic Symptoms ofEhlers-Danlos Syndrome

In general, these patients are athletic, so diagnosis of EDS is often delayed

Mild hypermobility may have some advantages for pregnancy and childbirth

But not much later in life, the number of surgeries they have may exceed their age

http://www.marieclaire.co.uk/opinion/ehlers-danlos-syndrome-living-with-eds-and-finding-treatment-10731

Inflammatory Diseases and EDS


Autoimmune and EDS: Bechet Disease in the NFL/Choroid

http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0004-27492017000200069&lng=en&nrm=iso&tlng=en

Autoimmune and EDS: Fibromyalgia and the Cornea


Autoimmune and EDS:Rheumatoid Arthritis

http://webeye.ophth.uiowa.edu/eyeforum/atlas/pages/Scleromalacia-in-RA/index.htm

RA and Scleromalacia

http://webeye.ophth.uiowa.edu/eyeforum/atlas/pages/Scleromalacia-in-RA/index.htm

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Rheumatoid Arthritis and EDS: Joint Support Ring Splints

https://youtu.be/tWMjl0iLk50

Other Ocular Consequences of Ehlers-Danlos Syndrome

Exposure Keratitis Corneal Hysteresis Refractive Error Strabismus Postural Orthostatic

TachycardiaSyndrome

https://decisionmakerplus.net/case-report-post/exposure-keratopathy-secondary-to-lagophthalmos-2/#1454791209937-f372e282-b6d16c55-bb67

1. Exposure Keratitis and EDS

https://decisionmakerplus.net/case-report-post/exposure-keratopathy-secondary-to-lagophthalmos-2/#1454791209937-f372e282-b6d16c55-bb67

Treating Dry Eye in EDS:Ant-Inflammatories

https://www.slideshare.net/drajayslide/dry-eye-19808747https://www.goodrx.com/fml?drug-name=fml

Treating Dry Eye in EDS:Salagen (oral pilocarpine)

https://www.goodrx.com/salagen?drug-name=Salagen

2 .Corneal Hysteresis in EDS:Ocular Response Analyzer

http://www.reichert.com/product_details.cfm?pcId=652&skuId=2976&skuTk=1036239258#.WnG8xK2ZOu4

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Why You Won’t Often See Blue Sclera in EDS

Blue sclera is normal in newborns and the elderly

Adult patients with thin blue sclerae have a brittle cornea and ectasia risk

The weak cornea and sclera puts the patient at risk for retinal detachment and globe rupture with ocular injury

https://globalgenes.org/raredaily/ehlers-danlos-syndrome-6-spells-multiple-problems-for-dagmara/

Why Refractive Surgery is Contraindicated in EDS

http://www.reviewofcontactlenses.com/content/d/irregular_cornea/c/60783/

Treating Post-LASIK Ectasia in EDS: Scleral Contact Lenses

http://lasikadvisory.blogspot.com/2013/03/avedro-ccl-treatment-for-kerataconus-or.html

Scleral Lenses Treat Post-LASIK Ectasia and Dry Eye in EDS

Corneal transplants are a particular challenge for most EDS patients with keratoconus due to risk of a ruptured globe

Preceding penetrating keratoplasty, a 360 degree conjunctival peritomy must be done

Descemet’s membrane from the donor eye has to be sutured on in a ring first, followed by a PK months later http://globalrefractivesolut

ions.com/sclerallenses.html

Treating Post-LASIK Ectasia: Keraring

http://www.ijo.in/article.asp?issn=0301-4738;year=2011;volume=59;issue=6;spage=437;epage=443;aulast=Tunc;type=

3

Anterior Segment OCT for EDS after Keraring

http://www.ijo.in/article.asp?issn=0301-4738;year=2011;volume=59;issue=6;spage=437;epage=443;aulast=Tunc;type=3

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Treating Ectasia in EDS with Corneal Collagen Cross-Linking

http://www.corneaclinic.com/collagencrosslinking.html

3. Refractive Error in EDS

Most casual references to Ehlers-Danlos syndrome and the eye report high myopia in these patients

While scleral or corneal hyperextensibility would logically result in myopia, these patients are often too sick to report to us in an ambulatory setting

But they may have anotherconnective tissue disorder

https://medicalpictures.net/stickler-syndrome-pictures/

High Myopia in EDS?OD: -8.00 D, OS: -14.00 D

Wright 3, figure 12-1

EDS Differential Diagnosis: Stickler Syndrome

Also called Hereditary Progressive Arthro-Ophthalmopathy is an autosomal-dominant connective tissue disease

