2018 Victoria Conference Workbook Part 22018 Victoria Conference Workbook Part 2 SATURDAY, July 14 PAGES Beth Kinoshita Corneal Ecstasias 112 – 118 James Kundart Visual Consequences

2018 Victoria Conference Workbook Part 2

SATURDAY, July 14 PAGES Beth Kinoshita Corneal Ecstasias 112 – 118 James Kundart Visual Consequences of Chiari Malformation 119 – 127 Anthony DeWilde Managing Unilateral Optic Nerve Edema 128 – 156 SUNDAY, July 14 James Kundart Macular Cherry Red Spots 157 – 165 Lee Carr Recognizing Red Flag Headaches 166 – 175 Beth Kinoshita Coatings and Treatments and Agents 176 – 180 Anthony DeWilde Rethinking Gonioscopy 181 – 193 James Kundart Climate Change, Eclipses & the Eye 194 – 202

Corneal Ectasias

Beth Kinoshita, OD, FAAO 2043 College Way

Forest Grove, OR 97116 503-352-3140

[email protected]

Course Description This course will review the types of corneal ectasias and their possible etiologies and treatment options with an emphasis on keratoconus. Cases will be used to highlight diagnosis and management options.

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

• Be familiar with the difference between a corneal dystrophy and degeneration• Be able to identify the different ectasias with corneal topography• Identify keratoconus and the various treatment options• Be familiar with the corneal crosslinking procedure and criteria for referral• Be familiar with the contact lens management options for ectasias

Course Outline • Corneal Ectasia

o Non-inflammatoryo Bilateral thinning of the central, paracentral or peripheral cornea

• Dystrophy vs. Degenerationo Controversial classificationo Case for dystrophy

Genetic basis• Family history in 10% of cases

o Found in twins / families with 2 or more generations• Increased prevalence in 1st degree relatives• Increased prevalence in trisomy 21 (Down Syndrome)

o Case against dystrophy Sporadic (in an individual only) Causative associations with eye rubbing and atopy Insufficient evidence of clear genetic basis

• Genetics of Keratoconuso Found in identical twins / families with 2 or more generationso Prevalence in 1st degree relatives

15-67 times higher than the general pop.o Associated genes

Chromosome 21, chromosome 17 (Leber’s congenital amaurosis),chromosome 13

o Autosomal dominant inheritance with variable penetrationo In the Japanese, human major histocompatibility complex (HLA) antigens

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mailto:[email protected]

HLA-A26, B40 and DR9 associated with early onset• Corneal Ectasia

o Keratoconuso Keratoglobuso Pellucid Marginal Degenerationo Posterior Keratoconuso Post-LASIK ectasiao Terrien’s Marginal Degeneration

• Keratoconuso The incidence of keratoconus is approximately 1 in 2000o What we know about keratoconus

The condition occurs in every country throughout the world Occurs equally in men and women? Usually begins between the ages of 12 and 32 Condition of unknown etiology

o Associated Conditions Atopic disease

• Oxidative stress? Eye rubbing Hereditary CL wear?

• CLEK study Do CL stop or slow the progression?

o Only 10% of People with KC Undergo Corneal Transplant Surgeryo Unilateral keratoconuso Hallmarks of Keratoconus

Decline in visual acuity Changes in cylindrical power and axis

• Scissor reflex on retinoscopy Topographical changes Squinting of the eyelids, artificially creating a pinhole effect Appearance of halos around street lights

o Morphological Changes in Keratoconus Epithelium

• Basal cells degenerate - grow towards Bowman’s layer Stroma

• Reduction and disorganization of lamellae Decrease number of keratocytes Descemet’s membrane

• Hydrops Endothelium

• Change in cell shape with cells pointing towards the coneo Clinical Changes in Keratoconus

Corneal nerves more visible Scissor reflex with retinoscopy Charleaux oil drop

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Fleisher’s ring• Iron deposition at the bse of the cone

Straie• Compression of Descement’s membrane

Corneal thinning Corneal scarring Hydrops Munson’s sign Rizutti’s sign

o Puberty Onset Keratoconus Begins in early adolescence approximately age 12 to 16 Usually bilateral with one eye affected worse than the other The younger the patient, the more severe the condition.

o Late Onset Keratoconus Usually begins in late 20’s or early 30’s Both eyes can be affected the same The incidence of progression reduces greatly with the age of onset

o Keratoconus Fruste A mild non-progressive form KC Can occur anytime throughout life No positive slit lamp findings associated with KC Normal corneal thickness Often diagnosed with topography

o National Keratoconus Foundationo Classification

Morphology• Nipple

o Cone is ≤ 5 mm round near the central or paracentralcornea

• Ovalo >5 mm and paracentral or peripheral

• Keratoglobuso Cone is throughout 75% of the cornea

Disease evolution• Four stages

Index-based• Topography• OCT• Aberrometry

o Treatment Options Spectacles

• Need more regular cornea to be a good option Corneal GP lenses

• Potential for great acuity• Adaptation to comfort• Case example of GP contact lens fit

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Soft contact lenses• Potential for similar (or better) acuity as spectacles• Stability of vision

o Consider large astigmatism correction Custom soft contact lenses

• No CL vs. over CL• Initial base curve selection

o Mean K + 1.00 mm• Select fitting curve

o 8.3 mm, 8.6, mm 8.9 mm• Select overall diameter

o 10.0 mm to 17.0 mm• Material

o Hydrogelo Silicone hydrogel

Lathe Reproducibility

• Case example for custom SCLo A 23-year-old presents with a chief concern of vision that

has gotten worse OD>OS for the past 2 years and isseeking a second opinion regarding refractive surgery

o Exam findings Decreased best corrected acuity, distortion with

keratometry Anterior segment is unremarkable Topography – inferior steepening with

superior/nasal flatteningo Treatment

Custom SCL with increased center thickness Scleral GP lenses

• Potential for great acuity• Less adaptation to comfort• Cost• Anatomy of a Scleral Lens

o Central zone, peripheral zone, limbal zone, and scleral zone• Fitting Goals

o Clearance across the central corneao Increase limbal clearance

Bright ring of fluorescein at the limbuso Scleral alignment

All pressure, weight and bearing of the lens shouldbe on the sclera

• What is the Appropriate Apical Clearance?o 200 to 400 microns

• Limbal Clearance Zone

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• Appropriate scleral landing zone• Case example for scleral GP fit

Implantable Intracorneal Rings Segments• Flatten the cornea and decrease irregular astigmatism• Need minimum of 450 um at incision site• Removable

Corneal Cross-Linking• Hope to stabilize / slow progression• Generally still needs some type of vision correction• Concept first introduced in 1998• Strengthen tissue by photosensitization and chemical cross-linking• Exposed to measured dose of UVA radiation

o Free radicals are produced covalent bonds betweencollagen molecules and glycosaminoglycan molecules

o Exact mechanism is not understood• April 2016 - FDA granted approval to Avedro Inc. for its corneal

cross-linking system to treat patients with:o Progressive Keratoconuso Post LASIK Ectasia

• Dresden Protocolo Epithelial debridement over the central 9mmo Topical riboflavin is instilled every 2 minutes x 30 minutes

Saturation of the stromal with riboflavino UVA (365nm) irradiance of 3.5 mW/cm2 x 30 minuteso Riboflavin every 2 minutes x 30 minuteso Antibiotic and steroid drops + bandage CL

Removed when epithelium heals• Normal Corneal Anatomy = 540 um• In Corneal Crosslinking the Epithelium is Removed• Minimal stromal thickness is 400 um• Most of UV energy dissipated in the anterior 400 um

o Energy level at the endothelium 0.18 J/cm2

o Half of the endothelial damage threshold• Transepithelial Cross-linking

o Epithelial is not removedo Thinner corneaso New formulations of riboflavin and/or longer pre-op

loading time (45-60 minutes) may contribute to improvedstromal uptake

o Possibly higher rates of progression vs. Dresden Shallower treatment depth

• Accelerated Cross-linking (Law of Reciprocity)o Twice the level of irradiance (30mW/cm2 x 3 minutes)

• Effects on the corneao Early apoptosis of keratocytes to 300 um

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Keratocyte repopulation after 3-12 months,contributes to post-op haze

• Stromal edema• Loss of sub-epithelial nerve pelxus• Loss of midstromal nerve fibers• Increased reflectivity in the mid-stroma

o Contributes to post-op haze in the anterior stromao Plateau in 1-3 months then declineso Generally does not affect acuity

• Increased corneal stabilityo Increase in collagen fiber diameter (12.2% anterior stroma

and 4.6% posterior stroma)o Resistance to enzymatic degradationo Increase in corneal rigidity by 328% (Wollensack, Spoerl

and Seiler)• Visual Acuity

o Worsening acuity up to 1 montho Improvement 6 months to 1 year

• Keratometryo Steepening up to 1 montho Flattening 6 months to 1 year

• CXL Complications• Patient selection

o Progressive keratoconus Changes to keratometric (Sim K) measurements

• Increase in maximum value of 1.00 D in ayear

Change in refraction? Change in CL base curve Clinical judgment

o Minimal stromal thickness of 400um• Contraindication

o History of herpetic eye diseaseo Pregnant or nursingo Central corneal opacityo Stroma thickness less than 400um

Treatment Options• Protect against oxidative damage

o Use UV filterso NSAID

Placibo effect?o Preservative-free artificial tearso Ophthalmic antihistamines / mast cell stabilizerso Minimize corneal microtrauma

• Pellucid Marginal Degenerationo Rare

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o Thinning of the inferior corneao Onset during 4th and 5th decadeo Slowly progressive band of thinning down to 1 mm from the limbuso Topography - Generally high ATR astigmatism

Early to moderate stages can be corrected with a toric SCL Case example of PMD SCL fit

• Posterior Keratoconuso Affects the posterior cornea and may not be neutralized with a contact lenso Posterior corneal imaging

• Post-LASIK ectasiao Treatment and management similar to keratoconuso Screening for ectasia prior to refractive surgery

• Terrien’s Marginal Degenerationo Rareo Unknown etiologyo Mostly asymptomatico More common in males >40 years oldo Early

Stromal opacification superiorlyo Late

Thinning superiorly and circumferentiallyo Perforation is uncommon but may occur spontaneously or with traumao Topography - ATR or Oblique astigmatism

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James Kundart OD MEd FAAO FCOVD-A

1

Visual Consequences of Chiari Malformation

2018 VICTORIA CONFERENCEJAMES KUNDART OD MED FAAO FCOVD-A

PACIFIC UNIVERSITY COLLEGE OF OPTOMETRYFINANCIAL DISCLOSURE: NOTHING TO DISCLOSE

https://www.conquerchiari.org/index.html

Learning Objectives1. Which cause of Chiari malformation is most

common? What are the presenting symptoms?

