course handouts - university of houston

Course Handouts

INTERCONTINENTAL HOTEL 15201 Dallas Parkway Addison, Texas 75001

CE in the Southwest hosted by

PROGRAM LOCATION

INTERCONTINENTAL HOTEL 15201 Dallas Parkway Addison, Texas 75001

PROGRAM AGENDA

Saturday, March 22, 2014

7:00 am to 8:00 am Registration/Continental Breakfast/Visit Exhibits

Lectures presented Peter Kehoe, OD, DOS, FAAO:

8:00 am to 9:45 am Primary Care Electrodiagnostics COPE ID #36509-GO

9:45 am to 10:15 am Break/Visit Exhibits

10:15 am to 11:05 am Excellence in Optometric Patient Care COPE ID #34316-GO

11:05 am to 12:00 pm Prescribing Sports Specific Sunwear COPE ID #40708-GO

12:00 pm to 1:00 pm Lunch provided by UHCO and UIW

Lecture presented by Jennifer Deakins, OD:

1:00 pm to 2:45 pm Neuroimaging in Optometry COPE ID #40448-NO

2:45 pm to 3:15 pm Break/Visit Exhibits

Lecture presented by Bruce Onofrey, OD, RPH, FAAO, FOGS:

3:15 pm to 5:00 pm My Doc told me to get an eye exam because..... COPE ID #37212-PH CEE Available

Sunday, March 23, 2014

7:00 am to 8:00 am Registration/Continental Breakfast/Visit Exhibits

Lecture presented by Bruce Onofrey, OD, RPH, FAAO, FOGS:

8:00 am to 9:45 am GLC-Not Just IOP, Think DPP, OMG! COPE ID #37209-GL CEE Available

9:45 am to 10:15 am Break/Visit Exhibits

Lecture presented by Richard Sharp, OD:

10:15 am to 12:00 am Adult Acute Binocular Diplopia COPE ID #40698-SD

12:00 pm to 1:00 pm Lunch provided by UHCO and UIW

1:00 pm to 2:45 pm Diagnosis and Management of Secondary Glaucomas COPE ID #40699-GL

2:45 pm to 3:15 pm Break/Visit Exhibits

Lecture presented by Jennifer Deakins, OD and Jenny Terrell, OD:

3:15 pm to 4:05 pm Community-Based Eye Care: Optometry's Role in Public Health

COPE ID #40472-GO

Lecture presented by Jenny Terrell, OD:

4:05 pm to 5:00 pm Professional Responsibility COPE ID #40651-EJ

Primary Care Electrodiagnostics Peter H. Kehoe, OD, DOS, FAAO

Diplomate – American Board of Optometry 2-Hour General Optometry

COPE Course ID: 36509-GO

Neuro-Physiology of Vision o Phototransduction o Visual Pathway

Visual Evoked Potential (VEP) Electric signal registered at the occipital region in response to a visual stimuli.

o VEP Visual – patient observes a visual stimulus Evoked – generates electrical energy at the retina Potential – measure the electrical activity in the visual cortex

o Measure the function of the entire vision system; no patient response required

VEP – Previous Limitations

VEP – Current In-Office Technologies

VEP Stimulus o Flash o Pattern

Contrast Sensitivity Visual Acuity Color

VEP Components o Repolarization o Depolarization o Amplitude o Latency o High Contrast o Low Contrast

International Society for Clinical Electrophysiology of Vision o http://www.iscev.org/standards/proceduresguide.html

American Academy of Ophthalmology Preferred Practice Patterns

American Optometric Association Clinical Practice Guidelines

VEP and Other Ophthalmic Diagnostic Tests

Psychophysics of Vision o Visual Acuity o Contrast Sensitivity o Visual Field Test

http://www.iscev.org/standards/proceduresguide.html

Diopsys NOVA-TR o User-Defined Protocol o Customize testing parameters specific to each patient and pathology o Pattern Type & Size, Contrast level, Eye o Testing times are flexible and depend upon the customized settings

Diopsys NOVA-TR o Different Spatial Frequencies o Building Protocols o Building Option Sets o Multiple Sclerosis o Amblyopia – Vision Therapy o Neuro – Rehab - TBI

Prescribing and Response to Treatment

Diopsys NOVA-LX o Fixed Protocol

Pattern Type and Size are pre-determined o Normative Database for Glaucoma o Easy to interpret results for doctor and patient

VEP and Glaucoma – Well Defined Science o The Visual Evoked Potential in Glaucoma and Ocular Hypertension: Effects of Check

Size, Field Size, and Stimulation Rate Invest Ophthalmology Vis Science 24:175-183, 1983

o “The finding that is of clinical importance is the presence of abnormally long VEP latencies in some patients with ocular hypertension.

o The abnormal prolongation of VEP latency in these eyes may reflect subclinical optic nerve lesions that have not been uncovered with other techniques.”

Why VEP? o VEP is an objective, functional test that can help discriminate between healthy and

glaucomatous eyes2

How We Test o Low Contrast

Demonstrates degradation of magnocellular pathways

An early indication of glaucoma o High Contrast

Demonstrates degradation of parvocellular pathways

An early indicator of central vision loss and issues caused by problems before signal reaches optic nerve

Running Tests o Simple, automated protocol guides technician through the test o Operator friendly - anyone in the office can be trained to run the test1 o Patient set-up to printable results in as little as 4-6 minutes

Reading the Results o Quickly interpret results to enhance medical decision making and treatment

planning o Easy-to-read reports allow clinician to demonstrate therapeutic results and monitor

disease progression Normal or Abnormal – Red – Yellow - Green

Incorporating VEP in a Comprehensive Optometric Practice o Incorporating Any Technology in an Office

Does it do something our other technology doesn’t? Will it provide clinical information that will impact the treatment of our

patients? Can it be incorporated into our office? Space – Patient Flow - Staff Is it “standard of care” or “leading edge”? Is it “patient friendly”? Will it be profitable and/or Practice Builder?

Efficiency – Billable - Referrals

Clinical Example #1 – 11 year old Female o Complicated History o Normal VEP

Successful Vision Therapy Outcome

Clinical Example #2 – 63 year old Female o Unusual OCT and VF o Abnormal VEP leads to early treatment decision

Clinical Example – pERG #1

Clinical Example – pERG #2

Incorporating VEP in Our Practice o Space o Patient Flow o Staff o InfantSEE® Exams

Our Glaucoma Protocol including VEP o Annual Exam o 3-4 months later: gonio, IOP + VEP o 3-4 months later: HRT, HVF and OCT

Profitability of VEP o Comparison with other procedures o 95930 Reimbursement and limitations o Diagnosis codes associated with 95930

Referrals and Marketing due to VEP

Diopsys NOVA-PERG (Pattern ERG) o Available Fourth Quarter 2012

Test takes less than 2 minutes Allows simultaneous display of VEP and PERG Can help distinguish between retinal and cortical pathway issues Will display retinocortical timing

o Clinical Protocol o Profitability

Potentially TWO codes performed simultaneously

Summary – VEP + ERG o Good for The Patient o Patients accept and understand the technology o Objective data with no patient stress o Good for The Practice o Valuable clinical data for a variety of diagnoses o Easily incorporated into practice flow o A source of professional and patient referrals o One of the highest reimbursed procedures in the practice

Questions

Excellence in Optometric Patient Care Peter H. Kehoe, OD, DOS, FAAO

Diplomate – American Board of Optometry Cope: Applied

Course Description: You will learn the fundamentals of Excellence in Optometric Patient Care. Patient Expectations, office set up, staff, equipment, a review of clinical guidelines for specific disease states, and coding and billing will be discussed. An action plan will be provided to participants depending on the goals of the practitioner. Course Objectives: 1. You will learn the challenges and opportunities of Excellence in Optometric Patient Care,

regardless of the practice setting or modality. 2. The incidence and clinical practice guidelines for several common eye and systemic diseases

that are routinely discovered and managed in an optometric practice will be the basis of describing the infrastructure and staffing necessary to successfully provide Excellence in Optometric Patient Care in a corporate or traditional optometric practice including office layout and equipment.

3. Clinical Practice Guidelines with be the framework to outline a plan of action for certain ocular and systemic disease states and discuss where to learn proper coding and billing concepts, specifically the challenges of medical insurance versus vision insurance.

Introduction

Patient Expectations a. What Patients Expect from their Eye Doctor

The commitment necessary by the doctor and Staff Doctor and Practice Goals

Revenue

Patient Diversification

Introducing Medical Optometry

Primary Care Optometry

Total Patient Care

Philosophy

Optometry is THE primary eye care provider

Vision is our history but medical eye care is our future

The commitment necessary from the doctor

The commitment necessary from the staff

Meeting the total patient care needs – and expectations – of ALL your patients

Excellence in Optometric Patient Care and Doctor Driven Dispensing are closely linked.

Healthy Eyes - Healthy People – Healthy Practice

Incidence and Clinical Practice Guidelines for Common Conditions in an Optometric Practice

Review – Vision Problems in the U.S. – Prevalence of Adult Vision Impairment and Age-Related Eye Disease in America

o Cataracts o Age-Related Macular Degeneration o Glaucoma o Ocular Allergies o Dry Eye o Ocular Side-Effects of Systemic Disease

Diabetes Hypertension Cancers Emotional Disorders

Review – Children’s Vision and ocular health statistics o Refractive Error o Binocular Vision Issues o 3-D Vision

Review AOA Clinical Practice Guidelines for a Variety of Common Eye Conditions that can be managed in an optometric practice

o Dry Eyes o Red Eyes o Glaucoma o Macular Degeneration o Diabetic Patients

Necessary Office Infrastructure

Physical Plant Layout o Rooms and Patient Flow

Paperwork needs – health history, insurance information o Documentation for Medical Records and Medical – Legal o Patient Education

Staffing Needs o Patient Flow o Training Opportunities

Instrumentation o Disease Specific o Patient Education Opportunities o Getting Started with the Basics o Advanced instruments for advanced practices

Staffing

Phone Contact – triage versus information gathering – setting patient expectations

Understanding and Communicating the Concept to patients throughout the encounter

Mining for patient needs, wants and desires

The role of staff and need for additional training – Certified Paraoptometrics

The Optometrist(s)

Training is adequate – but is the commitment and desire equal to the training? o Where/How to gain additional confidence

Throughout the exam – extending the history and understanding the needs of patients.

Gaining or refreshing additional expertise – where, how and in what order

Skills necessary – always within the comfort zone!

Communicating the conditions and offering the provision of services

Setting the expectation that the optometrist is THEIR eye doctor for ALL eye conditions The Concept of Prescribing

Doctor Driven Dispensing Basics for vision needs of your patients

Prescribing special testing o Disease Specific o Based on Clinical Practice Guidelines

Prescribing the follow-up examination o Disease Specific o Based on Clinical Practice Guidelines

Coding and Billing in a Total Patient Care Mode

Discuss the philosophy and challenges of vision versus medical insurance and how to communicate with patients.

Discuss the concepts of proper billing and coding for common medical eye conditions

Review resources for learning the proper coding and billing procedures, including AOA and other sources

Summary

Review Concepts Excellence in Optometric Patient Care

Develop an Action Plan of implementing Excellence in Optometric Patient Care in an optometric practice

Prescribing Sports Specific Sunglasses

Course Description: A thorough and up-to-date review of sunglass options for the weekend and elite athlete will allow the

prescriber to offer patients research and medically recommended eyewear, both prescription and non-

prescription for protection and vision enhancement. The major sunglass manufacturers/brands that are

typically found in an optometric or optical practice will be shared with prescribing guidelines, marketing

messages, and competitive comparisons for golf, fishing, boating, cycling and many other popular

sports.

