Differential Diagnosis - Pacific University

2012 NORTHWEST RESIDENTS CONFERENCE
Pacific University College of Optometry – Jefferson 224
Monday, June 4, 2012
8:00 am – 6:50 pm
TABLE OF CONTENTS
Jason Bleazard, OD
VAMC Puget Sound
Judy Posner, OD
VAMC Jonathan Wainwright
Anna Griffith, OD
Pacific University & Associated Clinics
Jessica Dennis, OD
Eye Care Associates of Nevada
Oliver Kuhn-Wilken, OD
VAMC Puget Sound
Jonee Brandt, OD
VAMC Puget Sound
Kelvin So, OD
Pacific University & Associated Clinics
Alison She, OD
IRIS Ophthalmology Clinic
Prevention & Treatment of Pseudophakic Bullous Keratopathy Pages 2-9
Herpes Stromal Keratitis PAGES 10-19
TBI: Treatment and Management of Accommodative and Vergence
Dysfunction
PAGES 20-26
A Partial Cranial Nerve Three Palsy PAGES 27-35
BREAK: 10:00-10:20
The Problem with Prostaglandins: An Assessment of the Risks and
Contraindications
PAGES 36-40
Etiology & Management of Posner-Schlossman Syndrome PAGES 41-45
Case Studies in Pediatric contact Lens Correction Modalities for
Myopic Refractive Error & Myopia Control
PAGES 46-53
Endothelial Cell Changes Associated with Intraocular Lens Surgery PAGES 54-58
Lunch: 12:20 – 1:00
Bic Trinh, OD
Eye Care Associates of Nevada
Amy Pedersen, OD
Portland VA Medical Center
Erin Bender, OD
Lebanon VA Medical Center
Allison Coit, OD
Spokane VA Medical Center
Kendra Kallemeyn, OD
Roseburg VA Medical Center
Persistent Epithelial Defect in Post Corneal Graft: A Case Study PAGES 59-64
One Conjunctivitis Away From Endophthalmitis: A Case Report of
Blebitis
PAGES 65-69
A Very Lumpy Nerve: A Case of Optic Nerve Head Drusen PAGES 70-76
Postoperative Endophthalmitis: A Case Report PAGES 77-80
Valsalva Retinopathy PAGES 81-87
BREAK: 3:30-3:50
Brett Richardson, OD
Spokane VA Medical Center
Keely Hoban, OD & Grace Tsan, OD
Portland VA Medical Center
Zachary Oswald, OD
VAMC Jonathan Wainwright
Kevin Riedel, OD
Portland VA Medical Center
Benjamin Taylor, OD
VA Southern Oregon Rehabilitation
Center & Clinics
Hypotensive Crisis: Vision loss secondary to non-ocular surgery PAGES 88-92
An Assessment of the Diabetic Teleretinal Imaging Program (TRIP)
at the Portland Veterans Affairs Medical Center – A Retrospective
Study
PAGES 93-99
Radioiodine Therapy & Graves’ Ophthalmopathy PAGES 100-120
Long Term Ocular Complications of Rosacea PAGES 121-130
Ocular Manifestations of Carotid Occlusive Disease & Ocular
Ischemic Syndrome: A Case Study
PAGES 131-139
This program is sponsored in part by an unrestricted educational grant
from

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5/29/2012
Prevention, Diagnosis, and Management.
Jason Bleazard, O.D.,
American Lake Veterans’ Association, Tacoma, WA
Five Layers
(anterior to
posterior)
◦ Epithelium
◦ Bowman’s
Layer
◦ Stroma
◦ Descemet’s
Membrane
◦ Endothelium
Endothelial cells are connected by gap
junctions and macular occludens and thus
make up a very slightly permeable membrane
between the stroma and aqueous humor.
Recall that the corneal endothelium is in fact a
specialized epithelial layer. The base of the
cells attach to Decemet’s, while the apices face
the anterior chamber.
• Water follows large molecules such as amino
acids and glucose into the stroma.
• The endothelial cells pump water out of the
cornea via Sodium/Potassium ATP-ase pumps
and aquaporins.
• A compromised endothelium may lead to
stroma edema
• The endothelial cells of the cornea do not
replicate.
• It follows that adult corneas have a lower
endothelial cell density than youngsters.
• Damage to the endothelium further decrease
endothelial cells counts.