2. Which cause of Chiari malformation is not evident with imagining, but may haveocular signs and symptoms?

3. What are the differential diagnoses forChiari syndrome?

4. What are the surgical and non-surgicaltreatments for Chiari malformation?

Definition of Chiari Malformation

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

Chiari malformation istraditionally definedas the cerebellartonsils being located3mm-5mm or morebelow the foramenmagnum asmeasured on an MRI

Problems with the Traditional Chiari DefinitionSome people

have large herniations with no symptoms

Others haveonly small herniations, but are severely symptomatic

http://en.wikipedia.org/wiki/Arnold-Chiari_malformation

Variable Symptoms of Chiari Malformation

https://www.conquerchiari.org/documents/presentations/SYMPTOMS%20Presentation.pdf

Chiari Symptoms

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4508727/pdf/nmc-53-847.pdf

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Chiari Signs

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4508727/pdf/nmc-53-847.pdf

Brainstem Compression in Chiari Malformation


Causes of Chiari: Increased CSF Pressure Chiari doesn’t require

obstruction, just higherCSF pressure

This is sometimes calledChiari Type 0, and resembles idiopathicintracranialhypertension (IIH), andmay beindistinguishable from it

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

High CSF-Pressure Chiari, “Type 0” (same as IIH?)

One of my first Chiari suspects

Causes of Chiari:Small Posterior Fossa

This is the default“anatomical determinism” theory

When this occurs,transient but recurrent hydrocephalus can result

In these cases, surgerymay be the best option

https://www.conquerchiari.org/documents/presentations/OVERVIEW%20Presentation.pdf

Causes of Chiari:Connective Tissue Disorders “There is one published large

study that has looked at the association between type 1 Chiari and EDS

This was undertaken by Milhorat et. al. in 2007 at The Chiari Institute in New York

They looked at 2813 patients with a known diagnosis of type 1 Chiari malformation

They found that 357 (12-13%) had features of EDS”

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Causes of Chiari:Tethered Cord (?)

“Tethered cord is a relatively new entity, medically speaking, and as such there is still quite a bit of controversy surrounding it

There is even occult TCS since the tethering is not apparent on MRI

A second area of controversy involves therelationship, if any, between tethered cord and Chiari and/or syringomyelia”

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5738018/

How Common is Chiari?(and does IIH mimic it?) The US Association of

Neurological neurologicalsurgeons performs 10K Chiari surgeries per year

Chiari may be as common as 1:1000 patients in the US. Also…

“Cerebellar tonsil position in patients with IIH was significantly lower than that in age-matched controls, often times peg-like, mimicking Chiari”

http://www.ajnr.org/content/33/10/1901

Gender and Ethnic Trends in Chiari Malformation

Chiari is oftendiagnosed inyoung adults

Women getChiari moreoften thanmen

It affects allethnicities

https://www.conquerchiari.org/documents/presentations/OVERVIEW%20Presentation.pdf

Three Types of Chiari

1. ChiariMalformation,Type I

2. Arnold-ChiariMalformation

3. ChiariMalformation,Type III

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

Three Types of Chiari

Wong, page 170

Classical Chiari Type I

Chiari malformation happens when the cerebellar tonsils protrude through the foramen magnum, pinch the medulla, and block CSF flow

http://www.mayfieldclinic.com/PE-Chiari.htm#.VXiR486VzPA

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Congenital Chiari Type I


Arnold-Chiari (Type II)

Much less common than Type I, this birth defect leads to fourth ventricle hydrocephalus

Expect childhood-onsetwith more severe symptoms

These patients are usuallyborn with paraplegia due to a defect (hole) in the spine and back called a myelomeningocele

http://www.fluidsbarrierscns.com/content/5/1/2/figure/F2?highres=y

Congenital Arnold-Chiari


Chiari, Type III

This terrible birth defectis characterized by cerebellar herniation outside the skull cavity, called an encephalocele

This happens when the neural tube does not close during the first trimester of gestation

Various teratogens like arsenic can cause this usually fatal condition

http://radiopaedia.org/articles/chiari-ii-malformation

Congenital Chiari Type III


Visual Symptoms of Chiari

Blurred VisionDiplopiaNystagmusPhotophobiaStrabismus


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Symptom ProfilesThat Mimic Chiari

https://www.conquerchiari.org/documents/presentations/DIAGNOSIS%20Presentation.pdf

Chiari Obscured by Morning Glory Disc

https://www.ncbi.nlm.nih.gov/pubmed/24802674

Chiari Malformation and Eye Movements

Mild cases of Chiari may result inintermittent diplopia

Often, this presentsas esotropia at farof the divergence insufficiency type

When this occurs,suspect CN VI palsy

http://www.neuroophthalmology.ca/textbook/disorders-of-eye-movements/iv-neuropathies-and-nuclear-

palsies/v-abducens-vi-nerve-palsy

Pursuits and Saccades in Chiari Malformation


Eye Movements in Chiari

Leigh & Zee, 5th edition

Syrinxes and Syringomyelia

A syrinx is a fluid-filled cyst in thespinal cord

This causes spinalcord edema,compromisingneuronal function

Permanent nervedamage can result

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Normal vs. Chiari Cerebellum & Syrinx


Spinal Cord Syrinxes and Chiari Symptoms

http://www.mayfieldclinic.com/PE-Chiari.htm

Syrinxes and Chiari Surgery


Surgical Treatments: Posterior Fossa Decompression


Craniectomy for Chiari

http://www.mayfieldchiaricenter.com/chiari_surgery.php

Opening the Dura in Chiari


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Dura Patch for Chiari



Surgical Time Course for Posterior Fossa Decompression

https://www.conquerchiari.org/documents/presentations/TREATMENT%20Presentation%20.pdf

Surgical Time Course for Posterior Fossa Decompression


Chiari Surgeries on the Rise


Surgical Outcomes for Posterior Fossa Decompression


Case #1: Chiari Surgery Relieves Cluster-Like Headache

http://www.ant-tnsjournal.com/Mag_Files/24-4/004.pdf

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Case #2: Pre-Op Signs of Chiari in 13 YOM with ↑BMI

A pre-operative sagittal T1-weighted MRI demonstrating CMIwith tonsillar herniation 5 mm below the foramen magnum

Case #2: Post-Op Signs of Chiari in 13 YOM with ↑BMI

A sagittal T2-weighted MRI performed 6 months after suboccipitaldecompression demonstrating the creation of a normal-sizedcisterna magna for sufficient CSF flow

Case #3: Chiari Causing Esotropia Pre-Op in 6 YOF


Case #3: Chiari Causing Esotropia Post-Op in 6 YOF


Non-Surgical Chiari Tx: Acetazolamide and Lasix

https://i.pinimg.com/originals/e7/80/67/e780675385d88cd1f

e507bc885c5072e.jpg

https://www.onlineclinic.co.uk/images/product/acetazolamide-

blister-pack-l.jpg

Future Directions in Chiari

Researchers are lookingfor a new way tomeasure Chiari severity

Focus areas includeadvanced MRI andengineering techniquesto quantifycerebrospinal fluid(CSF) flow, crowdingand compliance


GIF Animation of CSF flow in Chiari

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Questions? Thank you!


ProfessorPacific University

College of Optometry3D Performance [email protected]

Reading and References

For moreinformation, seeEye MovementDisorders byAgnes Wong(2007, seechapter 10 onthe cerebellum)

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Evidence Based Optic Nerve

Anthony DeWilde, OD FAAO

Kansas City VAMC

No financial disclosures

Goals

1. Understand Diagnostic Strategies

2. Learn Nuances of GCA

3. Develop Referral Strategy

Diagnosis

1. Possible

2. Probable

3. Prognostic

4. Pragmatic

Optic Nerve Edema

V - Vascular

O - Ophthalmic

I - Inflammatory

C - Compressive

Optic Nerve Edema

Vascular

AION

NAION

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Optic Nerve Edema

Ophthalmic

Drusen

CRVO

Hypotony

Optic Nerve Edema

Inflammatory

Infectious (syphillis, etc)

Non-infectious (collagen vascular)

Optic Neuritis

Optic Nerve Edema

Compressive

Tumor

Graves’ Disease

Chiasmal

Optic Nerve Edema

1. Possible

2. Probable

3. Prognostic

4. Pragmatic

Optic Nerve Edema

1. Possible

2. Probable - based on age

3. Prognostic

4. Pragmatic

Probable

Based on Age

40 and younger -- Optic Neuritis

50-60 -- mostly atypical

60+ -- NAION

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Optic Nerve Edema

1. Possible

2. Probable

3. Prognostic - GCA

4. Pragmatic - GCA

What is GCA?

Immune-Mediated Vasculitis

Focal arteritic lesions Ischemia

Affects medium, large arteries

~18 per 100,000

Rahman, et al. Giant Cell (Temporal) Ateritis: An Overview and Update. Surv Ophthalmol 50:415--428, 2005

What is GCA?

https://goo.gl/images/Tdi5Tr

How does the Temporal Artery connect to the eye?

Why is it so important?