Course Objectives: 1. A discussion on the potential market for Sports Specific Sunglass prescribing based on US sports

participation will be the framework for the course. 2. Peer reviewed research on specific tints and lens/frame materials will be reviewed both for lenses

and frames. 3. Attendee will gain a thorough understanding of available sunglass options for a variety of sports. 4. A basic understanding of specific prescribing recommendations from sports vision organizations will

be shared 5. Inventory, internal and external marketing and point of purchase recommendations will be

discussed. 6. Participants will leave with a road map for incorporating Sports Specific Sunglass prescribing into

their practice.

1. A discussion on the potential market for Sports Specific Sunglass prescribing based on US sports

participation will be the framework for the course. 15 minutes

2. Peer reviewed research on specific tints and lens/frame materials will be reviewed both for

lenses and frames. 15 minutes

3. Attendee will gain a thorough understanding of available sunglass options for a variety of sports.

30 minutes

4. A basic understanding of specific prescribing recommendations from sports vision organizations

will be shared 15 minutes

5. Inventory, internal and external marketing and point of purchase recommendations will be

discussed. 15 minutes

6. Participants will leave with a road map for incorporating Sports Specific Sunglass prescribing into

their practice. 10 minutes

Neuroimaging in Optometry

Jennifer Deakins, O.D.

Community Eye Clinic, Fort Worth, Texas

• Bio

• UHCO class of 2010

• Residency in Ocular Disease, Bridge Builders Eye Clinic

• Current associate at Eagle Mountain Family Eye Care, Lake Worth (formerly 1st Eye Care)

• You never know what’s going to walk in the door…

• Overview

• Neuroimaging role in eye care

• Importance of coordination with neuroradiologist, neurologist, and/or neuro-ophthalmologist

• Relevant Imaging

• X-ray

• Computed Tomography (CT)

• Magnetic Resonance Imaging (MRI)

• Magnetic Resonance Angiography/venography (MRA/MRV)

• Computed Tomography Angiography (CTA)

• Indications for Imaging

• Ordering

• Case Reports

• What is the role of Neuroimaging in Eye Care?

• Coordinated Care

• The Radiologic Technologist

• 2 yrs Associates degree or 4 yr Bachelor of Science

• Coordinated Care - Referrals

• Neurologist

• Pediatric Neurologist

• John Honeycutt, MD

• Hayden Head, MD (Ped Neuroradiologist)

• Neuro-Ophthalmologist (4 in the DFW area)

• John McHenry, MD

• Sam Abdul-Rahim, MD

• Terminology Review

• X-ray

• Electromagnetic waves pass through tissue soft tissue, are absorbed by denser tissue. Image is

developed onto film.

• Skull x-ray to pre-screen for metallic FB prior to MRI

• CT

• Based on standard x-ray attenuation by tissues of various densities

• Rapid rotation of x-ray tube around patients

• Denser material (like bone) blocks/attenuates the x-ray beam and is “brighter” while less dense

material (like air) allows the beam to pass through and is “darker”

• Radiation exposure = 115 chest x-rays or 1 yr of background radiation

• CT with contrast or without

• Contrast material - Iodinated

• Contraindications - prior allergic rxn or renal failure

• Improved sensitivity and specificity

• Should be used for most ophthalmic imaging

• Exception:

• Thyroid eye disease*

• CT with and without contrast

• CT of the orbit, head or both

• Orbital:

• Images obtained at a different angle using thinner slices (0.7mm vs 3-

4mm)

• Can be reconstructed to any slice thickness (usually 2mm)

• Most common planes are axial and coronal, sagittal views can be

reconstructed

• Coronal views show relationship btwn EOMs, optic nerve, and

surrounding bone structures

• Note - 3-D reconstructions popular but can “smooth” over abnormalities and 2-D images should

always be viewed as well

• Indications for CT

ACUTE conditions

ie. trauma, HA, papilledema, vision/visual field loss, diplopia

If there contraindications to MRI - claustrophobia, severe obesity, cochlear implant, ferromagnetic

aneursym clip, pacemaker or other metallic FB

• The ABC’s of CT

A Acute study needed (bleeding, trauma, hydrocephalus, emergent case)

B Bone (fracture, sinus dz)

C Calcification (meningioma, craniopharyngioma,

retinoblastoma)

• Calcified Lesions

• Thyroid Eye Disease

• MRI

• Based on detecting signal from resonance within a large magnetic field

• MR signal generated from interaction of hydrogen protons within the powerful magnetic field

Just how powerful you ask?

Fun fact…Tesla (T) is the unit that measures

the magnetic field created by the MRI

• Contraindications to MRI

• Absolute - cardiac pacemaker* and any retained or implanted metallic foreign body (in critical

location)

• Difficult patients - movement disorders, children, claustrophobia

• 15-20 minutes per study, typically 8-10 studies

• MRI

• Signal intensity

• Hyperintense, isointense, hypointense

• 2 most common pulse sequences T1 and T2 - weighted images

• Normal anatomy - T1

• Intracranial or other pathology - T2

• Both typically acquired as part of MRI of orbit and brain

• Most important tissue appearances on MRI

• FAT - bright/hyperintense on T1

• CSF - bright/hyperintense on T2

• Pathology on MRI

• Most impt T1 hyperintense substances

• Subacute hemorrhage

• Proteinaceous fluid

• Melanin (very hyperintense T1 and very hypotintense T2) very useful in

imaging choroidal melanomas or intracranial melanoma metastases.

• Pathology on MRI

• Hyperintense T2 pathologies

• Demyelinating lesions

• Ischemia

• Inflammatory dz

• Toxic or metabolic disorders

• Neoplasms

• Optic Neuritis (example)

• What is fat suppression?

• Allows better visualization

• Hyperintense fat signal can block contrast enhancement

• Can show content of fat-containing lesions ie orbital dermoid cysts and lipomas

• Should always use for post-contrast orbital T1 - evaluating optic nerve sheath menigioma or

optic neuritis

• Usually, post-contrast fat suppression is standard (no need to order separately)

• FLAIR - Fluid attenuation inversion recovery

• FLAIR sequences show pathological hyperintensity on T2 better

• Should order when looking for demyelinating disease

• Hyperintense T2 signal of CSF can mask pathology

• GRE - Gradient Echo Sequence

• Shows blood very well, even trace amounts

• When used with T1 and T2, age of hemorrhage can be determined

• Good for looking at hemes associate with AV malformations and traumatic brain injury

• Gadolinium Contrast in MRI

• Should be used for all neuro-ophthalmic imaging (unless CI)

• Minimal side effects - skin rash, sweating itching

• Previously thought safe for kidney dz, beware nephrogenic systemic fibrosis (NSF)

• MRI with contrast is no longer “no risk” for renal dz patients

• Contrast in MRI

• 2 is often better than 1

• CT and MRI together may provide a more complete picture

• Especially in lesions that affect soft tissue AND bone

• Assessing Vascular Lesions

• MRA and CTA has reduced need for invasive catheter angiography

• Iodinated contrast-filled vessels can be seen without interference from background tissue

• 3-D rotational images

• MRA

• 2 types

• Time-of-flight (TOF) MRA *preferred for ophthalmic imaging

• Phase-contrast (PC) MRA

• MRA advantages over CTA

• No iodine contrast

• Less nephrotoxic

• Increased signal-to-noise ratio

• Easier post-processing techniques

• CTA advantages over MRA

• Increased spatial resolution

• Technically easier, faster to study

• Less motion artifacts

• Third Nerve Palsy

• Pupil involvement?

• For partial/complete EOM involvement WITH pupil involvement

• Traditional method - invasive catheter angiography

• MRA or CTA

• Usually MRI/MRA



• Vasculopathic patients with complete external WITHOUT pupil involvement

• Can be observed - likely ischemic

• Without vasculopathic risk factors or vasculopathic patients that don’t improve or progress over

several months - imaging indicated**

• MRA and CTA - up to 98% sensitivity in identifying aneurysm leading to third nerve palsy

• MRA and CTA - other uses

• AV malformations


• Dural or carotid-cavernous fistula


• Supected carotid artery disease

• MRV and CTV

• MRV/CTV used to exclude dural venous sinus thrombosis in cases of papilledema from increased

ICP

• Cerebral venous sinus thrombosis (CVST) can have same symptoms of

idiopathic intracranial HTN (CVST is a rare stroke involving thrombosis of

dural venous sinuses that drain blood from the brain)

• Indications - Vision Loss

• Unilateral or bilateral vision loss

• Unilateral or bilateral optic neuropathy

• Junctional scotoma

• Bitemporal hemianopsia

• Homonymous hemianopsia

• Cortical blindness

• Indications - Pupillary Defects

• Efferent pupillary defects

• Anisocoria due to Horner’s syndrome or 3rd nerve palsy

• Afferent pupillary defects

• RAPD

• Light near dissociation

• Indications - Orbit

• Thyroid eye disease

• Orbital tumors

• Idiopathic orbital inflammation

• Orbital cellulitis

• Carotid-cavernous fistula

• Indications - Lid Abnormalities

• Lid retraction

• Lid lag

• Ptosis

• Orbital lid lesions

• Indications - Fundus Abnormalities

• Papilledema

• Optic atrophy

• Optic nerve hypoplasia

• Optic disc drusen

• Choroidal folds

• Ordering Imaging

• Relevant clinical findings

• Suspected lesion location

• Differential diagnoses

• Urgency of imaging request

• Where to send

• Private imaging centers

• Radiology Associates www.radntx.com

• Preferred Imaging www.preferredmri.com

• Hospitals

• OD privileges

• Wait time

• Form

• Reasons for Imaging in Eye Care

32 per 10,000 cases imaging was ordered (ophthalmic services in hospital)

1. Suspected compressive lesions in anterior visual pathway

2. Acquired ocular motility disturbance

3. Orbital lesion

4. Cerebrovascular event

5. Headache

6. Sinusitis

• Case Reports

1. Severely asymmetric glaucoma

2. CN 6 Palsy and Temporal Arteritis

3. Pseudotumor cerebri (presumed)

4. Bilateral Papilledema

5. Thyroid eye disease

http://www.radntx.com/

6. Ocular Ischemic Sydrome

• Asymmetric Glaucoma

• 68 Hispanic Female

• Presented to BB diagnosed with POAG (since 2007) treated in Mexico with Kryptan

(brimonidine, timolol, dorzolamide) and Xalatan

• LPI OU performed in Mexico

• Asymmetric Glaucoma

Clinical Findings

• BCVA OD 20/30 OS 20/25

• Mild/Mod DES and MGD

• LPI’s superior OU

• NS and cortical cataracts OU

• Gonio - open to CB, no pigment, very slight anterior bowing

• POAG OD>>OS

• Referred for CT

• Optic Nerve

• Visual Field

• OCT

• CT Results

• CN 6 Palsy and Temporal Arteritis

• 60 yo WF, slightly elevated cholesterol (diet and exercise)

• Sudden onset diplopia, after visit to chiropractor

• HA and tenderness on left side of head x 10 days

• BVCA OD 20/20 OS 20/20

• EOMs…primary gaze appeared to be left exotropia. (Pt was fixating on deviated image). True

findings: esotropia OD 15 pd, 3+ restriction of abduction OD

• Normal posterior/fundus findings, (-) AION

• Right CN6 palsy, suspected temporal arteritis

• Immediate MRI for motility disturbance

• CBC/Sed rate/CRP for temporal arteritis

• MRI Results

• Neurologist report

• Pseudotumor Cerebri (presumed)

• 37 black female

• Moderately overweight, hypertensive

• Reports ‘tension HA’ in the evening

• Hx of breast cancer surgery 2003

• Meds: Diltiazem, HCTZ, tylenol prn

• Clinical Findings

• BCVA 20/20 OD, OS 20/20

• IOP 20, 20

• 2 old corneal scars OD

• Mild HTN retinopathy

• Optic Nerve

• OCT

• MRI Results

• Pseudotumor - diagnosed

• 20 yo white female

• Reports HA (diagnosed with migraines). 2-3 times per week, variable location.