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Normal Endothelial
Mosaic
Corneal guttata
Depositions of basement membrane in
Descemet’s, cause thickening and bulging
into the anterior chamber.
Peripherally, these are termed Hassall-Henle
bodies
Centrally, the areas of thickening are called
guttata
Guttata represent thinning of the
endotheilum as well as a thickened basement
membrane.
Guttata – “Spotted, speckled, or drop-like”
Direct illumination of
advanced Corneal
guttata
Elaphe
Guttata
A damaged endothelium has a reduced ability
to pump water out of the stroma
Fluid accumulates between the fibrils of the
stroma, resulting in edema
Stromal edema results in blurry vision and a
painful eye
Guttata alone do not warrant a diagnosis of
Fuch’s, stromal edema must be present
Endothelial cell density
is critical in
maintaining a properly
hydrated cornea.
In children, the
average density is
3,000-4,00/mm 2
In adults, cell density
ranges from 1,000-
2,000/mm 2
In order to maintain a
functioning
endothelium, 500
cells/mm 2 are needed
The exact mechanism of endothelial cell loss is
unknown, however, there are a number of
theories:
◦ Histology has shown increasing amounts of apoptotic
endothelial cells in Fuch’s patients. These corneas
also show decreased anti-apoptosis gene expression.
◦ UV light (gets blamed for everything) has been shown
to induce DNA damage to endothelial cells. The longer
you live, the more UV you will have been exposed to.
◦ Fuch’s corneas have shown to have reduced
expression of the aquaproin-1 protein. This is an
integral protein in pumping fluid out of the cornea.
• Mouse models have shown that decreased aquaporin-1
expression results in slower recovery times in edematous
corneas
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Other factors that result in decreased endothelial
cell numbers (occur in otherwise normal eyes):
◦ Age
◦ Previous ocular surgery
◦ Ocular trauma or infection
◦ Angle closure glaucoma
◦ Pseudoexfoliation
◦ Long-term contact lens wear
◦ Sex- Filipino men had lower endothelial cells counts than
women
◦ Diabetes
• 10 years or more results in decreased endothelial cell
numbers and morphological changes.
• Endothelial cell loss after phacoemulsification is higher in
diabetics than normals
While not all Fuch’s patients progress to
bullous keratopathy, the risk for significant
corneal damage such as that in PBK is real.
Swelling of the cornea as a result of
iotrogenic trauma to ocular tissues.
PBK results in an extremely painful eye with
significant reduction in visual function.
Edema can be present in the stroma and the
epithelium
◦ Epithelial edema results
in bullae, which are
essentially corneal
blisters.
Subjective
◦ Decreased vision
◦ Pain
◦ Epiphora
◦ Foreign body sensation
◦ Photophobia
◦ Recent cataract surgery
Patients with PBK can present with mild to
severe findings on physical examination
Corneal findings:
◦ Corneal guttata
◦ Folds in Descemet’s Membrane
◦ Stromal edema
◦ Stromal haze
◦ Epithelial edema
◦ Bullae- may be ruptured
◦ Corneal neovascularization
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Other Ocular Findings:
◦ Cells/flare in anterior
chamber
◦ Subluxed IOL
◦ Shunt tube w/ current or
previous endothelial touch
◦ Elevated IOP
◦ Cystoid macular edema (CME)
has been associated with PBK,
especially in patients with an
anterior chamber IOL
As is the case with most conditions,
treatment depends on the severity of the
disease in each patient.
Mild cases may respond to medical therapy,
while moderate to severe cases often require
surgery.
Mild
◦ Edema
• Muro 128 (NaCl 5%) gtts QID
• Muro 128 (NaCl 5%) ung QHS
◦ Elevated IOP
• Antiglacuoma medications
• Avoid prostaglandin analogues to reduce risk of CME
◦ CME
• Treat as with other cases of CME
Surgical procedures are dependent on the
severity of the patient’s condition as well as
their visual potential.
Penetrating Keratoplasty Diagram
If a patient is a cataract surgery candidate
and has Fuch’s, measures must be taken to
protect the cornea.
For healthy corneas with guttata, viscoelastic
should be used
◦ Most surgeons use the soft-shell technique
• Combines cohesive and dispersive viscoelastic
◦ Viscoelastic protects the endothelium from the
energy released during phacoemulsification as well
as the trauma that is incurred during surgery
Corneas with stromal edema take special care
and consideration when cataract surgery is to
be performed.