Profound Vision Loss

Bilateral in 14 days in 1/3 if Untreated

Systemic Complications

Treatable

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Ophthalmic

Anterior Ischemic Optic Neuropathy (AION)

Central Retinal Artery Occlusion (CRAO)

Amaurosis Fugax

DiplopiaHayreh SS, et al. Ocular Manifestations of Giant Cell Arteritis. Am J Ophthalmol

1998;125:509-520

Systemic

Headache

Jaw Claudication

Scalp Tenderness

Neck Pain

Anorexia/Weight Loss

A-AION

Sudden, Painless Vision Loss

Amaurosis Fugax

Occurs > 50 years of age

1 out of 10

Management of ischemic optic neuropathiesIndian Journal Ophthal 2011. Vol 59, 2, 123-136


Ocular Symptoms

Vision loss

Amaurosis Fugax

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Amaurosis Fugax

From 7% to 50% of patients with GCA

Hayreh found 30%

In sharp contrast to NAION (2.5%)

Transient ischemia to ONH

Hayreh SS, et al. Ocular Manifestations of Giant Cell Arteritis. Am J Ophthalmol 1998;125:509-52

Hayreh SS, et al. Amaurosis Fugax in Ocular Vascular Occlusive Disorders. Retina 2013;0:1-8

Systemic Symptoms

Jaw Claudication (Odds Ratio 9.0)

Neck Pain (Odds Ratio 3.4)

Anorexia (Odds Ratio 2)

Hayreh SS, et al. Giant Cell Arteritis: Validity and Reliability of Various Diagnostic Criteria. Am J Ophthalmol 1997;123:285-96

Less Predictable

Headache

Fever

Scalp Tenderness

Malaise


Systemic Symptoms

Headache

A-AION - 46% had Headache

NA-AION – 54% had Headache

Could Mislead


Headache

0

22.5

45

67.5

90

112.5

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Average Number of Symptoms = 3

Occult GCA

Between 5 and 38% of cases

No systemic symptoms

Rahman, et al. Giant Cell (Temporal) Arteritis: An Overview and Update. Surv Ophthalmol 50:415--428, 2005

Contralateral Eye

Important for 2 reasons

1. Gives us clues about diagnosis

2. Make sure other eye stays healthy

C/D Ratio

Average C/D in Population = 0.4

Contralateral C/D in NA-AION

• 75% are < 0.3

• 33% are < 0.15

C/D Ratio

A-AION

• <0.3 = 50/725 = 1/15

• >0.4 = 50/275 = 1/5

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C/D Ratio

Some evidence says:

90% of C/D in NA-AION is <0.3

Then…

<0.3 = 50/860 = 1/17

>0.4 = 50/140 = 1/3

Testing

Labs – ESR, CRP, CBC, Platelets

Fluorescein Angiography

Ultrasound, PET, MRI – Limited Benefit

Temporal Artery Biopsy

FA


Labs

ESR

> 33 mm/h

Sensitivity 92%

Specificity 92%


Labs

CRP

> 2.45 mg/dl

Sensitivity 100%

Specificity 82%


Labs

CBC includes

WBC

RBC

Platelets


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ESR + CRP

Sensitivity 100%

Specificity 97%

PlateletsOdds Ratio:

ESR > 47 mm/hr = 1.5

CRP > 2.45 mg/dL = 5.3

Platelets > 400,000/μL = 4.2

All 3 elevated = 8

Walvick MD, Walvick MP. Giant Cell Arteritis: Laboratory Predictors of a Positive Temporal Artery Biopsy. Ophthalmology 2011;118:1201-1204

Additional Testing


Gold Standard

Case by Case

Side Effects

Necrosis, Infection, Nerve Damage

Bilateral?


If case is equivocal

ESR + CRP +

ESR + CRP -

ESR - CRP +

ESR - CRP -

Clinical Picture

Unilateral Optic Disc Edema

Age

Systemic Symptoms

Labs (ESR, CRP, Platelets)

Other Eye


American College of Rheumatology

Need 3 of the following 5

1. Over 50 years of age

2. New onset of Headache

3. Scalp tenderness

4. ESR > 50 mm/h

5. (+) Temporal Artery Biopsy

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American College of Rheumatology

Meeting this criteria yields:

94% Sensitivity

91% Specificity

NOT good enough with swollen optic nerve

Study of ACR Criteria

112 Patients in Neuro-Ophthalmology Clinic

25% with + TAB missed by ACR

28% with - TAB met criteria

Murchison, AP, et al. Am J Ophthalmol 2012;154:722-729

Case

62 Year Old Male

Sudden Vision Loss

Unilateral Optic Nerve Edema

What now?

More Information

More details….

• Other eye = C/D 0.5

• Systemic symptoms = Headache,Neck Pain

• Labs: ESR = 70 mm/h

CRP = 3.2 mg/dl

What If...

More details….

• Other eye = C/D 0.2

• Systemic symptoms = Headache

• Labs: ESR = 20 mm/h

CRP = 0.8 mg/dl

Treatment

Oral Steroid

80-100+ mg

VERY long taper

75% reached 5 mg/day at year

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Treatment

IV Steroid no better

Limited Evidence for Immune Modulators

TNF Blockers

Methotrexate

Clinical Picture

Unilateral Optic Nerve Edema

Systemic Symptoms

Lab Results

Other Eye

Referral

If AION suspect

Labs

Case History

Possible referral

Referral

Ophthalmology

Rheumatology

Neurologist

Urgent!!!

Giant Cell Arteritis

Affects Eyes

ION, CRAO, Diplopia, Amaurosis Fugax

Affects Systemic

Elevated Labs, Symptoms

Emergency!

MR. A

63 y/o White MaleNew onset headache, temporal pain, neck

painNO vision complaints

EOM fullNO APD

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MR. A

Labs

ESR = 56

CRP = 1.37

Pending Temporal Artery Biopsy

MR. A

Started on 40 mg Pred

When he tapers, headaches return

What about vision?

20/70 and VF reduction

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MR. A

When Pred resumed, vision returned to 20/25

Visual Field improved

MR. A

Has been on low dose Prednisone for 4 years!

MR. T

63 Year Old White Male

Presents to ER with vision loss OS

Progressed over the day

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MR. T

20/20 OD

NLP OS

MR. T

Anterior Segment normal

0.2 C/D OD

Edematous OS

MR. T

Scalp Tendernes

NO headache, jaw claudication, neck pain

Intermittent diplopia a month ago

MR. T

ESR = 96 mm/h

CRP = 6.9 mg/dL

MR. T

Admitted and started on IV corticosteroids

Temporal Artery Biopsy +

MR. T

12 years later on 5 mg/day Prednisone

If tapers off, symptoms start OD

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NAION

Sudden, Painless Vision Loss

3/4 Wake up with Vision Loss

Occurs 50+ years of age

9 out of 10

NAION

Systemic Risk Factors

HTNDMNocturnal HypotensionHyperlipidemia

NAION

More common in small optic cup< 0.15 in 33%< 0.3 in 75%

Small C/D NOT primary factor

NAION

“Disk at Risk”

NAION

“Disk at Risk”

Average C/D = 0.4

Incidence NAION = 10 per 100,000

citizen.org

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NAION

20/20 in 33%

> 20/40 in 50%

< 20/200 in 20%

nature.com

Classic VF?

NAION

Treatment?

Referral?

Case

64 Year Old White Male

C/O Blur OD

S/P PCIOL OU

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Case

+DM

+HTN

Only symptoms is neck pain

Case

ESR = 32

CRP = 0.22

Platelets = 180,000

Case

What’s the plan?

Case

Get opinion from Rheumatology

Treated with Corticosteroids

No benefit noted - tapered quickly

Ophthalmic

Hypotony

CRVO

Drusen

Ophthalmic

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Ophthalmic Ophthalmic

Ophthalmic Inflammatory

Infectious vs. noninfectious

MS

Inflammatory

Consider lab work/imaging with:

Age

Systemic health

Symptoms

Inflammatory

Infectious

Spirochete - Syphilis

Viral

Cat scratch

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Syphilis Syphilis

If suspected, it's tertiary

Need to evaluate CSF

Treated with infused antibiotics

Inflammatory

Non-Infectious

Sarcoidosis

Other connective tissue disorders

Optic Neuritis

Consider if 40 years old or younger

1/3 are swollen

2/3 retrobulbar

Optic Neuritis

+APD

92% pain on eye movement

Optic Neuritis

L'hermitte symptom

Uhthoff phenomenon

Numbness/weakness

Tingling

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Optic Neuritis

25% Optic Neuritis initial manifestation of MS

Optic Neuritis

MRI

At 10 years

Overall rate of developing MS was 38%

If no lesions on MRI, risk of MS was 20%

If 1 or more lesion, 56%

Optic Neuritis

MRI

At 15 years

If no lesions on MRI, risk of MS was 25%

If 1 or more lesion, 75%

Optic Neuritis

Treatment - current attack

Steroids

Plasmapheresis

Optic Neuritis

Treatment - prevention

Beta Interferon (Avonex, etc)

Copaxone

Immune suppression - monoclonal antibodies

Optic Neuritis

Treatment

IV steroid followed by oral steroid sped recovery (4 days compared to 15 days)

Reduced recurrence of Multiple Sclerosis by 2 years

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Optic Neuritis

Treatment

Oral steroids alone did not help

Increased recurrence

Optic Neuritis

CHAMPS Trial (Interferon)

50% of placebo progressed to MS in 3 yrs

35% of interferon treated progressed

Optic Neuritis

Referral

Neurology or Neuro-ophthalmology

Order MRI if available

Compressive

Graves’ Orbitopathy

Chiasmal Lesion

Optic Nerve TumorGliomaHemangiomaMeningiomaLymphoma

Graves’ Disease

80% are Hyperthyroid

Sweat, tremor, weight loss

10% are Hypothyroid

Cold, weight gain, hair loss

10% are Euthyroid

Graves’ Disease

30-50% of Graves’ patients have orbitopathy

2-5% serious complications

(Compressive Optic Neuropathy)

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Graves’ Disease

Dry eye

Injection

Eyelid retraction

Diplopia

Compressive Optic Neuropathy

Graves’ Disease

Increase in

Fibroblasts

Hyaluronic Acid

Collagen

Adipose

Orbitopathy

http://www.nature.com/nrendo/journal/v5/n6/images/nrendo.2009.61-f1.jpg

Graves’ DiseaseExophthalmos

Hertel

Asian upper limit = 18

White upper limit = 21

Black upper limit = 24

Graves’ Disease

Free T3 and T4

TSH

Anti-thryoglobulin (TSI)