• Thyroid disroder, seasonal allergies, anxiety

• Amitriptyline HCL, cetirizine, synthroid, tri-sprintec, tylenol 3

• BCVA OD 20/20, OS 20/20

• IOP OD 20, OS 21 mmHg

• Normal anterior findings

• Normal peripheral retina/vasculature

• Bilateral optic nerve edema OD>OS

• MRI ordered – orbits and brain, with and without contrast

• No compressive lesions. Fluid intensity lesion left lateral aspect of the sella, likely a Rathke cyst.

Follow up MRI of pituitary in 6mo.

• Questionable mild prominence of CSF in ON sheaths bilaterally. May be within normal limits, of

uncertain significance.

• Referred to neuro OMD, lumbar puncture performed. High opening CSF.

• Pt was treated with diamox, clinical improvement in HA symptoms

• Limited communication = difficulty in follow cases

• Bilateral Papilledema

• 12 yo WF

• Requests CL exam

• 20/20 OD, OS

• Bilateral elevated rim tissue and NFL

• HA symptoms revealed upon further questioning

• CT

• MRI

• Thyroid Eye Disease

• 68 Black Female

• Previously dx’d with HTN, hyperthyroid, age-related arthritis

• Meds: Synthroid, Clonidine, Lisinopril, Diltiazem, Premarin

• Reported OS more prominent than OD x 2 yrs, stable

• (-) dip, (-) pain with eye mvmt

• Clinical findings

• BCVA 20/20 OD 20/25 OS

• Asymmetric proptosis OS>OD, (-) EOM restrictions

• Mild bulbar hyperemia, no significant DES

• 3+ cortical and 2+ NS cataract OU

• Normal ONH, macula, and fundus

• MRI without contrast of brain and orbit

• Refer for cat sx

• MRI Report

Impression:

Bilateral, symmetrical proptosis. Mild symmetric emlargement of EOMs, lateral rectus spared.

Suggestive of thryoid eye disease. No evidence of compression of ONH.

• Ocular Ischemic Syndrome

• Pt referred by fellow OD for retinal evaluation

• Hx of squamous cell carcinoma of the base of the tongue, prior neck sx and radiation

• DM type 2, HTN, RA, carotid artery dz

• 20/30 OD, 20/25 OS. Normal IOP

• Normal anterior structures, no NV of angle

• Glaucoma?

• 67 Hispanic male

• 20/25 OD, 20/30 OS

• Mild cataracts

• CVF – restriction in left field

• IOP 28 OD, 31 OS

• Glaucoma?

• Glaucoma?

• Glaucoma?

• References

• Lee, Andrew G et al. Imaging for neuro-ophthalmic and orbital disease - a review. Clinical and

Experimental Ophthalmology 2009; 37: 30-53.

• Mathews, JP et al. Can ophthalmic requests for neuroimaging be improved? Eye, 2004; 18: 290-

292.

• Lee, Andrew G. Ten Pearls for improving your use of neuro-imaging in neuro-ophthalmology.

Pearls in Ophthalomolgy, 2009.

• Bose, Swaraj. Principles of Imaging in Neuro-Ophthalmology. Ophthlamology, 2nd Ed. Ed by

Yanoff, M. and Duker J. 1241- 1248. Mosby, 2004.

2/20/2014

1

ADULT ACQUIRED

DIPLOPIA

Rick Sharp, O.D. Assistant Professor, Rosenberg School of Optometry

Adjunct Assistant Professor, University of Houston College of Optometry

ADULT ACQUIRED

DIPLOPIA



ADULT ACQUIRED

DIPLOPIA



Diplopia cases at the VA in Baltimore

• Resident at Baltimore VAMC • Told preceptor I liked neuro • So, all diplopias given to me • Didn’t have a strategy at first • Felt stressed • Hospital inpatients • Walk ins

• I didn’t have a strategy to evaluate diplopia • So, I developed a strategy • Learned to like diplopias

• And to this day I like diplopias …….OK…not this well…..

“It’s a huge differential diagnosis,” said Nurhan Torun, MD, director of the neuro-ophthalmology service at Beth Israel Deaconess Medical Center and an instructor of ophthalmology at Harvard Medical School in Boston. “Diplopia tends to be intimidating for many practitioners.” Intimidation may even turn to dread. “When most ophthalmologists see a patient with a chief complaint of diplopia, they hate it,” said Michael S. Lee, MD, associate professor of ophthalmology, neurology and neurosurgery at the University of Minnesota in Minneapolis. “They often don’t know what to do with the patient.” What they do know, of course, is that the proper workup will take longer than a standard office visit. Well…………….good to know I was not the only one feeling this way initially.

The Baby Boomers are not coming….THEY ARE HERE!!!

• 2 years ago saw NP on Wed PM, was 6 now 11, all turned 65

• They get vascular TNP, SNP, FNP and decompensated heterophorias

You must know the common presentations but be ready for the

uncommon ones

• Non-isolated CN palsies (e.g., a TNP combined with a SNP, etc.)

• Thyroid eye disease causing diplopia

• Myasthenia gravis

• Internuclear ophthalmoplegias (i.e, brainstem origin)

• We will review these, uncommon but must be aware none-the-less

2/20/2014

2

The usual presentation with patients 65 and older…….

• A vascular (hypertensive or diabetic) TNP, SNP, or FNP

• A decompensated heterophoria (age, significant glasses change with cataract formation, or onset with a new oral medication). Usually age and Rx change.

• (Just make sure you are

stronger than your patients)

Simple easy approach Make sure binocular

diplopia

Rule out a Cranial Nerve Palsy

III, VI, and IV (use Maddox Rod for IV)

If a CN palsy – determine isolated

vs. nonisolated

If not CN palsy – evaluate for comitance

(use Maddox Rod)

If comitant than most likely a

decomensated heterophoria

Evaluate oral medications (esp.

new ones)

Rx prism

Use of the Maddox rod is KEY in evaluation of the Fourth Nerve and…… In diagnosis of decompensated heterophorias

Be on guard: • Any non-isolated CN palsy or pupil involvement • Myasthenia Gravis • Thyroid Eye Disease (muscle restriction) • Internuclear Ophthalmoplegia • Giant Cell Arteritis (ischemia of EOM), other signs • …..and more……

You walk into the exam room………

• If it’s a IIIn. Palsy • Easiest diagnosis • Ptosis • Eye is “down and

out” • Pupil involved or

not involved • Should take about

10 seconds after you walk in

Down because IV (superior oblique) is working Out because VI (lateral rectus) is working

Superior oblique


• It’s a Vin. Palsy

• You see it’s not a IIIrd

• Do quick lateral versions….there it is

• Should take about 10 seconds

• This is a LEFT sixth nerve palsy • Don’t get fooled by this presentation • Fixating with paretic eye (we will go further in detail about this)


• It’s a IVn. Palsy

• Ok, this is the tricky one

• Not a III or VI

• Maddox rod testing (this is the key)

• Diagnosis in about 3 minutes

We will discuss this diagnosis in detail

(note head tilt with this Left FNP)

OK, you’ve ruled out III, IV, VI……..

• So now you want to know if there’s comitance

• If so, decomp heterophoria • You will prescribe prism • Maddox rod comes in handy

here • If not comitant……..this is

where the real fun starts • But usually…it’s either III, IV,

VI or decomp phoria

• Any non-isolated CN palsy or pupil involvement

• Myasthenia Gravis • Thyroid Eye Disease (muscle restriction) • Internuclear Ophthalmoplegia • Giant Cell Arteritis (ischemia of EOM),

other signs • ….and more….

2/20/2014

3


diplopia




vs. nonisolated


(use Maddox Rod)




new ones)

Rx prism



Binocular or Monocular?

• Cover each eye individually and look evaluate their symptoms

• If you have monocular diplopia or triplopia or polyplopia you most likely have: – Uncorrected astigmatism – Pre-retinal membrane – Cataract with large vacuoles – ..combination of above

• Of course you can have monocular diplopia WITH a binocular diplopia (patients with pre-retinal membranes can have decompensation of their heterophorias too)

• You have to sort this out first • Usually you can do this in several seconds

MONOCULAR or BINOCULAR?

• First make sure they have their glasses on – If they have uncorrected astigmatism, they may

see two images with each eye or one eye

• Cover OD and ask, cover OS and ask

• With both eyes open ask

• If you don’t do this: – You may be on a “wild goose chase”

– Waste time

– Be angry with yourself at the end

Causes Monocular Diplopia

• Uncorrected asigmatism (ghost overlap – most common, esp. with new spectacle prescription)

• Pre-retinal membrane (metamorphopsia – fairly common)

• Dry or Wed ARMD (metamorphopsia)

• Looking through edge of bifocal (amazing but true)

• Dislocated IOL (rare)

• Monocular diplopia…………..but you mistakenly think it’s binocular diplopia

First is there a III, IV, or VI nerve palsy

• IIIn. Palsy – easy

– Don’t get tricked by an INO

– Make sure isolated

• Vin. Palsy – easy

– Don’t get tricked by fixation with paretic eye

– Make sure isolated

• IVn. Palsy – this is where most of trouble is

– Avoid mnemonic schemes, you may forget them

2/20/2014

4

The Usual Situations

• An isolated III, IV, or VI

– Either follow or order blood and imaging tests

• A decompensated heterophoria

– Rx glasses with prism

Will discuss INO’s later

I know, you can’t wait for that

o Bilateral pinhole – could keep trial frame with bilateral pinholes available o To grab anytime you have a diplopia case o Just pull it out and ask patient if they still have diplopia o PH will resolve:

• Uncorrected astigmatism • Pre-retinal membrane

What patients may report as “double vision”

D D Uncorrected astigmatism

Metamorphopsia

EOM Functional Anatomy

• Medial rectus (IIIn) – no problem

• Lateral rectus (VIn) – no problem

• Superior and Inferior recti (IIIn) – no problem

• Inferior oblique (IIIn) – maybe a problem

• The Superior oblique (IVn) this is where

most of the problem lies

• If the superior oblique is paralysed (an intorter and a depressor) then:

The inferior oblique will extort eye The superior rectus will elevate eye (hyper)

Patient sees this with extorsion

2/20/2014

5

Ludwig Edinger 1833-1890 1855-1918

Karl Friedrich Otto Westphal

I was taught……. This structure coordinated all the EOM movements. But now….

The EW nucleus actually only controls autonomic functions of the pupil – constriction and accommodation but NOT IIIn. EOM coordination. That’s done by IIIn. Nucleus.

YOUR LIBRARY

• No. 1 Neuro Book

• Paperback

• 30th edition available

• Not on Kindle yet

• F.J. Bajandas was a neuro-ophthal at UTHSC in San Antonio, killed in car accident 1981 who initially wrote this book


diplopia




vs. nonisolated


(use Maddox Rod)




new ones)

Rx prism



STEP 1 - R/O a THIRD NERVE PALSY

• This would be difficult to miss • Ptosis – many times a complete ptosis with no diplopia • The eye is down and out

– Down: nerve IV is still active and pulls eye down – Out: nerve VI is still active and abducts

• Double check for IV = the IIIn eye will intort with attempted infraduction (fun to watch while at the slit lamp)

• Doubt you will miss this • Do not confuse with:

– Internuclear ophthalmoplegia (INO)

• Pupil sparing – if older, HBP or DM, may not arrange imaging – How is the pupil spared in a TNP? (Pupilomotor fibers in the nerve

periphery, oculomotor nerves in the core of the nerve)

• Pupil involved - imaging • This diagnosis should take about 5 seconds

Third Nerve Levator

Superior rectus

Medial rectus

Inferior Oblique the only EOM with origin from within the orbit

Inferior rectus Superior oblique is CN IV

Lateral rectus is CN VI

2/20/2014

6

Third Nerve Palsy

• Ptosis (lid held up here). (There may be no c/o diplopia because of this) • “Down and out” – OS lateral rectus working (CN VI) out OS superior oblique working (CN IV) down • Pupil dilated (in some cases) – dilator unopposed by sphincter, dilation

Q: How does on evaluate the superior oblique during a IIIn. palsy?