If CCT is greater than 640um, a “Triple”
procedure may be considered
◦ Triple= Phacoemulsification+IOL implantation+cornea transplant
If the patient elects for CE without a
transplant, they MUST be educated that they
will likely need one in the future.
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For patients that qualify, the triple procedure
is preferred-
◦ One trip to operating room
• Reduces cost
• Less discomfort for patient
• Low risk for future corneal decompensation
◦ Cataract removed
◦ Surgery is the only true definitive treatment for
Fuch’s
Penetrating Keratoplasty (PKP) is a full-thickness
corneal transplant. Previously, it was the only
surgical treatment for patients with advanced
Fuch’s or PBK.
PKP may be indicated in a plethora of conditions:
• Fuch’s
• PBK
• Keratoconus
• Failed grafts
• Scarring
• Corneal thinning
• Corneal perforations
While more surgeons are familiar with PKP,
there are a fair amount of downsides to it…
• Even in uncomplicated cases, Post-op is very
involved -
• Topical corticosteroids
• QID*1mo
• QD*6mo
• Q o D *6mo
• This may be altered (usually increased)
• Systemic steroids or other immunosuppressants may
be warranted as well
• Endophthalmitis- most dreaded complication
• Treated aggressively
• Epithelial downgrowth
• Wound Leak- requires immediate intervention
• Epithelial defects (usually resolve w/ lubrication after a
few weeks)
• Glaucoma due to:
• Infectious keratitis
• Crystalline keratitis – usually 2’ streptococcus near suture
• Graft rejection
• 50% of rejection occurs w/in 6 mo
• The rest usually occur w/in the next 6 mo
• Most common type is also the most serious: Endothelial
rejection
• Tx= Repeat transplant
• 10% are epithelial
Nowadays, PKP is not always considered firstline
treatment, and is more of a last-resort
for PBK patients in the U.S.
Newer techniques are proving to be quite
effective and tend to have fewer side effects
and less severe complications
We will review some of the well-established
procedures and introduce a few new ones as
well
DALK = Deep Anterior Lamellar Keratoplasty
DSEK= Descemet Stripping Endothelial
Keratoplasty
◦ DSAEK= Descemet Stripping Automated Endothelial
Keratoplasty
◦ FS-DSEK= Femtosecond DSEK
DMEK= Descemet Membrane Endothelial
Keratoplasty
◦ Transplantation of Decemet’s membrane and
endothelium only
PTK = Phototherapeutic Keratectomy
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Began in 2003
Descemet’s Membrane and endothelium is
removed from the host cornea
Small portion of posterior stroma along with
Descemet’s and endothelium are harvested
and transplanted on posterior surface of host
cornea
DSEK
No corneal surface incisions
Little post-op astigmatism
Fewer suture related problems
Less wound dehiscence
Better, less variable visual
outcomes
Low rates of graft rejection
Usually done after cataract surgery
Higher endothelial density longterm
PKP
Significant corneal incisions
High and variable astigmatism
High rates of suture problems
Wound dehiscence
Variable, poor visual outcomes
Higher (double) graft rejection
rates
Done before cataract surgery
Lower cell denisty
In Koenig’s study, patients went from an
average of 20/100 preoperatively to 20/40
postoperatively @ 6 months.
DSEK and DSAEK have shown promising longterm
outcomes.
◦ Li’s study showed steady improvement in BCVA
from 6-12 months, from 12-24 months, and from
24-36 months, with a mean BCVA of 20/25.
◦ Ratanasit et al. showed 75% of patients were
20/20-20/40 @ 5 years, and not one patient lost
vision.
Successful In vitro
Descemet’s Membrane
transplantation in 1998,
2002
Descemet’s and
endothelium removed
from both host and
donor.
Both Descemet’s and
endothelium are
transplanted to host
cornea
No stroma
In vivo DMEK in 2006
◦ Single case- 20/20 vision
one week post-op
DMEK carries most of the same risks as DSEK
DMEK patients are more likely to experience a
graft dislocation.