Thyrotropin-Binding Inhibitory Immunoglobulin (TBII)

Thyroid Peroxidase (TPO)

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Graves’ Disease

Refer to Endocrine

Graves’ Disease

CT allows measurement of

Orbital fat

Lacrimal gland

Extraocular muscles

MRI for serial imaging

Graves’ Disease

Treatment

Quiet inflammation - Steroid

Stabilize Thyroid

Graves’ Disease

Stabilize Thyroid

Medication

Surgery

Radioiodine

Graves’ Disease

Treatment

Ocular Comfort

Prism

Surgery

Graves’ Disease

Surgery

Orbital Decompression

Strabismus

Eyelid

Cataract

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http://thyroideyes.org/resources/Thyroid

Graves’ Disease

Smoking makes disease worse

Smoking makes treatment less effective

Graves’ Disease

50 year old male

Complains of:

Diplopia

Swollen Eyelid OS

Red Eye OS

Exam

20/25 OD and OS

IOP 18/18

No APD

Diplopia in lateral and downgaze

Pain in lateral gaze

Exam

Exophthalmos OS

Hertel 19/23

Lagophthalmos

Conjunctival edema and injection

Eyelid edema

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Labs

TSH = 0.003 (normal = 0.47-5.00)

T4 = 20.3 (normal = 4.5-12)

Referral

Endocrine

Oculoplastics

Inform PCP of findings

5 months later

IOP 18/24

? APD OS

Start IOP Timolol 0.5%

Start Oral Pred (40 mg)

6 months later

IOP as high as 38/28

Oral Pred now 80 mg

+ APD OS

IOP 19/19 on Travatan, Cosopt, Alphagan

Refer for Orbital Decompression

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After Orbital Decompression

Develops Diplopia

But...IOP 12/14 on meds

Last exam

Now S/P:

Orbital Decompression

Strabismus Surgery

Eyelid Retraction

Now has 20/80 cataract

History

72 year old African American male

Blur OD x 3 months

Last eye exam 10 years ago

Ocular History

Mixed Mechanism Glaucoma

S/P LPI OU

Was on Xalatan qhs OU – no longer taking

Blunt trauma OD

Medical History

HTN

Anemia

CVA x 2

Hyperlipidemia

Kidney Disease

Amlodipine

Atenolol

HCTZ

Simvastatin

ASA

ExamBCVA OD: 20/320, OS:

20/25

+APD OD

Anterior Segment Normal

Except Mild NS OU

Gonio: Narrow with old PAS

S/P LPI OU

IOP 14/14

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Posterior SegmentOptic Nerve

0.75 OD - Pallor

0.90 OS

No maculopathy

No vasculopathy

Peripheral retina normal

Pallor Vs. Excavation

Pallor Vs. Excavation

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Differential

Glaucoma

Other Optic Atrophy

Traumatic

Compressive

Inflammatory

What Tests?

VF

OCT

VF - OD

VF - OS New Differential

Glaucoma

Compressive Lesion

CVA

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MRI MRI

Diagnosis

Pituitary Adenoma – 2.5 x 1.6 cm

Treatment

Monitor only

Due to other health factors

Patient reports vision is fine

Treatment

Goals

Normalize hormone levels

Pituitary gland function

Reduce signs/symptoms of tumor

TreatmentMedication (Micro)

Bromocriptine – Dopamine agonist

Hormone stabilization

Surgery (Macro)

Transsphenoidal

Transcranial

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Take Home

Check both eyes

Pituitary vs. Glaucoma

Pallor vs. Excavation

Urgency

Optic Nerve Edema

1. Possible

2. Probable

3. Prognostic

4. Pragmatic

Goals

1. Understand Diagnostic Strategies

2. Learn Nuances of GCA

3. Develop Referral Strategy

Thank You!

[email protected]

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James Kundart OD 6/20/2018

1

MacularCherry-Red Spots:

Causes and Consequences

2018 Victoria ConferenceJames Kundart OD MEd FAAO FCOVD-APacific University College of Optometry

Financial Disclosures: Nothing to Disclose

https://en.wikipedia.org/wiki/Cherry-red_spot

Learning ObjectivesToday, we will explore the varied causes and consequences of cherry red spots on the macula:

1. To cover some congenital and systemic causes behind central retinal artery occlusion (CRAO)

2. To review prevention and treatment of CRAO

3. To explore the varied presentation of the genetically-inherited lysosomal storage diseases, including Tay-Sachs, Niemann-Pick, Gaucher, and Sandhoff diseases

4. To differentially diagnose truaumatic causes of cherry red macular spots, like commotio retinae

Causes of Cherry Red Spots

1. Central Retinal Artery Occlusion

2. Tay-Sachs disease3. Niemann-Pick

disease4. Other Causes

(Gaucher,Commotio Retinae, Sandhoff disease) https://www.ncbi.nlm.nih.gov/

pmc/articles/PMC3864975/

1. CRAO:Diagnosis and Treatment


CRAO: Objective“Cattle Trucking”


CRAO: Fluorescein Angiography


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CRAO: Cilioretinal Artery Sparing with Acute RNFL Defects


CRAO: RNFL Improvement and Fluorescein Angiography


CRAO Triggers: Cataract Surgery Retrobulbar Injection

https://www.ncbi.nlm.nih.gov/pmc/artic

les/PMC5433131/

CRAO Triggers: Cataract Surgery Retrobulbar Injection

https://www.ncbi.nlm.nih.gov/pmc/artic

les/PMC5433131/

CRAO Triggers:Chiropractic Manipulation


CRAO Triggers:Chiropractic Manipulation


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CRAO Triggers:Chung-Strauss Syndrome


CRAO Triggers:Chung-Strauss Syndrome


CRAO Triggers: Pediatric Pneumonia


CRAO Triggers: Pediatric Pneumonia

Chest X-ray showed that two lung markings were increased, the high density lower right lung patchy shadows and a small right-sided pleural effusion at the initial presentation

b Chest X-ray showed that two lung textures were increased, the right lower lung had a high patchy density, and its edge was smooth


CRAO Triggers: Congenital Single Heart Atrium


CRAO DDx: Sickle Cell Anemia


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CRAO DDx:Pseudo-Cherry Red Spot in Dermato-myositis


Preventing and Treating CRAO



2. Tay-Sachs Disease

One of the gangliosides, diseases of sialic acid-containing material found in neural tissue like gray matter

If lysosomes don’t break these down efficiently, they accumulate in the brain and produce a spectrum of disorders, including a cherry-red spot in the macula

But Tay-Sachs disease is simply the most famous of the gangliodisoses

http://en.wikipedia.org/wiki/Tay-Sachs

Tay-Sachs and the Gangliodisoses

Tay-Sachs Disease (TSD), or acute infantile GM2, is often fatal by age 5

It is named for British ophthalmologist Waren Tay and American neurologist Bernard Sachs first described the cellular appearance of the disease in the 1880’s

It has a classic cherry-red macular spot that is pathognomonic in children

http://en.wikipedia.org/wiki/Bernard_Sachshttps://en.wikipedia.org/wiki/Waren_Tay

Tay-Sachs Cherry-Red Spot

The red spot is essentially a choroidal window at the fovea compared to the fatty accumulation elsewhere on the retina

The spot causes poor vision, that leads in turn to poor fixation

Poor fixation commonly results in nystagmus because of larger-than-normal tremors of the eye

Larger-than-normal drifts lead to strabismus as the eye goes to its phoric position in TSD

Classic Cherry Red SpotWright, Figure 7-5A, page 374

Ethnic Predilection and Late-Onset Tay-Sachs

Recessive carriers of Tay-Sachs are found in at least 1 in 30 in each of the following ethnic groups:

Eastern European (Ashkenazi) Jews (eradicated in the US?)

French Canadians

Louisiana Cajuns

Irish Americans have a 1 in 50 chance of being a carrier

In the general population, the incidence of carriers is 1 in 300

http://abcnews.go.com/Health/parent-carrier-test-eliminate-scourge-rare-childhood-diseases/story?id=12632510

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Other Clinical Signs of Tay-Sachs

Dymyelination of optic nerve, chiasm and tracts

Optic atrophy

Progressive loss of vision

Blindness by age 2

Flatline VEP early, with normal ERG late

Oculomotor ataxiaDegenerated Cherry Red SpotWright, Figure 7-5B, page 374

Stalling Saccades in Tay-Sachs Disease

Leigh & Zee, 4th ed.Tay-Sachs.mpghttp://en.wikipedia.org/wiki/Tay-Sachs

Bottom Line on Tay-Sachs

Some of these metabolic disorders are always fatal, others are not

All are autosomal recessive, meaning both the children of carrier parents are carriers themselves

The full disease in this family of conditions penetrate as often as about 1 in 4 of certain populations

Tear enzyme assay someday?

http://www.slideshare.net/aggabriel1/tay-sachs-disease-32430703

3. Niemann-Pick Disease

This loosely-knit group of metabolic diseases are characterized by abnormal accumulation of fats and cholesterol in visceral and neural tissue

This autosomal recessive disease happens due to missing enzymes to break down body fats which accumulate in the spleen, liver, and eyes

There are three identified types: Types A and B are caused by

lipid buildup in myelin sheaths of nerve cells

Type C is caused by cholesterol accumulation

http://imagebank.asrs.org/file/8651/niemann-pick-disease-type-b

Diangosing Niemann-Pick Disease (NPD – VIDEO)

Preschool children with NPD Type A first show “failure to thrive”

Next comes progressive vision loss and neurological deterioration

As in Tay-Sachs disease, NPD is characterized by cherry-red macular spots and eye movement disorders (shown here)

Niemann-Pick Saccades video from Leigh & Zee, 4th edition

http://bcove.me/oe9bo2r6

The Five Known Types ofNiemann-Pick Disease

The ophthalmic hallmark of NPD Type C is progressive supranuclearvertical gaze palsy

Look for hard blinks and head thrusts with vertical eye movements especially

Oculomotor and other striated muscle ataxia is common, as are learning disabilties https://www.epgonline.org/images/niemann-pick/2487.jpg

