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
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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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
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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
https://www.conquerchiari.org/documents/presentations/SYMPTOMS%20Presentation.pdf
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
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4757284/
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
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4757284/
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
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4757284/
Visual Symptoms of Chiari
Blurred VisionDiplopiaNystagmusPhotophobiaStrabismus
https://www.conquerchiari.org/documents/presentations/SYMPTOMS%20Presentation.pdf
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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
https://www.ncbi.nlm.nih.gov/pubmed/22864131
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
http://www.mayfieldclinic.com/PE-Chiari.htm#.VXiR486VzPA
Spinal Cord Syrinxes and Chiari Symptoms
http://www.mayfieldclinic.com/PE-Chiari.htm
Syrinxes and Chiari Surgery
https://www.ncbi.nlm.nih.gov/pubmed/14966661
Surgical Treatments: Posterior Fossa Decompression
http://www.mayfieldclinic.com/PE-Chiari.htm
Craniectomy for Chiari
http://www.mayfieldchiaricenter.com/chiari_surgery.php
Opening the Dura in Chiari
http://www.mayfieldchiaricenter.com/chiari_surgery.php
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Dura Patch for Chiari
http://www.mayfieldclinic.com/PE-Chiari.htm#.VXiR486VzPA
http://www.mayfieldchiaricenter.com/chiari_surgery.php
Surgical Time Course for Posterior Fossa Decompression
https://www.conquerchiari.org/documents/presentations/TREATMENT%20Presentation%20.pdf
Surgical Time Course for Posterior Fossa Decompression
https://www.conquerchiari.org/documents/presentations/TREATMENT%20Presentation%20.pdf
Chiari Surgeries on the Rise
https://www.conquerchiari.org/documents/presentations/TREATMENT%20Presentation%20.pdf
Surgical Outcomes for Posterior Fossa Decompression
https://www.conquerchiari.org/documents/presentations/TREATMENT%20Presentation%20.pdf
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
https://www.ncbi.nlm.nih.gov/pubmed/23931494
Case #3: Chiari Causing Esotropia Post-Op in 6 YOF
https://www.ncbi.nlm.nih.gov/pubmed/23931494
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
http://www.mayfieldclinic.com/PE-Chiari.htm
GIF Animation of CSF flow in Chiari
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Questions? Thank you!
James Kundart OD MEd FAAO FCOVD-A
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
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
Hayreh SS, et al. Giant Cell Arteritis: Validity and Reliability of Various Diagnostic Criteria. Am J Ophthalmol 1997;123:285-96
Systemic Symptoms
Headache
A-AION - 46% had Headache
NA-AION – 54% had Headache
Could Mislead
Hayreh SS, et al. Giant Cell Arteritis: Validity and Reliability of Various Diagnostic Criteria. Am J Ophthalmol 1997;123:285-96
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
Management of ischemic optic neuropathiesIndian Journal Ophthal 2011. Vol 59, 2, 123-136
Labs
ESR
> 33 mm/h
Sensitivity 92%
Specificity 92%
Hayreh SS, et al. Giant Cell Arteritis: Validity and Reliability of Various Diagnostic Criteria. Am J Ophthalmol 1997;123:285-96
Labs
CRP
> 2.45 mg/dl
Sensitivity 100%
Specificity 82%
Hayreh SS, et al. Giant Cell Arteritis: Validity and Reliability of Various Diagnostic Criteria. Am J Ophthalmol 1997;123:285-96
Labs
CBC includes
WBC
RBC
Platelets
Hayreh SS, et al. Giant Cell Arteritis: Validity and Reliability of Various Diagnostic Criteria. Am J Ophthalmol 1997;123:285-96
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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
Temporal Artery Biopsy
Gold Standard
Case by Case
Side Effects
Necrosis, Infection, Nerve Damage
Bilateral?
Temporal Artery Biopsy
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
Temporal Artery Biopsy
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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12
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!
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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
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4612404/
CRAO: Objective“Cattle Trucking”
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4764311/
CRAO: Fluorescein Angiography
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4764311/
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CRAO: Cilioretinal Artery Sparing with Acute RNFL Defects
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3822202/
CRAO: RNFL Improvement and Fluorescein Angiography
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3822202/
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
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3325618/
CRAO Triggers:Chiropractic Manipulation
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3325618/
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CRAO Triggers:Chung-Strauss Syndrome
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3714957/
CRAO Triggers:Chung-Strauss Syndrome
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3714957/
CRAO Triggers: Pediatric Pneumonia
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5148912/
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
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5148912/
CRAO Triggers: Congenital Single Heart Atrium
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4612404/
CRAO DDx: Sickle Cell Anemia
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4244145/
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CRAO DDx:Pseudo-Cherry Red Spot in Dermato-myositis
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3724690/
Preventing and Treating CRAO
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5148912/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4612404/
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)
http://imagebank.asrs.org/file/8649/niemann-pick-disease-type-b
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
http://imagebank.asrs.org/file/8648/niemann-pick-disease-type-b
4. Other LysosomalStorage Diseases
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4802848/
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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
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3831135/
Other Causes of Cherry Red Spots: Guacher Disease
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3831135/
Other Causes of Cherry Red Spots: Commotio Retinae
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4185168/
Other Causes of Cherry Red Spots: Commotio Retinae
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4185168/
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
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4202095/
Other Causes of Cherry Red Spots: Sialidosis
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4802848/
Other Causes of Cherry Red Spots: Sialidosis
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4802848/
Summary: Cherry Red Spots
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3864975/
Questions? Thank You!James Kundart OD
MEd FAAO FCOVD-A
Professor, Pacific University College of
Optometry
3D Performance Clinic
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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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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
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
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Eclipses, Climate Change, and the Eye2018 Victoria Conference
Pacific University
James Kundart OD MEd FAAO FCOVD-A
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
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