A: At slit lamp visualize the 12 oclock position of corneal limbus and ask the

patient to look down

The eye will intort with attempted downgaze, then you know for sure No. 4 is

OS

There are ISOLATED nerve palsies and not ISOLATED ones

• The not isolated and not so good friends are: – Bilateral ptosis (sign of a nuclear

TNP)

– Cerebellar ataxia

– Hemitremor

– Hemiparesis

– Altered consciousness

• So look/ask for these signs as well as another CN palsy

Isolated III, IV, and VI are the best ones to have

Nuclear TNP (extremely rare) Bilateral ptosis (both levators innervated by central caudal Nucleus)

Fascicle TNP – with ataxia

or hemitremor Usually ishemic, infiltrative (tumor), rarely inflammatory

Uncal herniation syndrome Dilated pupil (Hutchinson pupil) with altered consciousness, Then MR, IO, SO, IR

Posterior communicating artery Aneurysm Most common cause of nontraumatic IIIn. palsy with pupil involvement

Cavernous sinus syndrome May see TNP with IV, V, and VI TNPs tend to be partial Pupillary fibers are sometimes spared

Orbital syndrome TN spilts before entering orbital fissue Superior: Superior rectus & levator Inferior: IR, MR, IO, iris, ciliary musc Usually some orbit pathology (e.g. orbital cellulitis)

Pupil Sparing Isolated IIIn • Pupillomotor fibers of III travel in outer layers of nerve closer to nutrient blood supply surrounding the nerve as opposed to the nerve core blood supply • Diabetes, hypertension, athero- sclerosis

1 2

3 4

5

6

7

So why is the pupil fixed and dilated before the other ocular signs? • Pupillomotor fibers are in the nerve periphery • EOM motor fibers in the core This also explains pupil sparing with a vascular TNP, closer to nutrient blood supply

Uncal Herniation Syndrome

2/20/2014

7

Posterior Communicating artery aneurysm

• Third nerve is adherent to aneurysmal sac • A hemorrhage of the aneurysm may push blood into the substance of the nerve • Pupil may be spared, on occasion, as aneurysm compresses the nerve • Follow patient carefully for initial 5-7 days initially

About pupil sparing IIIrds

• Pupil spared in 80% of vascular TNP, not spared in 20%

• Pupil involved in 95% of compressive TNP

• So you manage: imaging or no imaging

• E.g.: 80yo with DM and HBP, isolated – I will follow, no imaging

• E.g.: with ANY pupil involvement I will get imaging

Q: What imaging and when?

A: Very soon, like the same day or next day if possible

• MRI (Magnietic Resonance Imaging) of brain with and without contrast

• MRA (Magnetic Resonance Angiography)

Should an OD be ordering imaging?

• It’s up to you and how comfortable you are

• They want your business

• Can go through the primary care provider

• Some insurances require go through PCP

Case in Point

• Female with Left pupil involved IIIn. palsy, thought to be isolated diagnosed by physician

• After about one week finally sent to eye doctor

• Eye doctor ordered MRI and MRA for next day after examination.

• Called imaging facility for results next day, patient expired before tests done. Ruptured aneurysm of posterior communicating artery

2/20/2014

8

Case in Point

• 80yoF with pupil involved IIIn palsy

• Diabetic and hypertensive

• Called PCP for blood work and imaging

• My staff called patient following week: appointment made to see local OMD in 3 months

• Called PCP back, he responded

• Sent letter to PCP

• Never saw patient again (a fee for service patient)

The Pupil will drive some of your decision making:

• 80yo diabetic with HBP and isolated TNP with pupil sparing – may decide no imaging, just follow. Three month resolution.

The Pupil will drive some of your decision making:

• 80yo diabetic with HBP and isolated TNP with pupil involved

• MRI and MRA

I got Burned!!!!

(well…….not really)

Interesting IIIn Presentation

• About year 1989 • Saw 40yo F, diabetic with intermittant diplopia • Had large exophoria, pupils normal, no ptosis • Dilated Fundus Exam: florid neovascularization of disk and

elsewhere OD and OS • Arranged to see retina next day for immediate PRP • Retinal specialist called next day saying “this patient has a

third nerve palsy, why was she sent to me” (BURNED) • Apparently, I caught the palsy very early in evolution and

more concerned with the retina (act quickly to avoid vitreous hemorrhage)….so, not really burned.

Medial Longitudinal Fasciculus

Remember this Convergence intact

Internuclear Ophthalmoplegia (INO) many time misdiagnosed as a “partial” IIIn. palsy.

* INO

2/20/2014

9

Don’t label an INO (internuclear ophthalmoplegia) as a “partial” third nerve. Usually MS patient. If vascular, the patient is usually seen as an inpatient with a non-isolated INO.

Cannot adduct eye with a version

Can with convergence

Case in Point

• 68 yo male c/o diplopia, constant

• Cannot adduct OS, thinking L INO, however, he cannot adduct during convergence (not an INO)

• Otherwise feeling well, isolated problem

• Does have OS ptosis but dermatochalasis, levator function was full and = to OD

• MRI, MRA, neurology consult

• Neurologist says L IIIn. Palsy (ah……no)

• MRA occlusion of blood flow to medial rectus

• Resolved completely within 2 months

• Never seen or heard of such a cause = “Miscellaneous”


diplopia




vs. nonisolated


(use Maddox Rod)




new ones)

Rx prism



The Sixth Nerve

• Sixth nerve starts in the Pons • Travels forward then vertical to enter Dorello’s canal • Then forward past internal carotid artery in cavernous sinus • Entering superior orbital fissue • On to lateral rectus

Don’t forget GCA and Elev ICP with pap

Brainstem Syndrome • V, VII, and VII, VIII may be involved bec of proximity • Ipsilateral conjugate horizontal gaze palsy (remember 6 sends fibers to contralateral medial rectus • Numerous other neurologic problems since in brainstem…….therefore not isolated you will get further eval.

VIII

VII

VI V

Elevated ICP • Downward stem displacement • VI stretched palsies, bilat • 30% Pseudotumor have SNP • More…

Petrous Apex Syndrome • SNP • Ipsil decr hearing • Ipsil facial pain • Ipsil facial paralysis • Following otitis media

Cavernous Sinus Syndrome • Involvement of III, IV, and V • Horners • Optic n. compression • Pituitary gland involvment • …..not isolated… further eval

Orbital Syndrome • Proptosis • ON atrophy, edema • Trigeminal ophthalmic

involvement • Tumor, trauma, orbit

inflamm, cellulitis

STEP 2 – R/O SIXTH NERVE (lateral rectus) PALSY

• The most straight forward evalution

• Only problem is could be thrown off by patient fixating with the paretic eye…the fellow good eye is turned in

• Reduced abduction of the affected eye

2/20/2014

10

Yoked – Herings Law of Equal Innervation

• LR OD and MR OS “yoked” both muscles receive the same innervation to move the eyes together

• Same for convergence

• Same for torsional movements

Constantine Hering – Hering’s Law of Equal innervation “Father” of homeopathy Founded Philadelphia College of Homeopathy Born: January 1, 1800

It takes a lot of effort

to move this paretic

eye from the adducted

position to the central one

The OD lateral rectus

and the OS medial rectus

are “yoked” muscles. The

normal medial rectus reacts

to a high level of effort

It takes less effort to

Abduct the normal

OD eye, less “yoked”

power to the OD –

Therefore will not turn

in as much and smaller

angle of diplopia

R. Six Nerve Palsy

Sixth Nerve Palsy (SNP) SIX NERVE PALSIES

• Q: The patient here has an isolated SNP, now, which eye has the palsy?

• A: It could be either one

• It depends on which eye the patient chooses to fixate with and many times they will fixate with the PARETIC eye - ?why

I chose to fixate with my paretic eye for

a very good reason!!

If I fixate with my left eye I see double like this:

When I fixate with my right eye I see double like this:

The eye with the SNP

So, I will fixate with my right paretic eye.

More effort to abduct eye with lateral rectus palsy

Means equal amount of innervation to the medial rectus and it (being normal) goes way in

• 78yo male with his two daughters

• c/o diplopia constant

• Fixating with OD

• OS eso

• Daughters say “he has a problem with his left eye”

• Has obvious R SNP

• I explain how problem is not the left but the right eye ……in detail

• They say, “OK, how are you gonna fix dad’s left eye”

2/20/2014

11

Management of Isolated SNP

• Age under 50: greater probability of neoplasm, therefore – MRI brain with and without contrast, MRA, LP, neuro consult

• Over age 50 (?50, is that old?): most likely ischemic mononeuropathy, if not resolved in 3 months then do comprehensive evaluation

– CBC, ESR, CRP(looking for GCA), GTT, ANA

Duanes Syndrome • Prenatal lesion, nuclear cells that

give rise to abducens nerve are absent

• Type I (85% of cases)(of three) is isolated abduction deficit, unilateral or bilateral, with or without an esotropia

• May be confused with a SNP • A portion of III innervates the

lateral rectus muscle • This causes co-contracture of MR

and LR and the characteristic retraction

• Symptoms, usually no diplopia


diplopia




vs. nonisolated


(use Maddox Rod)




new ones)

Rx prism



Fourth Nerve Palsy • The most difficult of the three nerve palsies

depending on how you think about it

• Typically learn mnemonic schemes which are totally unecessary and just not the way to go since you have to remember the mnemonic scheme, so you need a mnemonic to recall the mnemonic……..and so on…..