Like Marfan, it causes very highmyopia and possible retinaldetachment

It is seen as frequently as one in 7,500 patients

One characteristic feature is a vitreous veil, as seen here

Wright, Figure 5-5, page 241

Amblyopia, Strabismus andStickler Syndrome

One way in which a Stickler patient can present is with strabismus secondary to retinaldetachment

In this Stickler patient, an RD in OS resulted in LET

If the eye turn occurs before age 2, it is amblyogenic

More often, the poor VA in thestrabismic eye is because the detachment affects the macula and is not true amblyopia

https://medicalpictures.net/stickler-syndrome-pictures/

Anterior Segment Featuresof Stickler Syndrome: Cataract

Wright, Handbook of Pediatric Retinal Disease, Figure 6-5, page 184

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Posterior Segment Featuresof Stickler Syndrome

Other anterior segment complications are rare

For example, glaucoma is only seen in 5% of Stickler cases, although ocular HTN can occur

However, congenital, progressive myopia is universally seen

Retinal detachment is common Seen here is a “peripheral area of

circumferential lattice degeneration”, an early sign

Wright, Figure 5-6, page 241

Radial Lattice Degenerationin Stickler Syndrome

http://webeye.ophth.uiowa.edu/eyeforum/atlas/pages/radial-lattice-in-Sticklers-syndrome.html

Minor ocular trauma can cause vitreous hemorrhage and/or retinal detachments

The vitreous is typically liquified with midperipheral circumferentialcondensations

Radial perivascular patchesof lattice degeneration are present in the posterior poleor mid-periphery

These patients have a 50%lifetime risk of retinal detachment!

Progression of Lattice Degeneration in Stickler Syndrome

Wright, Handbook of Pediatric Retinal Disease, Figures 6-3 and 6-4, page 183

Systemic Features of Stickler Syndrome

Wright, Handbook of Pediatric Retinal Disease, Figures 6-6 and 6-7, page 185

Facial Features of Stickler Syndrome

http://syndromepictures.com/stickler-syndrome-pictures/

Systemic Features of Stickler Syndrome

Sensorineural hearing loss (25%)

High arched palate (25%) Progressive arthropathy (joint

disease), becoming pronounced by 4th or 5th

decade of life Conversely, instead of

stiffness, some havehyperextensible joints

Mitral valve prolapse is seen in almost half (45%)

http://syndromepictures.com/stickler-syndrome-pictures/

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Treating Stickler Syndrome

Many of these patients may need laser photocoagulation for retinal holes and tears

Some will need vitrectomyand scleral buckling for RD

Like Marfan, you will want to have these patients tested for heart and valve defects

A Haberman Feeder baby bottle can be used for Stickler babies with arched palate

https://en.wikipedia.org/wiki/Haberman_Feeder

4. Strabismus in EDS: CN VI andCavernous Sinus Leakage

http://www.nejm.org/na101/home/literatum/publisher/mms/journals/content/nejm/2011/nejm_2011.364.issue-

8/nejmicm1006035/production/images/large/nejmicm1006035_f1.jpeg

http://imagebank.asrs.org/file/8032/carotid-cavernous-fistula

Listening for Orbital Bruit inCarotid-Cavernous Fistula

https://www.ncbi.nlm.nih.gov/books/NBK289/

http://imagebank.asrs.org/file/8033/carotid-cavernous-fistula

Treating Indirect Fistula and DI:Diamox (acetazolamide)

https://www.goodrx.com/acetazolamide?drug-name=acetazolamide

5. POTS in EDS

https://www.top10homeremedies.com/wp-content/uploads/2016/09/postural-tachycardia.jpg

Visual Snow and POTS

http://robertjrgraham.com/wp-content/uploads/2010/10/page1-1001-full.gif

https://media.giphy.com/media/q4Au83JRI550Q/giphy.gif

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VF Loss in a 12 YO with EDS:Cured with Gatorade?!?(thanks to Drs. Diep & Nguyen)

http://commons.pacificu.edu/coofac/24/

Bottom Lines onEhlers-Danlos Syndrome

EDS tests all your optometricskills, from anterior to posterior segment

While there are many structure effects of EDS, the patient wants you to treat their symptoms

These patients will bring in multiple generations of their family with varying penetrance of the disease

Questions? Thank you!

James Kundart OD MEd FAAOProfessor

Pacific UniversityCollege of Optometry3D Performance [email protected]

http://genesthatdontfit.blogspot.com/2014/08/eds-article-about-how-body-with-eds.html

Readings and References

Today’s lecture was inspired by The Handbook of Pediatric Eye and Systemic Disease, edited by Kenneth Wright. MD.

See chapter 5, called “Connective Tissue, Skin, and Bone Disorders’, by Elias Traboulsi.