◦ Over 50% of patients had a dislocation
◦ In DMEK, dislocations are partial
◦ Partial dislocations require re-bubbling and are
relatively simple to correct
Price et al (60 eyes, two surgeons, both were
brand new to DMEK)
◦ Mean BCVA was 20/30 @ one month
• 84% were 20/40 or better
◦ Mean BCVA @ 3 months was 20/25
• 94% were 20/40 or better
• 63% were 20/25 or better
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DMEK
Better refractive predictability
DSEK
Fair predictability – Host stroma
adds to corneal thickness
Thinner post-op CCT (528um) Thicker post-op CCT (650um)
Endothelial cell density equal ---
Tearing of donor tissue
Less likely to tear
Can use one donor cornea for
DMEK + DALK
No hyaluronic acid- lower
host/donor interface issues
Lower start-up cost
Can only use donor cornea for
DSEK
Need to use hyaluronic acid
Higher start-up cost
(microkeratom)
Done by many corneal surgeons
Fewer experienced surgeons
Partial graft detachments common Graft detachment rare (2-3%)
Using 20/40 or better @ 6-12 months
post-op as a benchmark:
38-100% of DSEK pts
◦ Few reach 20/25
40% of PKP pts
95% of DMEK pts
◦ 75% reached 20/25
◦ Most are 20/40 on the day of surgery
Post-op endothelial cell density is reduced in
both DSEK and DMEK. This is due to (1) cell loss
during dissection and (2) endothelial damage
while the graft is being handled before and
during surgery.
DMEK and DSEK are comparable in cell counts
◦ 25-54% loss 6 mo Post op in DSEK
◦ 24-61% 1 yr post op in DSEK
◦ 30% loss at 1 yr in DMEK
◦ 40% 1 yr post op in PKP
Even with all the cell loss, most corneas are well
above the 500/mm 2 cutoff.
For patients with limited visual potential
unrelated to the cornea, phototherapuetic
keratectomy (PTK) is a good option for pain
management.
Collagen cross-linking has shown some
potential for pain management, but longterm
results are lacking.
It may be possible to inject prepared
endothlial cells into the anterior chamber as
they have shown the ability to migrate onto
the posterior surface of the cornea.
PKP is well-established, but has more serious
and frequent complications and poorer visual
outcomes
DSEK/DSAEK provides for predictable
outcomes but requires a long wait-time
before visual acuity is optimal
DMEK is new and looks promising, however
there are few surgeons who will do it and
graft dislocations are common.
PBK causes painful vision loss
It is largely avoidable
Careful examination, proper patient
education, and appropriate surgical care are
necessary to avoid PBK
DSEK is the most common option for
treatment of PBK or use in a tirple procedure
DMEK has shown very promising results and
will be implemented in many surgical centers
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5/29/2012
Ehlers, Justis P., et al. The Wills Eye Manual: Office and Emergency Room Diagnosis
and Treatment of Eye Disease, Fifth Edition. Baltimore, Lippincott Williams &
Wilkins, 2008.
Ghanem, Santhiago, Berti, Thomaz, Netto “Collagen crosslinkin with riboflavin and
ultraviolet-A in eyes with pseudophakic bullous keratopathy.” Journal of Cataract
& Refractive
Surgery. 36.2. (2010).
Kanski, Jack J. Clinical Opthalmology: A Sytematic Approach, Seventh Edition.
Elsevier Saunders, 2011.
Koenig, Steven B., Covert, Douglas J., Dupps, William J., Meisler, Daivd M. “Visual
Acuity, Refractive Error, and Endothelial Cell Density Six Months After Descemet
Stripping and Automated Endothelial Keratoplasty (DSAEK).” Cornea. 26.6 (2007).
Li, Jennifer Y., Terry, Mark A., Goshe, Jeffrey, Davis-Boozer, David, Shamie, Neda. “
Three-Year Visual Acuity Outcomes after Descemet’s Stripping Automated
Endothelial Keratoplasty.” Ophthalmology. March 2012.
Lin, Pei-Yu, Wu, Chih-Chiau, Lee, Shui-Mei. “Combined phototherapeutic
keratectomy and therapeutic contact lens for recurrent erosions in bullous
keratopathy. British Journal of Ophthalmology. 85 (2001).
Milla, Elena, Verges, Carlos, Cipres, Maricruz. “Corneal Endothelium Evaluation
After Phacoemulsification With Continuous Anterior Chamber Infusion.”Cornea.
24.3 (2005).
Price, Marianne O., Giebel, Arthur W., Fairchild, Kelly M., Price, Francis W.
“Descemet’s Membrane Endothelial Keratoplasty: Prospective Multicenter Study of
Visual and Refractive Outcomes and Endothelial Survival.” Ophthalmology. 116.12
(2009).