• The diagnostic approach I developed has worked great for me for decades

No need to memorize schemes

Parks 3 step

http://www.reactionface.info/sites/default/files/images/1311001790320.gif

2/20/2014

12

Nuclear –fascicular syndrome • Hemorrhage, infarction, demylenation, trauma

Subarachnoid space syndrome • The classic trauma cause • Causes bilateral FNP

Cavernous sinus syndrome • Associated III, V, VI, Horners

Orbital syndrome • Associated III, VI, proptosis, • Chemosis, conj injecion • Trauma, inflammation, tumor

STEP 2 – R/O FOURTH NERVE (superior oblique) PALSY

• For me, this was the most difficult to do

• I decided didn’t want to us mnemonic schemes (they would be forgotten)

• I didn’t want to spend much time doing cover testing

• Then was reading a book on dipolpia and saw that the IVn. was referred to as the “reading nerve”

FNP diagnostic approach

• The fourth nerve has also been called the “reading nerve” since eye in adducted and infraducted position while reading

• Diplopia increased with adduction of the involved eye, the eye with the FNP (reading position)

• Diplopia increased with infraduction of the involved eye (reading position)

So, • If you move into the field of paralysis the

diplopia will increase

• Adduction…….increase the reading nerve

• Depression…..increase the reading nerve

• Intortion (head tilt to same side shoulder)….increase

• OK ---- I didn’t want to do cover testing and prism measurement like orthoptists do, (I didn’t have all day) so I moved to……

THE MADDOX ROD

Ernest Edmund Maddox 1863 – 1933 OMD

Ernest E. Maddox, M.D. British OMD

This is the reflection you see, and the patient sees a solid red streak in same orientation

2/20/2014

13

(What you see)

(What they see)

OD sees H red streak

OS sees transilluminator light

NORMAL

(What you see)

(What they see)

So we have a left hyper (right hypo)

(I’m not including the tilt caused by the FNP if the OD was involved)

What you see

What they see

That becomes greater with adduction of hyper eye

What you see

What they see

That becomes less with abduction of hyper eye

What you see

What they see

More hyper with downgaze

What you see

What they see

Less hyper with head tilt to R shoulder

OS must extort

2/20/2014

14

What you see

What they see

More hyper head tilt to L shoulder

OS tries to intort, Unopposed SR pulls eye up

= LEFT FOURTH NERVE PALSY

• Most older patients cannot do this, stiff neck

• Must have assistant move

head with hands

HEAD TILT

FACE TURN

• All of my patients, when asked to tilt the head, instead do a face turn

• You must watch for this

About the Head Tilt

• Head tilt to R shoulder – OD tries to intort (sup obliq) and OS tries to extort (inf obliq) – Secondary action: Sup obliq tries to depress, Inf obliq

and Sup rectus counter elevates (antagonists)

– With FNP the eye elevates and elevates more with head tilt to same side of palsy

– Some patients figure out that if they tilt head to opposite side of palsy, their diplopia resolves

• Head tilt to L shoulder – OD tries to extort (inf obliq) and OS tries to intort (sup obliq)

Management of isolated FNP

• “Young person” – imaging, MRI brain and brainstem, CBC

• “Older person” if diabetic and hypertensive may choose to follow with no further testing

• From trauma - follow

Fourth is an intorter, if compromised the eye will extort and the patient will see the opposite - intortion, which can be quantified subjectively like this

Red white

R hyper with subjective intorsion

A cyclotorsion of more than 10 implies bilateral FNP

WHY NOT JUST DO THIS TEST INSTEAD OF MADDOX OD (as previously done)? • Is you patient that reliable? • You could

2/20/2014

15

Isolated FNP

• Congenital – usually discovered late (50’s and 60’s…what? 50’s are late?.....), head tilt

• Acquired and isolated – MRI for patients <45yo with no hx of head trauma

– MRI for patients 45-55 with no vasculopathic risk factors or hx of trauma

– BP, fasting blood sugar, glycosylated hemoglobin

– If GCA suspected: ESR, CRP, CBC

– If no resolution after 3 months: Neuro consult, MRI with and without contrast, MRA, LP

An 18-year-old with head tilt

complained of intermittent diplopia

for several months Muscle balance

measured 8Δ of right hypertropia in

primary position and 16Δ in left gaze

(adduction)..

CONGENITAL FOURTH NERVE PALSY with decompensation

Snapshots at ages 12 and 2 demonstrate habitual head tilt consistent with right superior oblique palsy

Age 12 Age 2

Age 18

Before surgery After surgery

• You may see decompensated fourth nerve palsies

• Their vertical fusional reserves will be higher than normal – like 4,5, 8, 10 etc.

instead of 1,2 or 3 • Just use a vertical prism bar, neutralize the hyper, then

go up and down to evaluated the reserves


diplopia




vs. nonisolated


(use Maddox Rod)




new ones)

Rx prism



A Decompensated Vertical Phoria

• Fairly common with aging

• Fusional reserves decline with aging

• Typically in 90s phorias decomp and need prism

• The larger the phoria and earlier the decomp

• Decomp with sickness and certain drugs

• The separation between streak and light stay same regardless of gaze up, down, left or right

• Its COMITANT

What you see

What they see

OK, right hyper

2/20/2014

16

What you see

What they see

What you see

What they see

What you see

What they see

What you see

What they see

PRISM!

• I measure phoria • Trial and error loose

prisms over glasses using phoria measurement as starting point

• Tell patient it will take 3 tries to get it right • Give about 75% of

maximal prism • Usually get it right first

time, if not second time • After about 3-4 years

usually need more prism


diplopia




vs. nonisolated


(use Maddox Rod)




new ones)

Rx prism



2/20/2014

17

Be on Guard for These

• Myasthenia gravis

• Thyroid eye disease (Graves)

• Internuclear ophthalmoplegia

• Non-isolated CN palsies

• Giant cell arteritis

• Cranial nerve palsies III, IV, VI, isolated or non-isolated • Decomp heterophorias

• Myasthenia gravis • Thyroid eye disease • Internuclear ophthalmoplegia • Non-isolated CN palsies • Giant cell arteritis

Myasthenia Gravis

• Keep your mind open to this, if suspect start asking more questions

• Mechanism: skeletal muscle acetycholine receptors blocked by antibodies

• Usually females in 20s and 30s • Ptosis, diplopia (worse with prolonged effort or as day

progresses) • Difficulty in swallowing/breathing medical emergency • May involve pharyngeal muscles change in voice taking on a

more nasal quality

Antibodies

MG continued

• Can mimic any CN palsy III, IV, VI • Lid droop accentuated by having pt maintaing upgaze for 2

min • Manually elevating more ptotic lid will cause other more

normal lid to become more ptotic (= “enhanced ptosis”) • From downgaze to primary position lids will overshoot then

come to rest in their customary position = Cogans sign • Upgaze paresis, unilateral or bilateral especially when

ptosis is present • Pseudo INO (internuclear ophthalmoplegia) • Blood test for MG antibodies available, not always accurate • Tensilon (block breakdown of acetylcholine, increases the

neurotransmitter at neuromuscular junction, dramatically reverses ptosis or diplopia)

Common Things, other than TNP, FNP, SNP, decompensation of heterophoria

• Myasthenia Gravis

– May mimic specific cranial nerve palsies

– Pupil never involved

– Variable presentation, diplopia for short durations, then longer durations, apparent SNP there one day and not the next

– Definitely does not act like a vascular or compressive CN palsy

• 40 something female

• Presented with what I thought was a mild L SNP. No ptosis. Just out of the blue.

• Followed in one week – resolved (not acting like a vascular or compressive)

• Later re-appeared Tensilon test in office, (+) for MG, her diplopia resolved with injection and she felt as if she “came back to life”

Case in Point Thyroid Eye Disease (TED)

• Elevation and abduction abnormalities most common defect

• Muscle fibers eventually start to degenerate fibrosis

• Muscle fibrosis increase in chronic inflammatory cells restrictive myopathy and diplopia

2/20/2014

18

#1

Inferior

Rectus

#2

Medial

Rectus

#3

Superior

Rectus

#4

Lateral

Rectus

Involvement of EOMS in TED

*

*

(restriction with elevation)

(restriction with abduction)

and last but no least

Giant Cell Arteritis • Mechanism: necrotizing vasculitis of

medium and large extracranial arteries, T cells invade the wall of the artery, macrophages enter and cause lumen to close ischemia

• Diplopia in 10-15% of presentations • Literature mainly reports pupil sparing TNP • Just ask about:

Transient visual loss Scalp tenderness Jaw claudication (pain with chewing,

ischemia masseter muscle) Loss of apetitie, weight loss, night sweats PMR – pain and stiffness in proximal muscle

groups worse in AM and after activity

• If suspect: ESR, CRP, CBC, see primary care physician


diplopia




vs. nonisolated


(use Maddox Rod)




new ones)

Rx prism



we are done

All right…………………diplopia!!

fini

2/20/2014

1

Definition of “secondary glaucoma” controversial

AOA definition =This type of glaucoma occurs as a result of an injury or other eye disease. It may be caused by a variety of medical conditions, medications, physical injuries, and eye abnormalities.

Glaucomas that are associated with separate and distinct and identifiable pathological processes

Some definions do not include pigmentary or pseudoexfoliative glaucoma but most do

Some have big warning signs and you have to follow carefully

Pigmentary Dispersion Syndrome

Pseudoexfoliative Syndrome

Retinal ischemia

Inflammation leading to pupil seclusion or PAS

Your using steroids and need to remember to monitor IOP

If you miss them some how, it can be devastating

If your treating, you typically must be more aggressive

So…….that’s why

Pigmentary Glaucoma

Pseudoexfoliative Glaucoma

Neovascular Glaucoma

Uveitic Glaucoma

Steroid Induced Glaucoma

How many kinds of glaucoma are there?

Becker-Shaffer’s Diagnosis and Therapy of the Glaucomas

Stemper, Lieberman, Drake

Mosby/Elsevier 8th ed. 2009

A. Angle closure glaucoma A. Primary angle closure

B. Plateau iris

C. Phacomorphic block

B. Secondary angle closures A. Neovascular glaucoma

B. Iridocorneal endothelial syndromes

C. Ciliary block glaucoma

D. Iris cysts E. Intraocular tumors

C. Open angle glaucoma

A. Primary open angle glaucoma D. Secondary open-angle glaucoma

A. Pigmentary glaucoma

B. Pseudoexfoliative glaucoma C. Steroid glaucoma

D. Lens induced glaucoma (3)

E. Glaucoma after cataract surgery (6) A. UGH syndrome

F. Glaucoma associated with intraocular hemorrhage (3)

G. Glaucoma after vitrectomy (2)

H. Glaucoma with uveitis (9)

I. Glaucoma with intraocular tumors (6)

J. Amyloidosis

K. Increased episcleral venous pressure (3)

L. Developmental glaucoma (anomalies of the anterior segment at birth)

A. Primary congenital glaucoma (present at birth) (4)

B. Secondary glaucomas (10)

This text: 76 different

types in total

R.P. Sharp, O.D.

Assistant Professor

University of the Incarnate Word

Rosenberg School of Optometry

Pigmentary Glaucoma



Uveitic Glaucoma


2/20/2014

2

These patients have a variation of anatomy that causes this problem and others PDS PG – greater fluctuations and peaks in IOP than POAG Retinal detachments They tend to be greater steroid responders Youger age

Common symptom is 20-40yo c/o blurred vision after exercise 1% to 2.5% of glucomas seen Predominantly young adults Strong association with myopia Mainly in Caucasians, rare in African Americans and Asians Typical patient is Caucasian in 20s or 30s Inheritance: sporadic

PDS and pigmentary glaucoma (PG) are two stages of the same disease process

The triad: Mid-peripheral radial iris

transillumination defects (“transillumination” and “retroillumination” describing same process)

Krukenberg Spindle Dense pigmentation of the trabecular

meshwork

Krukenberg’s Spindle (or K-spindle) – pigment deposited on corneal endothelium in vertical orientation (follows thermal flow pattern of pigment flowing from the posterior chamber) Extracellular pigment and.. Intracellular pigment phagocytized by

the endo

PDS has 10% risk of conversion to PG at 5 years and 15% in 15 years

Young myopic males with initial IOP of >21 are at increased risk of conversion

Anyone with PDS you must be vigilant

Baseline data Visual Field

Optic nerve and NFL imaging

Photos of retroillumination defects

Monitor for changes, at least annual or q6mo

Patient education

Have very deep anterior chambers, both central and peripheral

A concave curvature of the peripheral iris Can see during SLE and gonioscopy

Iris is larger

Mild iridodonesis (the iris can be seen jiggling anteriorly-posteriorly during small eye movements when observing with slit lamp)

The concave iris periphery

Gonioscopic appearance of The concave iris

Mechanical theory – the concave shape of the iris (as one views from the slit lamp) allows the iris to rub against the anterior lens zonules releasing pigment from the posterior iris epithelium

The posterior iris epithelium is highly pigmented

This released pigment then gets caught in the aqueous thermal flow – eventually depositing on the corneal endothelium (K-spindle) and in the trabecular meshwork (TM)

Outflow is compromised and IOP elevates

2/20/2014

3

Posterior Iris Epithelium – highly pigmented, to control light entering globe and zonules.