Ehlers-Danlos Syndrome has a great entry at Epocrates online if you upgrade to the disease database: https://online.epocrates.com/noFrame/showPage.do?method=diseases&MonographId=570&ActiveSectionId=11

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Assessing Diplopia MONOCULAR vs BINOCULAR?

• Often need to “test” the patient• “Are you seeing double now?”• “What if I cover this eye? The

other eye?”

OCCLUSION revealsthe monocular cases!(99% of the time)

Some Key Questions:

• When did this start?• What did you first notice?• Is it more like MULIPLE IMAGES or more like

BLUR or SHADOW IMAGES?• Is it CONSTANT or INTERMITTENT?• Can you clear it up with a BLINK?• How many TOTAL IMAGES do you see?• Are they all the SAME? Or do they DIFFER?• Are they all EQUALLY INTENSE?

Do they TOUCH?Do they OVERLAP?

Is there SPACE between them?

C.N.S. “Cerebral Polyopia”

• Very Rare!• Major C.N.S. Disease• “Monocular Diplopia”

persists when eithereye is covered!

• All images are equallyclear (unlike true monocular polyopia)

MONOCULAR POLYOPIA

ONE “STRONG” IMAGE+

One (or more) “GHOST” Images

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MONOCULAR DIPLOPIA#1: Ocular Media Problem

- tearfilm- cornea- LENS- secondary opacification behind IOL- massive vitreous floater

#2: Ocular Optics Problem- change in astigmatism

#3: Macular Problem- epiretinal membrane

Characteristic Complaint:

• “ghost image” or “blur” when viewingwith ONE EYE

• Overlap• One strong/One or more weak images

PEARL: C/O “Binocular Blur” with new BVA Rx on

• Does it clear up when one eye is covered?• Does it also clear up when the other eye is

covered?• Does it return when both eyes are uncovered?• Is it non-concommitant? Characteristic of small

angles of binocularmisalignment

Monocular Diplopia

• Usually OPTICAL issue– Cataract– Corneal surface wetting problem– Corneal distortion (other causes)– Corneal edema– Dislocated or subluxated lens– Uncorrected refractive error– Macular edema– Macular puckering from epiretinal membranes

Assessment of MONOCULAR DIPLOPIA• Slit-lamp• Topography and/or

Keratometry• RETINOSCOPY• Pinhole Visual Acuity

– Refraction– Re Slit-lamp if Pinhole

Resolves it, but RefractionDoes NOT

• Dilated Fundus Assessment

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Invaluable Diagnostic Tool: Assessing the

“Two Eye Stuff”

Binocular Diplopia• Causes of misalignment

– Cranial nerve palsy– Extraocular muscle dysfunction– Neuromuscular junction disease– Mass behind globe– Internuclear pathway disease– Supranuclear pathway disease

Paresis of Nerve/Musclevs

Restriction

• Force Duction Testing

Question: Which ONE of the following represents a “Positive Force Duction Test” result?

A) Right eye cannot be pushed into upgazeposition

B) Right eye cannot be pulled into upgazeposition

C) Left eye can be pulled into an upgaze positionD) Left eye can be pushed into an upgaze positionE) Patient is told to “Try to look up.” Right eye

cannot be pushed into an upgaze position.F) Patient is told to “Try to look up.” Right eye

can be pushed into an upgaze position.

BINOCULAR DIPLOPIA

Any Clues from the HISTORY????Any Clues from their MEDICATIONS???-Start or Stop one?

-Using systemic fluoroquinolones?

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How are the Images Seperated?

• Horizontal• Vertical• Diagonal

Oblique• How far apart?

– Commitant?– Noncommitant?

• Worse at FARorWorse at NEAR

What Maximizes/Minimizes the Diplopia?

• Gaze Direction• FAR vs NEAR• Reading Position

“What were you doing when you first noticed that you had double vision?”

Is there a Headtilt or Face Turn No ADduction? Are you sure?

• Can the patient CONVERGE???

Also

• Good External Exam• Good Review of Systems• Check Acuities OD, OS, OU• Check Pupils carefully!• DFE with careful disk assessment• Check fundus vessels

CRANIAL NERVE PALSIES

• Most often 6th Nerve Palsy– Usually ischemic

• Diabetes• Hypertension• Lupus

– Compressive is NOT uncommon– Always consider Cranial Arteritis

in patients over 50

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3rd Nerve Palsy Next Most Common

• Usually Ischemic– Diabetes– Hypertension– Lupus

• Beware: Aneurysms!!!• Tumors are NOT rare• Consider Cranial Arteritis

in patients over age 50

4th Nerve Palsies do occur

• Most often head/neck trauma• Congenital 4th nerve palsy next

– Decompensation of large phoria

• Ischemic 4th can occur—rarely• Compression by tumor—rarer still• Consider cranial arteritis

in patients over age 50

Recent Call for Consultation

• 71 year old male, Type-2 diabetic x 12 years• C/O: “Double Vision” when reading• Started 10 – 14 days prior to exam• “I notice he’s tilting his head toward his right

shoulder. I think he’s got a left 4th nerve palsy, Ithink. What should I be thinking?”