Ratanasit, Arlene, Gorovoy, Mark S. “Long-term Results of Decemet Stripping
Automated Endothelial Keratoplasty.” Cornea. 30.12 (2011).
Rosado-Adames, Noel, Afshari, Natalie A. Current Opinion in Ophthalmology. 23.1
(2012).
Remington, Lee Ann. Clinical Anatomy of the Visual System, Second Edition. T.
Louis. Elsevier, 2005.
Ruggeri, A, Grisan, E., Jaroszeski, J. “A new system for the automatic estimation of
endothelial cell density in donor corneas.” British Journal of Ophthalmology. 89
(2005).
Seitzman, Gerami D. “Cataract Surgery in Fuch’s Dystrophy.” Current Opinion in
Ophthalmology. 16 (2005).
Wollensak, Aurich, Wirbelauer, Pham. “Potential Use of Riboflavin/UVA Cross-
Linking in Bullous Keratopathy.” Ophthalmic Research. 41.2 (2009).
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A Case Presentation
Case Presentation
Introduction to Stromal keratitis
• Immune Stromal Keratitis (ISK) defined
• Necrotizing versus Non-necrotizing
Pathophysiology of the disease
Epidemiology
Workup
Landmark Studies – HEDS I and II
Current therapies
• Including surgery
Conclusion/Clinical Pearls
65 YOWM new patient presented for a
consult for a CVE
The consult was placed by their PCP for
vision changes thought to be related to
hyperbaric O2 treatments 2/2 a bleeding
bladder from radiation cystitis
• Vet was initially given radiation therapy for
prostate cancer
• Last tx received 04/11- total of 40 tx that started
in 02/11
Overview: Hyperbaric oxygen therapy
(HBOT) is breathing 100% oxygen while
under increased atmospheric pressure
HBOT is generally performed daily for a
minimum of 30 treatments
• Treatment is typically at 2 to 2.4 ATA for a total
of 90 minutes
• ATA = atmosphere absolute
• 1 ATA= atmospheric pressure at sea level
Delayed radiation injury (soft tissue and
bony necrosis) **
Diabetic retinopathy
Diabetic foot
Carbon monoxide poisoning
Decompression sickness
Selected problem wounds
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Increase in myopia*
Improvement in hyperopia
Vision changes more common after 20
treatments and in patients >40 years old
This is usually temporary and in the
majority of patients, vision returns to its
pre-treatment level about six weeks after
the cessation of therapy
CC: Decreased vision at distance OU, that
occurred suddenly after receiving O2 treatments
LEE: ~ 08/11 with Dr. X (a non-VA provider);
07/13/11 CVE at the Portland VAMC
Current Ocular Medications: Prednisone TID OS
prescribed initially by Dr. X for an “abrasion”
and a “viral infection” that he has been using
intermittently since ~08/11 (renewed by his PCP)
– had been off for 1 month and was about to
restart
Personal OHx: corneal abrasion OS with a
viral infection dx ~8/11
Family OHx: Unremarkable
Pertinent Medical Conditions: DM II,
COPD, Vitamin D deficiency, prostate
cancer
Autorefractor:
• RE:-1.25-0.75x091 LE:-1.75-1.00x013
Current Spec Rx: Bifocals
• RE:-0.50DS 20/60 PH:20/40
• LE:-0.25-0.75x033 20/150 PH:20/80
• ADD:+2.50
Pupils: PERRL (-)APD OU
EOMS:FROM OU
CF:FTFC OU
SLE:
• L/L: BE: flakes, lower lid laxity w/ mild proptosis
• Conj: BE: Ping N&T LE:1+ diffuse injection temp
• Cornea:BE: arcus 360 w/ krukenberg spindles
• LE: central areas of white patchy stromal haze
• Sectoral deep stromal NV from ~3:00-5:00
• Central folds and SEI, bullae superior cornea
• (+)staining over the neo with stromal filling
• A/C: Deep and Quiet OU
• Iris: Normal w/o NVI OU
• Tonomtery by Applanation: 15/16 @ 15:48
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DFE:
Periphery: Attached 360 w/o holes/tears
Lens: RE: 1+ milky NS w/ vacuoles LE:1-2+
milky NS
Vitreous: BE: syneresis
Optic Nerve C/D ratio: RE:0.35 rd HRT
LE:0.40 shallow HRT
Macula: Flat and Dry OU LE: hazy view 2/2
cornea
Vessels:1:2 with moderate tortuosity and
threadlike arterioles
1)Left Eye Stromal Keratitis with stromal
edema – likely related to Herpes virus
per patient history with Dr. X
2)Bilateral Nuclear Sclerotic Cataracts
3)Diabetes Type II without retinopathy
OU
4)Bilateral Retinal Vascular Changes –
likely related to hyperbaric treatments
received back in April
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1)Prescribed oral Acyclovir 800mg 5X/day
for 1 month
• Viroptic 5x/day OS
• Pred acetate 1% q2h OS
• A referral to Portland VAMC for a corneal consult
• Vet from Astoria, OR and would not be able to f/u in
Walla Walla
2-4)Baseline photos were taken, will
monitor.