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Other Ocular Manifestations of Niemann-Pick Disease, Type A

Mild corneal haze

Fine lenticular deposits

Cherry-red spot (50%)

Retinal “haze” that extends far beyond the fovea

Central vision loss, occurring later in the disease (age 2)


Niemann-Pick Disease: Type B vs. Type C

Type B is mostly respiratory, has less neurological involvement, and survival into adulthood

Expect orbital congestion due to increased orbital fat

A macular halo may be seen instead of a red spot in Type B

Not usually associated with vision loss (normal BCVA)

In Type C, cholesterol-laden “foam cells” accumulate, classically leading to:

Hepatosphenomegaly, all starting in late childhood

Progressive dementia or intellectual disability

Ataxia

Dystonia

Vertical gaze paresis

CNS Effects of Types B and C Niemann-Pick Disease

In type B, patients can develop psychosis due to accumulation of myelin in the central nervous system

Since Type B patients survive well into adulthood, when these mental health disorders emerge, they have to be managed, sometimes surgically

Seen here is the loss of gray matter in the brain of a Niemann-Pick Type C patient

https://neurowiki2012.wikispaces.com/Niemann-Pick+Disease

Signs and Symptoms of Niemann-Pick Disease, Type C

In terms of eye effects, you can expect at least 4 out of 5 Niemann-Pick patients to exhibit: Oculomotor ataxia Vertical gaze palsy Learning disabilities and

visual-perceptual problems Some have mental health

concerns

https://neurowiki2012.wikispaces.com/Niemann-Pick+Disease

Treatments for Niemann-Pick Disease

Like Tay-Sachs, there is currently no known treatment for any of the three types of Niemann-Pick

Types B and C have much greater longevity, and may be managed pharmacologically or surgically in some cases

These diseases can be slowly progressive and take a while to diagnose


4. Other LysosomalStorage Diseases


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Other Causes of Macular Cherry Red Spots

Gaucher disease

Trauma (CommotioRetinae)

Sandhoff disease

Others: Sialidosis

https://youtu.be/7zmbMMOZMG0

Other Causes of Cherry Red Spots: Guacher Disease


Other Causes of Cherry Red Spots: Guacher Disease


Other Causes of Cherry Red Spots: Commotio Retinae


Other Causes of Cherry Red Spots: Commotio Retinae


Other Causes of Cherry Red Spots: Sandhoff Disease

“Sandhoff disease symptoms are clinically indeterminable from Tay-Sachs

There are three types of Sandhoff disease: classic infantile, juvenile, and adult late onset”

https://ekjo.org/DOIx.php?id=10.3341/kjo.2005.19.1.68

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Other Causes of Cherry Red Spots: Sandhoff Disease

https://ekjo.org/DOIx.php?id=10.3341/kjo.2005.19.1.68

Other Causes of Cherry Red Spots: Sialidosis

A 53-year-old man, with non-consanguineous parents, presented to our hospital with a history of progressive decrease of visual acuity since the age of 26

At 36, he developed generalized myoclonus and ataxic gait

He showed low visual acuity, ataxic gait, dysarthria and difficulty in writing






Summary: Cherry Red Spots


Questions? Thank You!James Kundart OD

MEd FAAO FCOVD-A

Professor, Pacific University College of

Optometry

3D Performance Clinic

[email protected]

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Readings and ReferencesFor more

information on Niemann-Pick and Tay-Sachs diseases, see chapter 7 of Wright’s Handbook of Pediatric Eye and Systemic Disease

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5/10/2018

1

Recognizing“Red Flag”Headaches

Leland Carr, O.D.Oklahoma College of Optometry

Northeastern State [email protected]

Various Classification Systems

• Vascular Headache

• Myogenic H.A. (“muscle contraction”, “muscle tension”)

• Cervicogenic H.A.

• Tractional H.A.

• Inflammatory H.A.

Source 2

• Tension H.A.

• Migraine H.A.

• Ictal H.A.

• “Brain Freeze” H.A.

• Thunderclap H.A.

• Vascular H.A.

• Coital Cephalgia

• Sinus H.A.

• Rebound H.A.

• Red Wine H.A.

International Classification of Headache Disorders, 2nd ed.

(ICHD-II)

-- International Headache Society-- Cephalgia. 2004;24:1-160

“Any good references, Doc?”

• CEPHALGIA– Journal

– Online

PRIMARY vs. SECONDARY H.A.’s

• PRIMARY– USUALLY “safe”

– Principally NEUROCHEMICAL cause

• SECONDARY– MAY indicate a significant problem

– Associated with “pulling”, “pushing”, inflammation, or ischemiaof a Pain-sensitive structure

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Most Headaches are Harmless

• Most headaches are self-limiting

• Most headaches remain “idiopathic”

• Most headache sufferers get more thanone form of headache

BEWARE !!!!!

…..BUT I NEVER, EVER HAD A HEADACHE LIKE THIS ONE BEFORE…..

BEWARE !!!!!…..AND ALONG WITH MY HEADACHE (XXX) ISN’T

WORKING RIGHT, OR (YYY) HAS STARTED TO HAPPEN

TO ME…..”

The “Pearls”

• “….Headache by itself tells you nothing….”• “What is the company that headache is

keeping????”

• “What else is going on????”

Assessing Severity

• “Scale of 1 to 10…..”

• What Can’t You Do Because of thisHeadache?

• NOT USEFUL: “Do you get relief fromover-the-counter pain medications?”

New Form of Headache

• In elderly patients….R/O CRANIAL ARTERITIS

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Quiz:

The most important assessment for an

Optometrist to make on a Headache patient is?

Examine the Eye(s) !!!!!

• OD and OS

• OU

• The Oculo-Cranial Nerves

RED FLAG!

• Very recent onset…

• Acutely explosive pain…

• Intense, “Thunderclap-like…”

• “Unlike anything ever before…”– Check Pupils!

– Check Motilities?

– Check Vitreous?

Quiz 2

List the Cranial Nerves most often affected by elevations

in Intracranial Pressure (elevated C.S.F. pressure)

• C#2

• C#3

• C#6

• C#8

Mechanism of Headache

P

A

I

N

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Mechanism of Primary Headaches

P

A

I

N

Mechanism of Secondary Headaches

P

A

I

N

Primary Headache’s Componants

• Neurochemical

• Neurovascular

• Vascular

Tension-type

Migraine

Cluster

CLINICAL EVALUATIONof the Headache Patient

#1: “The History is Where It’s At” J. Lawton Smith, MD

#2: Ancillary Testing is Indicated for All Suspected Secondary Headache Cases

#3: Imaging Studies are considered Standard Level of Care in most areas MINIMUM: CT of the Head without enhancement

#4: Blood Tests are considered Standard Level of Care in most areas ESPECIALLY FOR PATIENTS OVER AGE 50!!!

“Pearls” for H.A. Workups• Check blood pressure in ALL cases• H.A. or Face Pain is Giant Cell Arteritis in all

patients > 50…..until proven otherwise!• Ocular evaluation should always include:

- assessment of corneal sensitivites- IOP- gonioscopy- evaluation for cell&flare- careful assessment of both optic nerves

-- always look for spontaneousvenous pulsations

What About Visual Fields?????

• Sometimes helpful; Oftentimes not

• If you run them---make them simple

• They never finalize a lesion’s location/They are not a substitute for imaging

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QUIZ: What % of Headache Patients have normal Visual Fields on initial fields

testing?

A. Less than 25%B. 25 – 49%C. 50 – 74%D. 75 – 90%

QUIZ: What % of Brain Tumors become associated with Visual Field defects at some point during their

development?

A. Less than 10%B. 20 – 30%C. 40 – 50%D. 75 – 85%

Always Check Pupils

• “Blown” Neurologic Pupil

• Sudden-onset, painful, Horner’s Pupil

Always Check Motilities

• Large Amplitude, Rapid Horizontal Saccades– ABductional ability of each eye (6th nerve)

– ADductional ability of each eye (3rd nerve & M.L.F.)

• Test horizontal gaze ADduction

• Test convergence ADduction

Try to determine Temperature

• Thermometer

• Patient’s Report– Signs & Symptoms

Check Neck Flexibility

• “Very Stiff and Painful” = Need to Rule-out:– Neck trauma

– Meningitis

– Subarachnoid Hemorrhage

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Palpate Temporal Arteries(if cranial arteritis not ruled-out)

• Swollen?• Hard?• Tender?

“Hurt to comb your hair?”“Sore at base of head?”“Jaw claudication?”“Unexpected weight loss?”“Night sweats?”

Additional Testing(when the Hx says, “Keep looking”)

- All Highly Acute Presentations

- All Rapidly Progressing Cases

- All Cases of Disc Edema

- All Cases with Neurologic Findings

Blood Tests

• Complete Blood Count with Differential

• Platelet Count

• Erythrocyte Sedimentation Rate

• C-reactive Protein

• Serum Fibrinogen (?)

May want to add:

• Tick Panel

• Sickle Cell Test

• Drug Screen – Blood

• Urine Toxicology

CT Scan of the Head

• 1st: WITHOUT contrast– Best for “fresh blood”

– Best for hydrocephalus

• 2nd: WITH contrast– Enhances soft tissue lesions

– Recommend obtainingblood urea nitrogen andserum creatinine tests in“at risk” kidney patients!!!

MRI of the Brain (and orbits?)

• What sequence to order???– MRI-brain, Stroke Protocol– MRI-brain, Parenchymal Study– MRI-brain, Vascular Study– MRI-brain, Cranial Nerve (#) Emphasis– T-1 with Fat Suppression

for orbital exam– T-2 with FLAIR

for exam of periventriculartissues (vital in M.S. workup)

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Lumbar Puncture

• Cerebrospinal fluid opening pressure

• With C.S.F. Analysis

KEYPOINT:Imaging indicated prior

to Punctures!!!!

r/o INTRACRANIAL MASSES

r/o ARNOLD-CHIARI SYNDROME

Brain & Neck M.R.A.