1) DEFINE THE “DOUBLE VISION” BETTER!2) PERFORM THE PARK’S 3-STEP TEST3) CONFIRM WITH THE BIELSCHOWSKY

HEAD-TILT TEST

NO history of Head/Neck Trauma

4) NOW what????5) Findings:

At Follow-up Exam findings are reported to patient findings are discussed with P.C.P.

A1c is ordered4) NOW what????5) Findings:

6) NOW what????

Think You’ve Got An Ocular Cranial Nerve

Palsy, Involving C#6, C#3, or C#4?

DON’T FORGET TO CHECK THE FUNCTION OF THE ADDITIONAL

MAJOR NERVES ASSOCIATED WITH THE EYES!

V-1Oculosympathetics

C#3, C#4, C#6

Assess: More than one cranial nerve involved?

• Is the Oculosympathetic Pathway involved?– Look for poor pupil dilation to dim light

• CHECK BOTH EYES!!!!• Horner’s Pupil

– #6 + O.S. pathway = Cavernous Sinus– #4 + contralateral Horner’s = midbrain/pons junction

• Is the cornea de-sensitized?– V-1

• Cavernous sinus• Orbital apex

IV IV

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Testing 4th nerve function in the presence of a 3rd nerve palsy

• Obliques are mainly torsional muscles– Superior oblique and IV are main intorters

Have the patient fully ABduct theeye with the 3rd nerve palsy;ask patient to look DOWN;observe for INtorsion

R/O Hemiparesis

• Loss of Strength/Function in contralateral ½ of body– 6th + hemiparesis: pons/

corticobulbar tract– 3rd + hemiparesis: ventral midbrain/

cerebral peduncle

Extraocular Muscle Disease as cause of Diplopia

Usually: Thyroid Eye DiseaseRarely: Idiopathic Orbital Pseudotumor

Thyroid Eye Disease• Enlarged, inflamed, edematous EOM’s• Inflammation within the Orbital Fat• PAINLESS!!! (almost always)• Morning “puffy eye” syndrome

– Lids + Conjunctiva

• Fibrotic Scarring of the Muscle– Loss of elasticity; can’t stretch– Inferior Rectus > Medial Rectus– Mueller’s Muscle– Lower lid Retractors

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NO correlation between thyroid hormone levels and orbital

disease!

• Radioactive Iodine treatmentscan worsen orbital disease!

• Smoking can worsen orbitaldisease

Thyroid Eye Disease can:raise the I.O.P. compress the optic nerve

Graves Disease

• Always Ask: “Any problems with intermittenteye lid droop?”– “Late in the

Day Ptosis”

Orbital Pseudotumor

• PAINful• Periorbital swelling• Proptosis• Red Eye• Possible optic neuropathy• Muscle + Tendon enlargement• Diplopia• Responds exquisitely to

systemic steroids!

Neuro-muscular Junction Disease as cause of Diplopia

Myasthenia Gravis Ocular Myasthenia

• Levator in more than 50%• Orbicularis Oculi• MR, IR, SR, IO > LR > SO

– Combinations not rare!

• NOT the pupil muscles!• (accommodation often

is affected)• NOT painful!!!!

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“Fatigability” + “Variability”

• Findings fluctuate• Exercise worsens weakness• Rest (“sleep test”) improves strength• Ice packs can temporarily improve

strength• Most often OD and OS involved

– Asymmetrically– Variably

50 – 80 % go Systemic

Ocular Myasthenia Myasthenia Gravis- Usually within 2 years- All skeletal muscles are vulnerable- Proximal muscles particularly

vulnerable- Diaphram muscle involved

in myasthenic crises- Swallowing/speaking often

affected transiently

Orbital TumorsAxial Proptosis

Non-Axial Proptosis

Orbital Tumors

• Usually painless• Meningioma• Glioma• Lymphoma• Metastasis from other

sites

InternuclearOphthalmoplegia

Lesion in the Medial Longitudinal Fasciculus

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Features of I.N.O.

• Adductional palsy during horizontal gaze• Intact adduction during convergence (usually)• Endpoint nystagmus in the Abducting eye• Often skew deviation with the eye

attempting to adduct “upshooting”

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