HPI: Vet reports symptoms started a year ago, with blurry
vision, pain and redness in the left eye
He was treated for an eye infection with numerous gtts (he
thinks herpes)
He denies any rash or eyelid lesions at the time
He had a recurrence after 3 months. He was seen in Walla
Walla, and was treated for HSV keratitis
His symptoms resolved after 2 weeks of treatment
Today he is pain free, but noted continued blurry vision in
both eyes. He was referred for evaluation by corneal
specialist to r/o interstitial keratitis OS
Habitual Rx Acuity:
• RE:20/100+1 PH:20/40-2 LE:20/400 PH:20/80
Pupils: Dilated OU
EOMS: FROM OU
Cover Test: No tropia
CF: FTFC OU
Ocular Medications: PF OS 5x per day,
Ocuflox TID OS, viroptic 5x/day OS,
acyclovir 800mg po 5x/day
SLE:
• L/L: No lesions OU
• Cornea: RE: WNL, +KS
• LE: trc PEE, IT pannus 1mm beyond limbus
• 1+ subepi haze
• 1+ diffuse stromal haze most prominent IT extending centrally
• Deep stromal NV IT
• Conj: 1+ diffuse injection
• AC: Deep and quiet
• Iris: WNL (-)NVI
• Tonometry: 14/14 @
DFE: Same as previous exam
OCT Scan: RE:261, no IRF/SRF LE:267, no IRF/SRF
1)Corneal Opacity, OS
• With extension to visual axis, and poor visual acuity (20/80)
• Possible interstitial keratitis, in the setting of presumed HSV keratitis, and
history of atopy (exzema)
• PPD negative
• Reports history of risk factors for syphillis
• Check RPR, ANA, RF, Lyme, EBV, ESR
• Continue PF, viroptic, ofloxacin, acyclovir
• F/U with cornea fellow next week
2)DM II, no retinopathy OU
• No CSME
• Continue good glycemic index
• Continue annual exams
3)Pigment Dispersion Syndrome, OU
• Stable IOP, nerves intact
4)Cataract OU
• Monitor.
Habitual RX Acuity:
RE:20/60-2 PH:20/30-2, LE:20/80-2 PH:20/40-2
Pupils: 2/3 (-)APD
SLE:
• L/L: No lesions OU
• Cornea:
• RE: Epi intact, trc subepi haze, +KS
• LE: Decreased corneal sensation, +KS
• Conj: White and Quiet OU
• A/C: deep and quiet OU
• Iris: TIDs peripherally OU
• Tonometry: 15/14 @
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1)presumed HSV stromal keratitis OS.
Clincal appearance consistent. RPR, ANA,
RF, EBV, ESR, wnl.