This is what does rubbing– posterior iris epithelium This is what

gets rubbed – the stationary zonules

As one might expect – asymmetry in iris transillumination defects between OD and OS of the same person Note the regularity and positioning

Cell thermal flow

Krukenberg Spindle Since the pigment is released from the posterior iris, all of the released pigment flows through the pupil causing the pigment to be caught in the vertical thermal flow. Hence, the expected vertical endothelial deposition.

Pigment deposited along iris valleys

Pigment deposited on posterior lens zonules – (not anterior lens zonules, pupil movement

Pigment deposition behind the lens

2/20/2014

4

The released pigment goes everywhere: angle, anterior iris surface, on the zonules, on the lens

A patient with pigmentary G can engage in sports activity, like basketball (jumping up and down), and experience a large release of pigment

Severe elevation of IOP

Corneal edema (endo pump cannot keep up with aqueous forcing it’s way in)

Halos (from corneal edema)

This can be blocked by use of topical Pilocarpine (pulls iris tight and reduces concave shape)

Regular pupillary block (as opposed to reverse block) This is mechanism for angle closure glaucoma (a.k.a. narrow

angle glaucoma) The pupil sphincter applies pressure against the lens making

it difficult for the aqueous to f low through Pressure builds up in the posterior chamber and pushes the

iris forward (iris bombe) causing TM block and a rapid and severe rise in IOP (up to and beyond 80mm Hg)

Pigmentary Glaucoma and Reverse Pupillary Block If you performed a laser peripheral iridotomy on a pigmentary

glaucoma concave iris, the iris straightens, and the pressure drops

This has led to the concept of reverse pupillary block

Normal aqueous flow

Pupillary block of aqueous flow

Iris bombe starts

Narrow Angle Glaucoma Mechanism

This is fascinating……

The act of blinking compresses the anterior chamber

Blinking pushes the iris and aqueous humor posteriorly pushing the iris against the lens zonules

The rubbing releases pigment which circulates creating the problems

During ultrasound biomicroscopy with normal lid position the iris is concave

B) Lid pressure bows iris backwards causing iris to contact zonules releasing pigment

A) Iris configuration when the lid is not in contact with the globe

The pupil then “burps” pigment into the anterior Chamber – this repeats itself over and over – pigment accumulates in the TM, up goes IOP

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With lid in normal position the iris is concave

Apply lid speculum which removes lid pressure from the globe

The iris gradually becomes LESS CONCAVE

Pressure builds in the posterior chamber pushing the iris forward

Remove the lid speculum and blinking is restored the original concave configuration is reestablished

Lens zonules are attached fairly close to the center of the lens Plenty of zonules for the iris to rub against

Blinking

Pupil dilation – try measuring IOP after dilation while in your office

Sports (especially jumping, “heading” the ball in soccer, boxing, jogging, every patient is different)

Head strikes in boxing or MMA fighting

PIGMENTARY DISPERSION SYNDROME (the anatomical tendency to release pigment is there to some degree – 0-100)

0 25 50 75 100 The continuum of disease presentation

PIGMENTARY GLAUCOMA

High tendency to go glaucoma

Low tendency to go glaucoma

This appears to be the case… Pigment dispersion can lessen with time

(This makes sense, once it’s rubbed away and replacement of pigment is reduced with the aging process)

The K-spindle becomes less prominent TM pigmentation becomes less prominent Increased aqueous outflow, so the IOP drops down to

normal levels May explain some nonprogressive cases of normal-tension

glaucoma i.e., ONH cupping, VF loss, normal IOP May have had pigmentary glaucoma and elevated IOP in the

past

With miosis, the iris is lifted away from the zonules

The transillumination defects fill in and can even disappear

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Take photos of iris transillumination defects

Measure IOP 1 hour after maximal dilation

Frequent gonioscopy

Pilocarpine is not well tolerated by younger patients

Medical therapy: CAI’s , B-Adrenergic antagonists, prostaglandin analogs

Be careful with miotics, could exacerbate a tendency for retinal detachments

A peripheral iridotomy should be considered to resolve the “reverse” pupillary block, use argon laser not YAG

Argon Laser Trabeculoplasty (ALT) is option, need lower power setting due to higher energy absorption by pigment. Selective Laser Trabeculoplasty (SLT) can be done as well.

Many patients eventually require a trabeculectomy

Reversing iris concavity Low concentration pilocarpine – ½% or 1% trial Can use Pilo ½% drop OU before immediately before sports

activity This pulls the iris away from the zonules MAKE SURE YOU DO DFE with attention to the periphery –

why? PG patients have higher incidence of lattice and retinal

detachments

Prevention of pigment release

Therefore – lowering the IOP

Prostaglandin analog works well (TravatanZ, Xalatan,etc.) with Pilo

Peripheral iridotomy Patient selection is key Those patients that have IOP spike after pupil dilation Patients under age 40 who have symptoms with exercise Use Argon laser, not the YAG laser – less pigment release

ALT and SLT good options Must keep power levels down to minimize pigment

release Works better in younger patients

Trabeculectomy The last stand, as needed

Before peripheral iridotomy

After peripheral iridotomy

Pigmentary glaucoma may diminish with age

E.g., treatment started at 30 may end and not be needed at age 60 or 70

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R.P. Sharp, O.D.

Rosenberg School of Optometry

University of the Incarnate Word

Pigmentary Glaucoma



Uveitic Glaucoma


Pseudoexfoliative Syndrome = PXS

Pseudoexfoliative Glaucoma = PXG

Pseudoexfoliative material, filaments = PXF

The “pseudo” is in reference to true exfoliation of the lens capsule that occurs with exposure to infrared radiation (glass blowers)

This is the problem, tangled balls of fine filaments……..?origin

Glaucoma – Science and Practice Morrison, Pollack Thieme

aa

C O N T R O V E R S Y Source of PXF material

Abnormal production of basement membranes vs

Elastic fiber degeneration

A basement membrane is a mixture of material secreted by epithelial cells throughout the entire body

Laminin, fibronectin, elastin, heparan sulfate and chondroitin sulfate

PXF is a disordered extracellular matrix synthesis

But where is it coming from??????

PXF is found in posterior iris epithelium with a disorganized and duplicated basement membrane with degeneration and disruption AND PXS PXG IS ASSOCIATED WITH IRIS TRANSILLUMINATION DEFECTS AS WELL AS EXCESSIVE PIGMENT IN THE ANGLE

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Normal elastic tissue consists of a central core of amorphous, insoluable protein – elastin

Surrounded by microfibrils

Guess what’s present in PXF?

Elastin

Tropoelaastin

Fibrillin

PXF material SHARES LIGHT MICROSCOPIC STAINING CHARACTERISTICS WITH LENS ZONULAR FIBERS

Similar in amino acid composition and structure to microfibrils of elastin

With PXS and PXG there is atrophy of the posterior iris epithelium and IRIS TRANSILLUMINATION DEFECTS in some cases (not in all)

With PXS and PXG there is an association of lens zonular fibers weakness which can lead to LENS DISLOCATION during/after cataract surgery or without cataract surgery

Single nucleotide polymorphyisms in the lysyl oxidase-like LOXL1 gene are associated with PXG in many patient populations

The LOXL1 gene is an enzymatic protein important in extracellular matrix metabolism and turnover.

Changes in the extracellular matrix of PXF tissues have been hypothesized to be the mechanism responsible for the development of PXG

• Zonular fibers at peripheral and equatorial region of lens

• Granular balls of PXF


Accumulation of material on lens

Broken zonular fibers

Pseudoexfoliative material

SCANNING EM


Schlemms canal (sc) Arrows show tangle of randomly arranged fine filaments and

thicker fibrils Glaucoma – Science and Practice Morrison, Pollack Thieme

Schlemms Canal

(added resistance to movment

of aqueous into Schlemms Canal)

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There is PXF throughout the eye and body

PXF in conjunctiva, optic nerve sheath, EOMs, eyelids

PXF in lung, heart, liver, skin and gallbladder

Streeten, B.W., et.al. Pseudoexfoliative fibrillopathy in visceral organs of a patient with pseudoexfoliation Syndrome. Arch Ophthalmol 1992;110(12):1757-62

Note use of term “fibril”

PXF associated with vascular disease (cardiac, cerebral, vessel, etc.), sensorineural hearing loss, elevated homocysteine levels

Associations are WEAK and CONTROVERSIAL

PXS appears unilateral in about 50% of cases at the time of diagnosis

Probably a bilateral process with asymmetric presentation

Autopsy studies show fellow “normal” eye did have PXF distribution present

So….it’s probably there but not clinically apparent

In the Early Manifest Glaucoma Trial, 55% of patients with PXS developed PXG after a mean observation rate of 8.7 years

Therefore: must carefully watch your PXS patients

Consider diurnal IOP evaluation Come to office for two half days with a novel to read One AM, measure IOP qh One PM, measure IOP qh

Establish a baseline with ONH/NFL imaging Establish a baseline with VF At least annual exams And of course….patient education

“Target” with clear intermediate zone

Pupil must be dilated to see this

Material connects central disk with intermediate zone


PXF at pupil margin

Prior to dilation

Look again after dilation

Or might be able to see on lens (phakia) before dilation

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Repeated pupil movement “peels” material

After cataract extraction, material on anterior hyaloid face of vitreous


PXF material causes degenerative changes in the iris

Iris retroillumination defects*** (ddx PG and many other things that cause iris trans defects)

Increased vascular permeability and impairment of the blood aqueous barrier function

Pupils are difficult to dilate for this reason

Iris ghost vessel

PXF surrounds the obliterated lumen

Note: pigment is liberated from the iris (not rubbed off like pigment

dispersion) and is deposited in the trabecular meshwork

This is postmortem

This PXF presence (or origin disease) can weaken the zonules

Lens dislocation (without surgery)

Implant dislocation during or after catarat surgery

May need to remind cataract surgeon that patient is PXE, PXS, PXG

• Mother with pseudoexfoliative glaucoma needed cataract surgery • Toni discussed PXG with cataract surgeon

• Surgeon was chosen for experience with PXG patients

• Lens dislocated

• Vitreous prolapsed

• Retinal detachment

• Multiple complications

• A nightmare

Iatrogenic zonular dehiscence causing vitreous prolapse into the anterior chamber

Complete or partial lens prolapse into the vitreous cavity

Posterior capsular tears created during cataract surgery

Poorer dilation so smaller capsulorhexis making sugery less easily visualized

Increased postoperative cell and f lare, so need to keep on steroids longer This is due to a propensity for PXF iris vessels to leak serum

PXF/PXG patients should have their cataracts removed earlier – less stress on zonules when you are phacoemulsifying a “softer” nucleus as opposed to a more hardened nucleus

Mature cataract dislocation with PXS


Dislocated lens with PXE on zonules

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Material released and deposited on corneal endo

Yes, similar to PDS or PDG but a totally different mechanism NOT due to rubbing of zonules on the posterior iris epithelium… So, you don’t have that specific pattern…. And yes, excessive pigment in the angle (just like PDS or PDG) but with white flakes of PXF


Pigmentary G Pseudoexfoliative

Q - Which is more predictive that your PXS patient will develop PXG?

a. amount of PXF

b. amount of pigment in the angle Ans =b

6w p CE, chafing from IOL haptic

7 years after CE, iris chafing (not same eye as above)

Mechanical chafing by IOL haptic, vision blurred while playing golf

Iris atrophy after Herpes Simplex Uveitis

Patients who have had cataract surgery will commonly show some kind of iris retroillumination defect

The smaller the pupil at the time of surgery the higher the probability Ultrasonic energy

used to “emulsify” cataract

You want the iris out of the way of this energy – devices to help open the pupil

• Here the phaco tip “ate” it’s way through the iris causing this defect, note small pupil

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Small white round KPs

OD OS

(the same person)

Ernest Fuchs Austrian Ophthalmologist

Keratic Precipitates

AA

Figure 14.60 Fuchs uveitis syndrome. (a) and (b) Keratic precipitates; (c) stromal iris atrophy rendering the sphincter

pupillae prominent and small pupillary nodules; (d) stromal nodules and mature cataract; (e) posterior pigment layer atrophy seen on retroillumination; (f) angle vessels (Courtesy of C Pavesio - figs b and d)

Iris transillumination defects here

PXF decreases aqueous outflow

Pigment release also decreases aqueous outflow

PXF – on surface of lens or IOL

Up to 20% of pseudoexfoliative cases are missed if examined with undilated pupils (1)

Pupils may not dilate well with PXS/PSG

May see phacodonesis (abnormal lens movement or “jiggling” with small eye movements)

May see iridodonesis

(1) Forsius H. Pseudoexfolation sydrome in various ethnic populations. Acta Ophthalmologica 1988; 66(suppl 184):71-85.