• When arterial lesions are suspected, but M.R.I.-brain was negative/inconclusive

• Brain & Neck M.R.V. indicated if venous disease is suspected– Differentiating Indiopathic Intracranial

Hypertension from Cerebral Venous Thrombosis

Well-guided Referral

• Neurologist

• Neurosurgeon

• Neuro-ophthalmologist

• Family Practice Physician– Comprehensive physical exam

– No “frightening findings”

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The Critical Clinical Tool:

CASEHISTORY

“What Else is Going On?”• Any Triggering Events?

• Any Trigger Points?

• Other Painful Areas

• Changes in Head or Body Functions?

• NAUSEA? VOMITING?

• CHANGES IN VISION?

Many Migraine PatientsDemonstrate

RAYNAUD’S PHENOMINON

The “Big Three”

• MODE of Onset– Sudden, Acute vs. Progressive

– Sudden “Explosion” vs. Prolonged Buildup

• WHEN & HOW 1ST Noticed– Initial features

• TIMELINE (Progression over Time)– Episodic & Intermittent vs. Constant

The Useful “Fourth”

• INTENSITY

–“How bad on a scale of 1-10?”

–“How disruptive is it?”

–“What can’t you do becauseof your headache? (Face pain,eye pain, etc.)

Helpful “Fifth”

• CONSTANT vs. INTERMITTENT

– “How long does each attack last?”

– “How long is each episode?”

– “Are the attacks Similar orDifferent?”

– “Do you know when an attack iscoming on?”

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Other Useful Questions

• Experiencing Visual Phenomina?

• Light Sensitivity?

• Odor Sensitivity?

• Sensitive to Noise/Sounds?

• Any Ringing in the Ears?

Treatments Tried?

• Did they work?

• Do they still work?

• Who prescribed them?

REBOUND HEADACHE

• “Medication Overuse (MOU) Headache”

• May involve Addiction

• Does involve Dependency

• MANAGEMENT– Patient education

– Do NOT “cold turkey”

– DO Taper off…..

RED FLAG!

• Very recent onset…

• Acutely explosive pain…

• Intense, “Thunderclap-like…”

• “Unlike anything ever before…”– Check Pupils!

– Check Motilities?

– Check Vitreous?

RED FLAGS!

• HEADACHE + NECK PAIN + SHOULDER PAIN + STIFF NECK

• HEADACHE/FACE PAIN + SHOULDER PAIN + ARM PAIN + HEAVY SWEATING

• SUDDEN-ONSET, HYPER-INTENSE “THUNDERCLAP” HEADACHE (especially following a valsalva manuever”

RED FLAGS!

• HEADACHES ASSOCIATED WITH SEIZURES or FOCAL SEIZURES

• HEADACHES ASSOCIATED WITH LOSS OF CONSCIOUSNESS or WITH CONFUSION

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Ictal Headaches• “Headache Associated with Seizures”• Rarely occur simultaneously

– Pre-ictal HA– Post-ictal HA

• Intensity varies by patient,and by episode

• Some patients experience hallucinations– Unusual thoughts– Unusual sensations– “Neurological Aura”

Orange-Red Flag!

• Steadily building…

• Increasing intensity…

• Steadily progressing…

• Steadily more intrusive…

• “Started several days (or weeks)ago…relentless. Just won’t stop.”

Yellow Flag

• Episodic pain…

• Definite pain-free intervals…

• “Has been going on for awhile…”

• Stereotypical for that patient

Post-Migraine Headache

• Exhaustion

• Mood Alteration

• Cognitive Alteration

Usually resolves in 24-48 hours

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Coatings and Treatments and Agents Oh My!

Beth Kinoshita, OD, FAAO 2043 College Way

Forest Grove, OR 97116 503-352-3140

[email protected]

Course Description The course will review the state of the contact lens industry and how contact lens dropout affects the growth of the contact lens modality. Minimizing contact lens discomfort may be key in reducing dropout rates. The role of contact lens treatments and coating will be explored to see if this may be the key to keeping patients comfortable in contact lenses. Course Leaning Objectives After participating in this course, the participant should be able to:

• Be familiar with the growth and dropout rates in the different contact lens modalities • Understand the role of contact lens dropout and what fit and material factors may

contribute to dropout • Understand coefficient of friction and how the industry is trying to improve contact lens

discomfort • Be familiar with how lens care products may help or hinder the comfort of a contact lens • Understand the distinction between plasma treatment and a true coating of a contact lens

Course Outline

• State of the Industry o 40.9 million Americans (16.7% of the US adult population) wear contact

lenses o Soft contact lens (SCL) market is growing o US CL market $2.7 billion

Steady growth but slowing? o Contact lens wearers make up 36% of a typical practice

Gross revenue: 32% Net Profit: 27%

o The CL industry is healthy Most practitioners (67%) believe that CL will grow in their practice

o What are we fitting? Soft contact lenses: 88% Gas permeable: 9% Other: 3%

o Replacement Schedule • Dropout

o A sustained or permanent discontinuation of CL wear o New fits = 29% o Mean dropout in the USA ~16% o Higher in other parts of the world

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o Improvingo Primary reason for discontinuing wear is discomfort

• A Contact Lens and The Eyeo A well fit soft contact lenso The average eyelid

• Soft Contact Lenseso Materials

29% Hydrogel 71% Silicone hydrogel

o Hydrogel (polyhydroxyethylmethacrylate or pHEMA) Start as a cured, hard plastic lens that absorbs water and forms a soft,

flexible material Oxygen permeability dependent on the water content

o Silicone hydrogel Combines hydrogel monomers with silicone Oxygen permeability dependent on the silicone content

• Interactions of the CL and the Eyeo Lid

Lid Wiper Epitheliopathy Contact Lens Papillary Conjunctivitis

o Cornea Epithelial Stromal – edema Endothelial changes – Morphologic and density changes

o Conjunctiva Bulbar

• What Is CL Discomforto Difficult to defineo Lack of clinical signs that correspond with symptomso No pre-existing dry eye conditiono Approximately 50% of CL wearerso TFOS Definition

A condition characterized by episodic or persistent adverse ocularsensations related to lens wear, either with or without visualdisturbance, resulting from reduced compatibility between the contactlens and the ocular environment, which can lead to decreasing wearingtime and discontinuation of contact lens wear.

o Multifactorialo Symptomso Identifying the Problem

Contact lens related Patient related Environmental

• Contact Lens Relatedo Coefficient of friction*o Oxygen permeability

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o Wettability o Surface modification o Modulus o Dehydration o Replacement frequency o Design o Thickness o Edge design

• Contact Lens Related o Improved comfort with…

Low water content More frequent replacement Thin designs Thin, tapered edges Less lens movement on blink

o Deposits Active lysozymes (major tear protein) had a significant positive

correlation with subjective comfort Tear dried material can change the friction force

o Coefficient of Friction Force that prevents one surface from sliding over another Tribology

• Microtribometer • Atomic force microscopy method • Inclined plane method • Finger lubricity method

Factors impacting measurements • Substrate choice – should mimic the chemistry, roughness and

softness of the ocular surface • Dynamic contact • Force pressure • Sliding speed – generally test at a lower speed (CoF is usually

highest) • Sample preparation • Lubrication fluid – try to mimic the tears but no standard

composition Lubricity

• Visual acuity • Physiological • Treat the lens • Submerge the lens

o Treat the Lens Silicone hydrogel naturally hydrophobic

• Surface treatment – gas plasma technique o Plasma coating (25nm) – N&D

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o Plasma oxidation - PVo Plasma coating + oxidation - Miru

• Internal wetting agent• Inherent lens properties - Biofinity

o Bind to water moleculeso Submerge the Lens

Lens Care Products• Preservative – increases disinfection efficacy• Surfactant – improve cleaning• Viscosity – buffer the ocular tissue from the preservative and

surfactant• MPS vs. H2O2

Poor compliance• Compliance - Replacement Schedule• Compliance – Lens Care Products• What LCP are we recommending?

o Topping offo Rub vs. No Rub

• Patient relatedo Non-modifiableo Modifiable?

• Environmentalo Few well controlled studieso Low humidity (RH <30%)o Low humidity + Temperatureo Wind and airflow – exacerbate evaporationo Occupation

• The Eye or the Lens?o Effects of Three Interventions on Contact Lens Comfort in Symptomatic

Wearers: A RCT (Navascues-Cornago 2015) Three interventions after 5 hours of CL wear None of the interventions had a meaningful impact on end-of-day

comfort• Plasma Treatment

o Gas permeable lenseso Not a coatingo Front surface of the lens is sterilized via exposure to cold plasma gas in a

reaction chamber Removes all residue = clean and wettable lens surface

o Improved initial comfort Wears out with time Avoid abrasive cleaners

• A True Coatingo Hydra-PEG (Ocular Dynamics – Menlo Park, CA)o Tear Film

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Lubricates, moisturizes, oxygenates, cleans and protects the ocular surface

Mucin o Hydra-PEG Study

Habitual SCL wearers with self-reported symptoms of CLD • Contact Lens Comfort

o Personalize prescribing o Innovations in the area of material, design, lens care o Novel approaches to contact lens comfort

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Rethinking GonioscopyFundamentals and Future Tech

Anthony DeWilde, O.D.

Goals

Misconceptions about angle closure

Prognosis/Treatment

New Technology

Indications

Elevated IOP

Asymmetric IOP

Vascular

CRVO, DM, OIS

Trauma

Every Glaucoma patient!!

Indications

Every Glaucoma patient!!

Role of IOP = assess risk

Role of gonioscopy = determine treatment

Contraindications

Hyphema?

Open Globe

Compromised Cornea

Underutilized

Only 50% of Glaucoma patients have gonio recorded

74% of referred patients had no angle status

Am J Ophthalmol 2018;188:16–29

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Underutilized

Don’t understand value

Difficult to handle equipment

Difficult to interpret

Subacute

Most primary angle closure is subacute

Spend months to years asymptomatic

May not catch during exam

Acute closure is uncommon

Risk of closure

Wilensky. AJO 115:338-346. March 1993

90%

9% 1%0%

Not all angle closure is acute

Not all acute glaucoma is angle closure

Not all angle closure is acute

Most is subacute

Not all acute glaucoma is angle closure

Rubeosis

Uveitis

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Difficult

Technically difficult to handle

Practice

Few good references

gonioscopy.org

eyecalcs.com

Difficult

assconnection.s3.amazonaws.com/703/flashcards/1084703/jpg/gonioscopy-exam132643198565

http://biomechanical.asmedigitalcollection.asme.org/data/Journals/JBENDY/27152/036004jby1.jpeg

How Do Angles Close? How Do Angles Close?