• h/o atopy
• Continue PF qid
• Reduce acyclovir to 400mg po bid
• d/c viroptic
• d/c ocuflox
• Return 4 wks, MRx next visit
Herpes Simplex Type I and Type II
Cytomegalovirus
Epstein-Barr Virus
VZV
Ocular herpes affects each corneal layer differently
and can vary in presentation as categorized below:
• Corneal epithelial disease
• Dendritic keratitis
• Geographic (ameboid) ulcer
• Marginal keratitis (limbitis)
• Corneal Stromal Disease**
• Necrotizing
• Non-Necrotizing
• Disciform, immune rings, limbal vasculitis
• Endothelitis
• Neurotrophic keratopathy 4,5
Management depends on the layer affected
By definition - “Immune” refers to the fact that
typically at this corneal level, the virus has been
reactivated and the patient has developed an
immunity/humoral response
The immune reaction represents a delayed
hypersensitivity reaction by T lymphocytes to
viral antigen
There are two types of ISK that may occur during
herpes infection:
• Necrotizing and Non-necrotizing
Presenting signs and symptoms:
• Reduced vision
• Pain
• Photophobia
• Lacrimation
• Blepharospasm
• Decreased corneal sensation
Presentation may be either unilateral or
bilateral
A history of prior episodes in patients with
recurrent disease may exist
There may be single or multiple patches of infiltration and inflammation
within the corneal stroma
Typically concurrent stromal edema
Stromal neovascularization may be present but is not necessary for the
diagnosis
The overlying epithelium is usually intact
If there is epithelial disruption, it will be much smaller in area than the
underlying inflammation
The inflammatory deposits are thought to represent complexes of viral
antigen with antibodies and complement – may take the form of a ring
infiltrate (Wessely ring)
Secondary anterior uveitis may be present
Endothelial folds and keratic precipitates are common
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Corneal thinning - secondary to chronic
inflammation
Corneal Scarring – secondary to stromal
neovascularization that can result in
profound vision loss**
Fibrosis, pannus, and lipid deposits from
stromal neovascularization
Occurs in 20-60% of eyes with recurrent HSV, and
90% of recurrent stromal keratitis 3,4
It does not usually move toward ulceration and
perforation
Untreated non-necrotizing ISK runs a self-limiting
course over several months; however if left
untreated severe vascularization and scarring
can result in profound vision loss thus treatment
is indicated 7
More severe form of herpetic stromal keratitis
• Manifests as dense, cheesy, yellow-white stromal infiltration
• Epithelial ulceration
• Stromal edema
• Dense vascularization
• Profound corneal thinning
• Possible perforation (major complication)**
The use of topical corticosteroids without antiviral
coverage may be a possible risk factor for its
development
It is much less common than the non-necrotizing type
Coursebook Page 15 of 139
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5/29/2012
Occurs mainly by 2 mechanisms:
1) Reactivation of the virus in the trigeminal
ganglion
• Migrates down the nerve axon to replicate and
infect ocular tissue
2) The cornea itself
• The virus may subsist latently within corneal tissue
(stromal keratocytes) and reactivate
• May also cause donor-derived HSV disease in
transplanted corneas
Conditions causing ISK include:
• Herpes simplex and zoster
• Epstein-Barr virus
• Syphillis
• Tuberculosis
• Lyme disease
• Mumps and measles
• Acanthamoebe
• Sarcoidosis
• Onchocerciasis
• Idiopathic
The most common cause of active ISK is the herpes
simplex virus, accounting for 70% of unilateral
cases 2
Frequency
• United States
• 80-90% of the US population has been infected with the
herpes virus – many with no history of clinical herpes
• ~ 20,000 new cases of ocular HSV occur annually
• >28,000 reactivations occur annually
• ~24% - 36% of patients with ocular disease will
experience recurrence within 2-5 years after the first
episode***
• International
• An estimated 1/3 of the population worldwide suffers
from recurrent infections 7
Mortality/Morbidity
• HSV keratitis IS THE MOST FREQUENT cause of corneal
blindness in the United States
• A leading indication for corneal transplantation
• Most common cause of infectious blindness in the
Western world
Age
• Affects mainly adults, and occurs many years after the
primary infection
• In children it involves the corneal epithelium
• Risk of binocular disease
• A high recurrence rate
• Amblyopia
Corneal Abrasion
Recurrent Corneal Erosion
Herpes Zoster
Bacterial Keratitis
Fungal Keratitis
Interstitial Keratitis
Keratoconjunctivitis Sicca
Corneal Ulcer
Coursebook Page 16 of 139
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5/29/2012
Diagnosis is primarily made based
on clinical features of the corneal
lesion **
Epithelial scrapings with Giemsa
stain:
• Show multinucleated giant cells
• Which are coalesced infected
corneal epithelial cells and
intranuclear viral inclusions 7
viral DNA can be detected in the:
• Corneal epithelium
• Conjunctiva
• Skin
• Anterior chamber tap
Negative cytology results do not
exclude HSV infection
Classic case of a multinucleated herpes simplex virus-infected cell 17
Enzyme-linked virus inducible system
(ELVIS)
• Very specific for detecting herpes virus
• Results in 24hrs!