If you do NOT routinely dilate pupils: You’re going to miss

fundus pathology You’re going to miss

PXS/PXG You will not be able to

appropriately manage anything that has to do with cataracts

1) More difficult to control than COAG

2) Higher IOP than COAG

3) Poorer response to ocular medications

4) May cause weakened lens zonules – a risk associated with inevitable cataract surgery (zonular rupture during cataract surgery, a little higher risk factor)

So, your going to have to fight this guy as aggressive as he tries to get you

PXG Monster

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Medial therapy similar to COAG Meds:

B-adrenergic agonists A-adrenergic agonists Miotics CAIs Prostaglandin analogs – Xalatan, Travatan, Lumigan

Sequence: Monotherapy Adjunctive therapy Maximal medical therapy Surgical intrvention

Good response to SLT or ALT

Good response with Trabeculectomy (same as COAG)

Some statistics (Thorburn W. The outcome of visual function in

capsular glaucoma. Acta Ophthalmologica 1988;66(suppl 184):141-147)

The old term for PXG is “capsular glaucoma”

Before patients died, 61% had undergone either ALT or Trab

25% became blind in at least one eye

8% blind in both eyes

15% with bilateral PXG became blind

(Published in 2010)

Pigmentary Glaucoma



Uveitic Glaucoma



A nightmare

A nightmare

Retinal ischemic tissue releases vasoproliferative substance (otherwise known as VEGF, vascular endothelial growth factor) which migrates past/around/through the vitreous to the anterior segment

Pre-existing vessels sprout new vessels which easily tear, hemorrhage, leak, and leak fibrin molecules with myofibroblasts

If enough fibrin molecules are leaked, a fibrin membrane can form which can contract (thanks to the myofibroblasts)

If the membrane is attached along a surface, that surface will be pulled together


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Movement of vasoproliferative substance

(1) Hemi BRVO,

vigilant, gonio first visit, check iris

(2) CRVO, some CWS, more vigilant – gonio every visit, r/o NVI

(3) CRVO, ischemic, very vigilant – gonio every visit, r/o NVI

(4) Very ischemic CRVO, extremely vigilant – same as above but more effort in looking

Vein Obstructions When does one need to be vigilant for

neovascular glaucoma?

(1) (2)

(3) (4)

Gonio every visit

Careful search NVI every visit

Treatment by Retinal specialist (they will be looking too)

Proliferative Diab Ret

CRAO’s can be obstructed from 1% to 100% so ischemia can vary

Look for NVI and do gonio

Frequency depends on amount of ischemic signs

Central Retinal Artery Obstructions

Must take some

time to carefull search

Start at rim and go out

Try red fee filter too

Neovascularization of Iris (NVI)

New blood vessel

leaks fibrin

The fibrin

accumulates…

..and accumulates…

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..and accumulates…

..then contracts…

A B

A B

The myofibroblasts cause contraction of the fibrous membrane

Retina

Choroid

& RPE

Fibrovascular Membrane –

attached to retina

Fibrovascular Membrane –

attached to retina

The fibrovascular (neovascular)

membrane contracts pulling the

retina with it

and there you have a

TRACTIONAL RETINAL

DETACHMENT (TRD)

As opposed to a:

Rhegmatogenous RD

Serous RD

Tractional retinal detachment

The membrane pulls the retina away from the RPE and forms another plane of tissue

Fibrovascular membrane

Progressive PAS formation in neovascular glaucoma

The neovascular membrane contracts and pulls the flaccid iris up against the

angle forming PAS

The iris is actually pulled

inside out, the posterior iris

epithelium is pulled out on

the anterior iris surface = ectropion

uvea

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NVG is a “pulling” mechanism, where

the iris is pulled up to the angle by

fibrovascular membrane contraction

NAG is a “pushing” mechanism

where the pupillary block causes

pressure to build behind the floppy

iris and it is pushed forward

Myofibroblasts in the

fibrovascular membrane

contract pulling the iris

up to the angle forming

peripheral anterior

synechiae (PAS)

Most likely etiologies: (1) ischemic central retinal vein obstruction and (2) proliferative diabetic retinopathy (again, ischemia)

NV starts at pupil margin, this is a 10 on a 1-10 scale

NV forms in the angle causing PAS

Ectropion uvea

Using the Volk G4 with

flange (better control)

I go mm by mm, slowly, 360

degrees

Rule out NV

No diversions

…concentrate…..

How I evaluate angle for NV

Initially we’re utilizing a retinal specialist the day of

diagnosis (a true emergency)

Intravitreal anti-VEGF injection (about 6 weeks for full

effect)

PRP (pan retinal photocoagulation)

Topical glaucoma medication

Atropine and topical steroid if photophobic

A glaucoma surgeon for the rest

Trabeculectomy or aqueous shunt

NVG - treatment

Must be looking for NVG when you think you have an acute

Narrow Angle Glaucoma attack in your chair

Many times the cornea is edematous and you may have difficulty

seeing iris details

Be suspicious when:

Patient is diabetic and fellow eye has signs of retinal ischemia

(NFL infarcts, moderate changes, etc….)

The fellow eye chamber is deep (it should be similar to eye with

NAG attack)

Comments NVG

2/20/2014

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The key to managing NVG is to

watch any patient with retinal

ischema carefully looking for

NV of iris and NV in the angle

Early detection, early treatment

and avoidance of glaucoma

E.g., with an ischemic CRVO

you might see the patient every

week

The Key to NVG

Uveitic Glaucoma

Pigmentary Glaucoma



Uveitic Glaucoma


Uveitis-induced ocular hypertension

• There is no optic nerve damage or field loss

• But, there is elevated IOP

• So, not uveitic glucoma

Uveitic Glaucoma or Inflammatory

Glaucoma

• There is evidence of optic nerve damage or field

loss, etc.

Terminology

About 25% of uveitis patients will develop increase in IOP at some time during course of inflammatory disease

More common with granulomatous as opposed to nongranulomatous

Main problem is obstruction of outflow

Can produce a glaucoma that is severe and not treatable with medical therapies

Statistics

The longer you treat a uveitis the greater the chances you will have a complication that elevates IOP, so, tighten up the follow up as time progresses

Look for the following problems

Sometimes the patient will for whatever reason stop steroid or mydriatic use and help create problems

….or…they won’t show up for f/u appointments…then finally show up with complications

The trouble is…..uveitis can produce a glaucoma that is not only severe but resistant to all medical therapies

In general:

2/20/2014

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Obstruction of TM by inflammatory cells

Pupillary block

Formation of PAS (peripheral anterior

synechiae)

Uveal effusion

Neovascularization

Use of steroids and steroid response

More likely to happen in chronic uveitis

as opposed to acute uveitis

How many ways can uveitis cause glaucoma? Let me

count the ways.

Inflammatory cells, circulating through the pupil, can cause the iris to adhere to the anterior lens

This is a posterior synechiae

If the adherence becomes 360 degrees it can block the exit of aqueous and cause an iris bombe and angle closure and the need for a Laser Peripheral Iridotomy

Posterior synechiae

How does one avoid?

Use a dilating agent and proper dosing that allows the pupil to stay mobile

You don’t want a static pupil, large or small

How does one break posterior synechia? High doses of atropine and time

Posterior synechia (continued)

Inflammatory cells and fibrin

deposit in TM, the fibrin molecules contract pulling the iris up and against the TM

Can “zip up” and eventually block all aqueous exit

Avoid this with steroid treatment

Peripheral Anterior Synechia (PAS)

A steroid response while you are treating a uveitis

Treat with topical glaucoma medications, except:

• Prostaglandin analogs

B-blockers and CAI’s are good since they reduce

aqueous production (outflow may be compromised by

the inflammatory exudates)

Steroid-Induced Ocular Hypertension/Glaucoma

beta blockers (like Betaxolol) – reduces aqueous production

carbonic anhydrase inhibitors (oral Diamox, topical Trusopt) – reduces aqueous production

apraclonidine (Iopidine) – decrease aqueous production and uveoscleral outflow

brominidine (Alphagan) – same mechanism as above

G meds to use

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Prostaglandin analogs (like Xalatan) – increases

uveoscleral outflow, reported to produce inflammation

and cystoid macular edema

Miotics – may contribute to posterior synechiae, cause

ciliaty body muscle spasm, enhance blood-aqueous

barrier

G meds to NOT use

Basically trying to break the

adhesion between the iris

and the TM

Making a direct opening into

the canal of schlemm

Goniosynechialysis or Trabeculodialysis

Direct outlet of aqueous

from anterior chamber to

subconjunctival space

Express Shunt

Cryogenic “old school” produces ischemic necrosis of CB and ciliary epithelium

Ciliary Body Ablation

Contact diode laser – destruction of ciliary epithelium

aa

Endoscopic Cyclophotocoagulation

Endoscopic view during procedure

Diode laser

Rick Sharp, O.D.

Associate Professor – Rosenberg School of Optometry

Adjunct Assistant Professor – University of Houston College of Optometry

2/20/2014

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Pigmentary Glaucoma



Uveitic Glaucoma


Steroid Responders – people who have an increase in IOP when using steroids

Steroid Glaucoma – G caused by steroid use

Steroid Induced Ocular Hypertension

Terminology

Steroids cause changes in the TM Cellular – function and morphology Biochemical – extracellular matrix production increase Molecular – cytoskeleton , gene cell expression AND THESE CHANGES RESEMBLE THOSE OF POAG!!

Outflow is reduced This typically takes weeks sometimes days depending on

the individual IOP elevates Glaucoma Children age 5-6y old are more likely to be a steroid

responder thought to be due to a difference in the TM anatomy at this age (functional immaturity). By age 8 functional maturity is reached

Mechanism Mechanism

EFFECT OF STEROID ON TM CELLCYTOSKELETON

Normal TM cell actin microfilament bundles forming linear arrays of stress fibers

Steroid induced reorganization of microfilaments into these stellate figures call cross linked actin networks

Steroids suppress phagocytic processes of the trabecular endothelium causing accumulation of debris in the meshwork

….which decreases aqueous outflow

Mechanism

-Armaly MF. Statistical attributes of the steroid hypertensive response in the clinically normal eye. Invest Ophthalmol 1965;4:187-197

-Becker B. Intraocular pressure response to topical corticosteroids. Invest Ophthalmol 1965;4: 198-205

Steroid Responders

Two studies independent from each other in 1960s

Dexamethasone and betamethasone (not prednisolone)

.1% drops tid or qid x 4-6 weeks

Results: 4-6% termed “high responders”, IOP >31 (or greater than

15 above the subjects baseline IOP)

33% termed “moderate responders”, IOP 20-31 (or 5-15 above baseline)

Remainder (let’s say 100-(33+5)=62%) 62% were termed “nonresponders”

So lets round off at 60 non/40 low with 5% high responders

2/20/2014

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Ahh…..no

Elevated IOP can persist in some cases Pre-existing glaucoma, just now off steroids?