Risk Factors

Age

Race (Asian, Eskimo)

Shorter Axial Length

Shallow Anterior Chamber

Lens

Accuracy

Classify type of glaucoma

Leads to better treatment

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Accuracy

POAG

NTG

Angle Closure

Rubeotic

Uveitic

Pigmentary/Pseudoexfoliation

Accuracy

Many different methods

Van Herrick

Shaffer

Spaeth

Accuracy

Many different methods

Van Herrick

Shaffer

Spaeth

Why Change?

Gonioscopy should grade occludability

Why Change?

Spaeth tells us

Occludability

Relationship of Iris to TM

Easier to monitor for change

Spaeth Method

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Spaeth Method

Normal Angle - Video

Video from gonioscopy.org - Used with written permission

Spaeth Method

eyecalcs.com

Angle of Insertion

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Steep or Regular Steep or Regular

TM – Iris Relationship

Go to most narrow angle

A = Anterior to TM

B = Behind TM

C = Scleral Spur

D = Deep (Ciliary Body)

E = Very Deep

Compression

If angle is narrow, may need compression

How far back does it go?

Check for PAS

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Compression

Compression Gonioscopy - Video

Video from gonioscopy.org - Used with written permission eyecalcs.com

Occludable

Who is occludable?

30 and 40 are not

10 and 20 are

Not all occludable angles will occlude

Who needs treatment?

No controlled clinical trials

Not everyone needs treatment

Only 10% of occludable angles

Who needs treatment?

Increased IOP

ONH and/or VF progression

PAS - current or aborted

Symptoms

Other eye

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Provocative Tests

Dark Room

Water

Dilation

Prone

Provocative Tests

All test suffer from

Poor specificity

Tedious

Provocative Tests

Dark Room

Gonio (after 1.5 hours)

66% sensitivity

80% specificity

Provocative Tests

Dark Room

OCT (after 3 minutes)

90% sensitivity

57% specificity

J Glaucoma 2012 Mar;21(3):155-9

Provocative Tests

Friedman - AJO 1972

Sensitivity

Dark room 48%

Prone 71%

Pharmacologic 58%

Provocative Tests

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Treatment

Laser Peripheral Iridotomy

Argon Laser Iridoplasty

Cataract Surgery

Acute Treatment

Diamox not fast enough

Isosorbide and Osmoglyn not available

Paracentesis

Cannot do this if angle is narrow

Acute Treatment

Meds!

Consider Iopidine

Acute Treatment

Cornea is edematous

- Underestimate by as much as 20%

If cornea is clearing, IOP is improving

Acute Treatment Quigley

Two factors influence risk of closure

Iris proximity to TM

Iris volume

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Quigley

Possible mechanisms:

Iris volume increase on dilation

Choroidal expansion

Advanced Tech

Ultrasound Biomicroscopy (UBM)

Scheimpflug photography

Anterior Segment OCT (ASOCT)

Ophthalmology 2013;120:1985-1997

Advanced Tech

Benefits

Good visualization of angle

Documentation

Patient education

UBM

Similar to B-Scan

Uses higher frequency

Images anterior segment

UBM

Pros

Quantitative/Qualitative view of ACA

Correlates well with gonioscopy

Plateau Iris

Confirm efficacy of LPI

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UBM

Cons

Best imaging requires coupling with eye bath

Inconvenient

May be difficult to interpret

Scheimpflug

Anterior Segment images from slit lamp

Noncontact optical system

Common system is Pentacam

Scheimpflug Scheimpflug

Pros

Inexpensive

Good correlation with gonioscopy

Scheimpflug

Cons

Not as good as OCT or UBM

No view of angle structures

ASOCT

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OCT

Objective measures

Iris curvature

Lens vault

Iris volume

Anterior chamber depth

Anterior chamber width

OCT

OCT

Pros

Can do in dark room

Good sensitivity

Many doctors familiar with OCT

OCT

Pros

Good visualization - even with corneal pathology

Good on uncooperative patients

OCT

Con

May overestimate risk

Questionable specificity

Cannot visualize behind iris

OCT

Con

Uses scleral spur as landmark, not TM

Cost

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ASOCT

Am J Ophthalmol 2018;188:16–29

Imaging

All technology is a complement to gonio

Cannot visualize angle as well as gonio

Cannot compress

Imaging

Need prospective trials

LPI vs Monitoring

None can predict which angles close

[email protected]

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James Kundart OD MEd FAAO FCOVD-A 5/28/18

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Eclipses, Climate Change, and the Eye2018 Victoria Conference

Pacific University


Focus Questions1. What are the functions of carotenoids in the body, and where can

they be found in the diet?2. What are the functions of flavinoids in the body, and where can

they be found in the diet?3. What are the functions of phytopigments in the body, and where

can they be found in the diet?4. What are the main ocular manifestations of subclinical vitamin C

deficiencies?5. What are the best dietary sources of vitamin C?

Solar Keratopathy: Subjective

Solar Keratopathy: Objective

Solar Keratopathy: Assessment

Solar Keratopathy: Plan

Solar Retinopathy: Subjective

Solar Retinopathy: Objective

Solar Retinopathy: Assessment

Solar Retinopathy: Plan

Antioxidants You Should Know: Beta Carotene

Beta Carotene Is NOT Found in the Retina¡ ”It is unlikely that the AREDS I benefit was related to β-carotene since it is not present in the retina!¡Supplementation of male smokers in Finland with 20 mg/day of β-carotene for six years did not decrease the risk of AMD compared to placebo¡A placebo-controlled trial in a cohort of 22,071 healthy US men

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to placebo¡A placebo-controlled trial in a cohort of 22,071 healthy US men found that β-carotene supplementation (50 mg every other day) had no effect on the incidence of age-related maculopathy — an early stage of AMD¡Recent systematic reviews of randomized controlled trials have concluded that there is no evidence that β-carotene supplementation prevents or delays the onset of AMD”

Beta Carotene and Smoking

Antioxidants You Should Know: Lutein¡Lutein belongs to a class of oxygenated derivatives of carotenes called xanthophylls (Eperjesi, page 92)¡This fat-soluble colored pigment gives the macula lutea its name, and it absorbs light best below 500 nm¡It is also found in the lens, and may prevent cataracts¡It is the most heat-stable of the carotenoids¡The food with the highest concentration of lutein is maize, or Indian corn (60 mol%, Eperjesi, page 93)¡However, corn is also high in omega-6 fatty acids, that are essential to the diet, but pro-inflammatory

Antioxidants You Should Know: Zeaxanthin¡The typical western diet contains seven times more lutein than zeaxanthin, BUT…¡Zeaxanthin predominates over lutein in the macula 2:1 (Eperjesi, page 95). Why?¡Maximum light absorption for zeaxanthin is above 500 nm. What is the peak of the macular cones?¡The food with the highest concentration of zeaxanthin is orange peppers (37 mol%, Eperjesi, page 93)

Food Sources of Carotenoids

Antioxidants You Should Know: Lycopene¡Lycopene is a pigment that gives vegetables and fruits their red color•Examples: tomatoes, pink grapefruit and watermelon

• Recent meta-analyses of observational studies reportedan inverse association between blood lycopene concentration and risk of developing prostate cancer. To date, most small-

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an inverse association between blood lycopene concentration and risk of developing prostate cancer. To date, most small-scale intervention studies found little-to-no benefit of lycopene supplements in reducing incidence or severity of prostate cancer in high-risk patients

Lycopene and Inflammation

Lycopene in

Retinal Re-Attachment

Lycopene in

Common Foods

The Universal Antioxidant: Vitamin C

• We are one of the few mammals that cannot produce our ownvitamin C (ascorbic acid)

• We get vitamin C from our diet alone, by active transport fromthe small gut to end up in whte blood cells

• Ascorbic acid is 70-90% absorbed through diet, but only 50%absorbed from megadose (1g) supplements

• Note that the corneal epithelium has the highest concentration ofvitamin C in the body, with the lens coming in fifth

Vitamin C Concentration

in Human Tissues

Semba, Table 9-2, page 374

What are the Functions of Vitamin C?

Vitamin C is vital in the synthesis of the following:

1. Collagen2. Cephalosporin3. Norepinephrine4. Oxytocin5. Tyrosine and pyridine6. Vasopressin

How Much Vitamin C is Needed?

See Semba, Table 9-3, page 375

• The RDA for prevention of scurvy in adult males is only 90 mg ofvitamin C daily

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• The RDA for prevention of scurvy in adult males is only 90 mg ofvitamin C daily

• To prevent chronic disease, much higher doses are needed• For example, the AREDS I dose was 500 mg

Recommended Dietary Allowance (RDA) for Vitamin Chttp://lpi.oregonstate.edu/infocenter/vitamins/vitaminC/

Where Is Vitamin Cin the Diet?See Semba, Table 9-1, page 373• Generally, colorful fresh fruits and vegetables are the bestsources

• Supplements often get vitamin C from rose hips (pictured)• Meats and dairy products have little to no vitamin C, which is whysailors came down with scurvy in the days before refrigeration

Dietary Sources of Vitamin Chttp://lpi.oregonstate.edu/infocenter/vitamins/vitaminC/

Clinical Manifestations of Vitamin C Deficiency1. Hematoma2. Exophthalmos3. Corneal edema4. Corneal ulceration5. Cataract6. Retinal phototoxicity

7. Vitamin C Deficiencyand Hematoma¡“The marks on her forehead are from being handled in the hospital, probably from a hemorrhagic disease and the skin eruptions are consistent with a condition in Barlow's disease (infantile scurvy) where blood pools under the skin and then sores erupt on the surface, called "extravasation" and form poorly healing skin ulcers, but they also look like cold sores and could be from a blood infection following a Hep B vaccination forced on the family at birth.”