The steroid “converts” the eye to POAG

Using topical steroids with POAG patients produces a moderate or high response in nearly all subjects (Armaly MF. Effect of corticosteroid on intraocular lpressure and fluid dynamics, II: the effect of dexamethasone in the glaucomatous eye. Arch Ophthalmol 1963;70:492-499….and….Becker B, Hahn KA. Topical corticosteroids and heredity in primary open-angle glauocoma. Am J Ophthalmol 1964;57:543-551)

This is important!!! Your glaucoma patients getting cataract surgery or trabeculectomy surgery will be on steroids afterwards – expect the IOP to elevate You might mistakenly conclude the trabeculectomy has

failed, it may be fine with IOP elevation due to steroid use

No big deal – just stop the steroids, right?

Now isn’t THIS special!

Families of patients with POAG tend to be

responders

There seems to be a link between the glaucoma gene GLC1A, TIGR and steroid induction into the TM

High steroid responders are more likely to develop POAG

Diabetics and high myopes have higher rates of steroid responsiveness

Responders and POAG

IOP elevation directly related to dose

Topical - eyedrops

Periocular administration – subconjunctival injection, retrobulbar injection

Systemic – oral or injected

Inhaled

Transdermal

Intranasal

In other words….all routes of steroid treatment

What steroids are we considering?

General practitioner or PA may prescribe a topical

steroid or antibiotic-steroid combination – not too often these days

Then refills are given and given and given and the patient continues to take the meds

I have met several patients with severe VF loss who have sued their PCPs over this

General Practitioners and refills

Initally the patient has undiagnosed glaucoma and

elevated IOP

Uveitis starts and the CB produces less aqueous and the IOP goes down. You then measure IOP.

You start prednisolone acetate (Pred Forte) and after two weeks the IOP goes up and up as the CB recovers and makes more aqueous

You conclude the patient is a steroid responder

You eventually take them off the steroid

The IOP does NOT go down (your back to the unknown and undiagnosed glaucoma situation from the beginning)

The Uveitis-Steroid Pitfall

Your patient is being treated with a long term steroid

(oral or transdermal), IOP goes up, optic neuropathy goes so far

Then the steroid is stopped and the IOP goes down

You then see the patient with glaucomatous changes and VF loss with normal IOP and conclude patient has NTG

The Normal Tension Glaucoma Pitfall

Isn’t THAT special!

2/20/2014

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You have a uveitis that is not therapeutically responding

to topical steroid (you’re in the Uveitis-Steroid Pitfall) and your patients IOP is at a normal level

You do sub-tenons steroid injection without knowing if your patient is a steroid responder

The patient just happens to be a high responder

The IOP goes up to 75mmHG

You can’t get the steroid out (cannot aspirate out)

You start topical and oral meds to lower the IOP

May even need a trabeculectomy

This is a known risk anytime you do a sub-tenons

Risk of NOT sub-tenon vs. doing the sub-tenons

Sub-tenons depo nightmare

Isn’t THAT special!

From most likely (and most effective) to least likely (and less effective):

Durezol (difluprednate ophthalmic emulsion) – fabulous, no BAK, ?effect on IOP, be careful

Dexamethasone

Prednisolone (Pred Forte)

Flurometholone (FML), Rimexolone (Vexol), Loteprednol (Lotemax)

Topical steroids less likely to cause a response

fini

Boulder Colorado

CE Outline for CE in the Southwest –Dallas, TX (March 22-23, 2014)

Jennifer Deakins, OD and Jenny Terrell, OD

Community-Based Eye Care: Optometry’s Role in Public Health

I. Community Eye Clinic

a. Brief history of the clinic

b. Patients served

c. Educational component

II. Patient Access

a. Professional services

b. Medications

i. Insured

ii. Uninsured

1. Individual manufacturers

a. Most companies have their own patient assistance program

(PAP)

2. “Clearinghouse” websites for assistance

a. www.needymeds.org (non-profit resource info about PAP)

b. www.rxhope.com (supported by PhRMA and companies)

c. Follow-up visits

i. Transportation issues

ii. Updated contact information

III. Barriers to Healthcare

a. Health literacy level

b. Patient’s budgeting priorities

c. Co-morbidities

d. Citizenship/residential status

IV. Referrals for surgical/tertiary care

a. Local medical society may provide assistance

b. Building relationships with retina, cornea, etc

c. Specific challenges to emergency care

V. Adding Philanthropic Care to Your Practice

http://www.needymeds.org/

http://www.rxhope.com/

a. Patients to sign waiver

b. Community based organizations

c. How to find the resources in your community

VI. Community Resources

a. Local churches

b. United Way -211

c. FQHC’s

d. County hospitals

e. Challenges in coordinating care with non-profit orgs

CE in the Southwest March 23, 2014 Speaker: Jenny Terrell, OD Course Title: Professional Responsibility (1 hr)

I. Prescriptions, ophthalmic and drug a. Optical Board Rule 361.359

1. Ophthalmic lens prescription must include: a. Signature of the optometrist or therapeutic optometrist (not

printed or stamped) b. The information and parameters the optometrist or therapeutic

optometrist considers relevant and necessary. ii. The prescription may not contain a restriction that limits the parameters to a

private label not available to the optical industry as a whole. b. Drug Board Rule §280.10(d)

i. A therapeutic optometrist may prescribe oral medications only in the following classifications of oral pharmaceuticals: (1) one 10-day supply of oral antibiotics; (2) one 72-hour supply of oral antihistamines; (3) one seven-day supply of oral nonsteroidal anti-inflammatories; (4) one three-day supply of any analgesic identified in Schedules III, IV, and V of 21 U.S.C. Section 812; and (5) any other oral pharmaceutical recommended by the Optometric Health Care Advisory Committee and approved by the board and the Texas State Board of Medical Examiners. (d) A therapeutic optometrist may independently administer oral carbonic anhydrase inhibitors for emergency purposes only and shall immediately refer the patient to an ophthalmologist. (e) A therapeutic optometrist may inject appropriate medication for a patient who has an anaphylactic reaction to counteract the anaphylaxis. The therapeutic optometrist shall immediately refer the patient to a physician.

c. Doctor identification on prescriptions II. Definition of Standard of Care

a. Why is it important? b. Standard of Care Defined:

i. standard of care n. the watchfulness, attention, caution and prudence that a

reasonable person in the circumstances would exercise. If a person's actions do

not meet this standard of care, then his/her acts fail to meet the duty of care

which all people (supposedly) have toward others. Failure to meet the standard

is negligence, and any damages resulting therefrom may be claimed in a lawsuit

by the injured party. The problem is that the "standard" is often a subjective

issue upon which reasonable people can differ. (See: negligence, duty of care)

ii. Medical: Standard of care: 1. A diagnostic and treatment process that a clinician

should follow for a certain type of patient, illness, or clinical circumstance. In

http://legal-dictionary.thefreedictionary.com/negligence

http://legal-dictionary.thefreedictionary.com/duty%20of%20care

legal terms, the level at which the average, prudent provider in a given

community would practice. It is how similarly qualified practitioners would have

managed the patient's care under the same or similar circumstances. The

medical malpractice plaintiff must establish the appropriate standard of care

and demonstrate that the standard of care has been breached.

III. Reclassification of hydrocodone a. Schedule II

i. “Substances in this schedule have a high potential for abuse which may lead to severe psychological or physical dependence.”

b. Schedule III i. “Substances in this schedule have a potential for abuse less than substances in

Schedules I or II and abuse may lead to moderate or low physical dependence or high psychological dependence.”

c. Currently, hydrocodone alone is classified as Schedule II but drugs containing less than 15mg of hydrocodone per dosage unit or in combination with acetaminophen are classified as schedule III controlled substances

d. APhA joint letter on Nov 11, 2013: i. “While we appreciate the efforts of the FDA to address the serious issue of

prescription drug abuse, we believe rescheduling hydrocodone is not the solution,”

e. New requirements for pharmacies that will increase burden such as “the provision of additional secure storage, recordkeeping, and inventory management.”

f. Reclassification may present problems in allowing patients in need access to the drugs g. No more phone orders h. Patients need more frequent visits to prescribers to obtain prescriptions since schedule

II drugs may not be refilled. This will cause more emergency room visits and ultimately drive the cost of health care higher

i. ASHP: (American Society of Health-System Pharmacists): Nov 5, 2013 i. “Based on an assessment using the criteria the [DEA] considers when

determining whether to control or reschedule a drug, ASHP believes that hydrocodone combination products are similar to other controlled substances found in Schedule II and should therefore be assigned to Schedule II,”

j. What does it mean for optometry? i. Reclassification would mean that OD’s could no longer prescribe any drug with

hydrocodone for pain management. 1. Vicodin 2. Lortab

IV. Medicaid Fraud and Abuse audits a. CMS definitions

i. Fraud – making false statements or representations of material facts to obtain some benefit or payment for which no entitlement would otherwise exist.

ii. Abuse – practices that, either directly or indirectly, result in unnecessary costs to the Medicare Program.

1. Misusing codes on a claim 2. Charging excessively for services or supplies, and 3. Billing for services that were not medically necessary.

b. Fraud

i. How does the ACA address fraud and abuse? 1. Uses a web-portal to identify providers that have been terminated. 2. Increases provider screening and enrollment requirements. 3. Requires states to suspend Medicaid payments in cases where there are

credible allegations of fraud or abuse 4. Gives states the power to temporarily suspend activity among new

providers to prevent waste, fraud and abuse 5. Requires state Medicaid programs to establish Recovery Audit

Contractor (RAC) programs to identify and recover overpayments and underpayments.

6. Mandates the use of the Nation Correct Coding Initiative (NCCI) 7. Encourages data system enhancements to identify fraud and abuse.

Federal funds are made available to help states implement such systems 8. Requires that physicians document a face-to-face encounter (telehealth

permitted) with a Medicaid beneficiary before ordering home health services, medical supplies or equipment.

c. States cracking down i. Primarily other health care professions

1. Be careful to bill properly 2. Be careful of anti-kickback violations

a. The Anti-kickback statute prohibits, giving, receiving or soliciting any items of value, either directly or indirectly for the purposes of inducing or rewarding items or services that are reimbursable by the federal government.

b. Violators are subject to monetary penalties, imprisonment or both

ii. Safe harbor regulations 1. According to the Office of the Inspector General, safe harbor

regulations: a. “describe various payment and business practices that,

although they potentially implicate the Federal anti-kickback statute, are not treated as offenses under the statute.”

b. Examples include lease of space, lease of equipment, warrantees, discounts and many more

c. Each example has a number of stipulations that must be met d. A complete list of Safe Harbor Regulations may be found at :

http://oig.hhs.gov/compliance/safe-harbor-regulations/ V. Peer Assistance Program

a. Professional Recovery Network i. Established in 1981 by the Texas Pharmacy Association

ii. Optometry was added September 1, 2010 iii. Helps professionals, students and professional staff in the fields of pharmacy,

optometry, dentistry and veterinary medicine overcome potential impairment due to substance abuse issues or mental illness.

iv. The reporting and treatment are confidential v. The goal is to provide public safety while preventing disciplinary action against a

professional license. vi. The above criteria apply if the individual complies with their treatment program.

b. Referrals i. Self

ii. 3rd party iii. Investigator iv. Board Order

c. Contact information: i. PRN Hotline: 1-800-727-5152

ii. PRN Address: 6207 Bee Caves Road, Suite 120, Austin, TX 78746 iii. Website: http://www.txprn.com/

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