2. Vitamin C Deficiencyand Exophthalmos

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and Exophthalmos

3. Vitamin C Deficiencyand Corneal Edema• Semba says that human tears contain higher concentrations of

vitamin C than plasma (665 micromol/L), or about 150 times

more than blood plasma

• This probably has to do with its important role in collagen

synthesis

• Aqueous ascorbic acid levels are 20-25 times higher than blood

plasma

4. Vitamin C Deficiencyand Corneal Ulceration• Which tissue has the highest vitamin C concentration? See slide

27! ___________________

• Because ascorbic acid helps active transport to mitochondria, a

deficiency slows corneal wound healing

• Thus, corneal ulcers can result from vitamin C deficiency!

5. Vitamin C Deficiencyand Cataract • Cataracts are not associated with scurvy, because it’s an acute

condition

• But chronic vitamin C deficiency can lead to cataracts. How?

• It serves as a UV filter

• It protects the lens from oxidative stress

6. Vitamin C DeficiencyRetinal Phototoxicity• Semba says that vitamin C may protect the retina from

phototoxicity

• Healthy retinas show concentrations of vitamin C twenty times

higher than the plasma

• With UV and short-wavelength visible light exposure, oxygen free

radicals are released and can cause oxidative damage

• Vitamin C can reverse this damage

What are the Side Effects of Excess Vitamin C?• Those who are not accustomed to vitamin C can get diarrhea

from even small doses

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• Those who are not accustomed to vitamin C can get diarrheafrom even small doses

• However, tolerance to higher doses can be achieved if they areconsumed regularly

• For instance, Nobel Laureate Dr. Linus Pauling believed that 2grams of vitamin C per day were vital for health and long life

Adverse Effects of Vitamin C

Vitamin C in Diurnal vs. Nocturnal Mammals

Vitamin C and Nonheme Iron¡ “Vitamin C strongly enhances the absorption of nonheme iron by

reducing dietary ferric iron (Fe3+) to ferrous iron (Fe2+) and forming an absorbable, iron-ascorbic acid complex

¡ Polyphenolic compounds in coffee, black tea, and herbal tea can markedly inhibit the absorption of nonheme iron. This effect may be reduced by the presence of vitamin C”

Vitamin C and Iron

¡ Enhancers of nonheme iron absortion include vitamin C ¡ Vitamin C strongly enhances the absorption of nonheme iron by

reducing dietary ferric iron (Fe3+) to ferrous iron (Fe2+) and forming an absorbable iron-ascorbic acid complex

¡ Other organic acids: Citric, malic, tartaric, and lactic acids have some enhancing effects on nonheme iron absorption”

Iron and Vitamin C¡ Vitamin C strongly enhances the absorption of nonheme iron by

reducing dietary ferric iron (Fe3+) to ferrous iron (Fe2+) and forming an absorbable iron-ascorbic acid complex

Potatoes and Vitamin Chttp://www.potato2008.org/en/potato/factsheets.html

The Antioxidant Catalyst, Zinc• While there is no specific zinc stores in the body, is is found in

higher concentrations in some tissues than others• Most is found in skeletal muscle, bone and the central nervous

system• There is also a high amount in the pancreas, liver and spleen,

with rapid turnover

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• There is also a high amount in the pancreas, liver and spleen,with rapid turnover

• However, the highest concentration of zinc is in the choroid andretina

Zinc in Human TissuesSemba, Table 8-2, page 358

What are the Functions of Zinc?Zinc serves many purposes in the eye:• It is found in the plasma membranes of the photoreceptors• It responds to photons in the all-trans to 11-cis transformation of

retinol• It catalyzes vitamin A and taurine metabolism• It modulates synaptic transmission

Functions of Zinc in the RetinaSemba, figure 8-1, page 359

How Much Zinc is Needed?¡ Zinc requirements generally increase with body mass¡ They are generally higher in men than women, except in

pregnancy¡ Lactating women generally have higher needs for zinc, BUT…¡ Pregnant men require MUCH more zinc but are, fortunately, rare

Recommended Dietary Allowances (RDA) for Zinc

Where Is Zinc in the Diet?• Because zinc is found in high concentrations in skeletal muscle,

it makes sense that it would be found in dark meats• White meats are fattier and like all unpigmented foods, lower in

nutrients• Other high protein foods like dairy products, beans and nuts also

have zinc in moderate amounts• Zinc intake should be increased in patients with AMD, as shown

by AREDS I

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by AREDS I

Dietary Sources of Zincsee also Semba, Table 8-1, page 357

Clinical Manifestations of Zinc DeficiencySemba, table 8-4, page 362

Acrodermatitis Enteropathica• Literally, “dry skin of the extremities”• In the eye, this disease can cause blepharitis, conjunctivitis, and

photophobia, likely due to keratitis• The corneal epithelium and Bowman’s membrane thins, though

corneal sensitivity is reportedly normal

Zinc and Cataract¡“Zinc nutrition has been loosely linked to cataract¡In a study from India, 140 patients with senile cataract had reduced plasma levels of zinc, among other micronutrients, compared with age-matched controls¡Zinc deprivation (also) causes cataract in fish”

Zinc and Ocular Surface Disease¡“Severe zinc deficiency appears to cause ocular surface disease¡Animal models of zinc deficiency demonstrate conjunctivitis, corneal opacity, and corneal neovascularization¡In humans, ocular surface disease has been described in zinc deficiency, predominantly in acrodermatitis enteropathica”

Zinc and Dark Adaptation¡The ocular manifestations of zinc deficiency in humans include impaired dark adaptation and nyctalopia¡Shown here: Oguchi’s disease¡We learned it as Congenital Stationary Night Blindness¡Remember, these are the patients whose retina looks like a tapetum lucidum!

What are the Side Effectsof Excess Zinc?• Taking zinc on an empty stomach can cause nausea, so it should

be taken with food

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• Taking zinc on an empty stomach can cause nausea, so it shouldbe taken with food

• Copper deficiency can result from zinc consumption over 50mg/day

• The average diet contains 10 mg/zinc per day, sosupplementation should not exceed 40 mg

• The AREDS 2 formula included zinc (80 or 25 mg) and copper (2mg) for this reason

Upper Limits of Zinc Intake

Questions?

Readings and References¡ Most of today’s material comes from chapters 2.6 and 2.7 in Eperjesi’s Nutrition and the Eye, and chapters 7 and 8 in Semba’sHandbook for Nutrition and Ophthalmology¡Also see Preedy, chapers 31-32 and chapter 60¡The Linus Pauling Institute at Oregon State Micronutrient Information Center is here: http://lpi.oregonstate.edu/infocenter/¡The NIH has an Office of Dietary Supplements (ODS) with a great website: ¡http://ods.od.nih.gov/Health_Information/Information_About_Individual_Dietary_Supplements.aspx

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2019 Island Eyes Conference

January 20 – 26, 2019 Fairmont Orchid Resort, Hawaii Island

Up to 30 hours of optometric continuing education and 9 hours of Paraoptometric education. Speakers include:

Steve Laukaitis, MD; Nate Lighthizer, OD; Brian Mathie, OD; Stuart Richer, OD, PhD; Stan Teplick, MD; and Maria Walker, OD,

MS; Dennis Fong, OD; Michelle Hoff, OD. www.Pacificu.edu/islandeyes

GLAUCOMA SYMPOSIUM Saturday, January 12, 2019

Willows Lodge, Woodinville, Washington 7 hours of CE with Howard Barnebey and Murray Fingeret

HOMECOMING CE Saturday, October 20, 2018

Jefferson Hall, Pacific University Up to 5 hours of CE

Check out our new offerings:

“Utilizing OCT in Patients with M.S.” “Obstructive Pulmonary Conditions – Ocular Implication” “TB and the Eye” “Introduction

to Neuroimaging in Eye Care” “Prescribing for Pregnant and Nursing Mothers” “Cranial Nerve Testing” “Diabetic Keratopathy”

https://online-ce.opt.pacificu.edu/

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PACIFIC UNIVERSITY CONFERENCE EVALUATION Victoria Conference

July 13 ‐ 16, 2017

As a result of attending the 2018 Victoria Conference Strongly

DisagreeDisagree Neutral Agree

Strongly

AgreeNA

1I have developed new strategies to manage glaucoma, retina disease, corneal disease,

cataracts and dry eye1 2 3 4 5

2 My ability and skills have been improved 1 2 3 4 5

3 I have identified changes I will implement in my practice 1 2 3 4 5

4 I will significantly change the way I will treat and care for my patients. 1 2 3 4 5

5 I expect positive changes in my patient outcomes 1 2 3 4 5

POOR EXCELLENT

Thursday, July 12 1 2 3 4 5 NA

1 Lee Carr ‐ Judicious Management of Eye Pain

2 James Kundart ‐ Epiretinal Membrane Update

3 Beth Kinoshita ‐ Contact Lens Complications

Friday, July 13

4 Anthony DeWilde ‐ Anti‐VEGF and the Eye

5 Lee Carr ‐ Judicious Prescribing, Government Oversight of Controlled Substances

6 Anthony DeWilde ‐Guide to Glaucoma Surgery

7 James Kundart ‐ Ehlers‐Danlos Syndrome and the Eye

8 Lee Carr ‐ Assessing Diplopia

Saturday, July 14

9 Beth Kinoshita ‐ Corneal Ecstasias

10 James Kundart ‐ Visual Consequences of Chiari Malformation

11 Anthony DeWilde ‐ Managing Unilaeral Optic Nerve Edema

Sunday, July 15

12 James Kundart ‐ Macular Cherry Red Spots

13 Lee Carr ‐ Recognizing Red Flag Headaches

14 Beth Kinoshita ‐ Coatings and Treatments and Agents

15 Anthony DeWilde ‐ Rethinking Gonioscopy

16 James Kundart ‐ Climate Change, Eclipses and the Eye

OTHER COMMENTS

I would like to learn more about:

Please return this completed form to the conference administrator.205 of 205

Documents

2018 Victoria Conference Workbook Part 22018 Victoria Conference Workbook Part 2 SATURDAY, July 14 PAGES Beth Kinoshita Corneal Ecstasias 112 – 118 James Kundart Visual Consequences