ELVIS test result is negative
• Cell culture for confirmation is recommended
Cultures obtained within several days of onset, prior to
antiviral therapy give a sensitivity of up to 70%
Enzyme immunoassay (EIA) tests can be
performed in the office
• HerpChek
The Captia test (Trinity Biotech) is a
blood test to detect antibodies to the HSV
• Unlike other tests it can differentiate between
HSV -1 and HSV-2
Combined CORTICOSTEROID and antiviral therapy –
• Viroptic or Zirgan and Pred acetate 1%
• Acyclovir 3% ophthalmic ointment is available in Europe but not in the US
• Cycloplegia and topical lubricants are used to ease patient discomfort
Dosing
• Viroptic (trifluridine 1%) dosing – q2h up to a maximum 9x/day for 7-14 days, then QID for
1-2 days after complete epitheliazation (not to exceed 21 days due to toxicity)
• Zirgan (ganciclovir 0.15%)- q3h up to 5x/day typically 7-10 days–then taper to 1-3x/day
for 7 days
• Pred acetate 1% q1-2h initially then tapered
One common recommendation is:
• Equal frequency of topical antiviral with a corticosteroid
Conducted by the National Eye Institute
Herpetic Eye Disease Study (HEDS) I – 1996
• Focused on stromal keratitis treatment
• Anti-viral alone
• Anti-viral + corticosteroid
• Anti-viral + corticosteroid + acyclovir
Herpetic Eye Disease Study (HEDS) II- 1998
• Focused on epithelial disease
• Looked at early treatment with acyclovir if it prevented progression to stromal
disease
• Patients with previous HSV disease not active within 30 days, if longterm
low dose treatment with acyclovir prevented recurrence
Focused on stromal keratitis (3 groups)
• Anti-viral alone
• Anti-viral + corticosteroid
• Anti-viral + corticosteroid + acyclovir
Results
1. Duration of inflammation and risk of progression were
significantly reduced in patient’s receiving prednisolone
2. The rate of epithelial HSV recurrence was not increased
3. The addition of oral acyclovir to topical corticosteroid and
topical antivirals provided no additional benefit**
• The role of external factors in triggering recurrence
Coursebook Page 17 of 139
8

5/29/2012
3 Main Studies:
1. Acute Epithelial HSV Keratitis
Study:
• Early tx with oral acyclovir
prevented progression to stromal
disease
2. Acyclovir Prevention Trial:
• If long-term tx with low dose oral
acyclovir (400mg BIDx1yr)
prevented recurrence
3. Ocular HSV Recurrence Factor
Study – looked at triggers
• Patients filled out questionnaires
every week for 52 weeks to track
acute and chronic stressors
Results:
1. There was no benefit from
addition of oral acyclovir to
preventing progression to
stromal keratitis
2. 41% reduction that any ocular
herpetic disease would recur
• 50% reduction in stromal keratitis
3. There are no results available
yet
Topical cyclosporin A 0.05% showed some
effectiveness in cases of HSK resistant to
corticosteroids
• It improves visual acuity
• Reduces inflammation and lesion size
• Regression of corneal stromal neovascularization 12
• Contraindicated with active epithelial herpes keratitis
Antiangiogenic agents, such as Avastin
A therapeutic vaccine designed to boost
protective CD8 T-cell population within HSV
latently affected ganglia
A triple-drug therapy targeting viral
replication with:
• Oral acyclovir
• Topical cyclosporin A
• Anti-VEGF
Randomized clinical trials needed
Penetrating Keratoplasty (PK)*
Deep Anterior Lamellar Keratoplasty
(DALK)
• Assumes healthy endothelium intact
• Not preferred secondary to viral latency in stromal
keratocytes
Conjunctival flap
• Still performed on select patients, not as common
• Helps quiet down an inflamed eye
• PK may still be performed through the flap
During active HSV infection AVOID
transplantation
• Unless perforation is eminent
Corneal neovascularization is the main
risk factor for immune rejection
• Recent studies show that topical and
subconjunctival bevacizumab (Avastin) is
effective in regressing neovascularization in
these patients 12
Prophylaxis with oral acyclovir
• Improves corneal graft survival
• Famciclovir and valacyclovir may be as effective
but have not been studied
Topical treatment with Zirgan given it’s
safety profile
Coursebook Page 18 of 139
9

5/29/2012
Non-Necrotizing ISK
• Treat with topical anti-viral (Viroptic or Zirgan) and Pred
Acetate 1% with equal frequency until the steroid is
tapered down to BID or QD
• Add oral acyclovir AFTER the virus is inactive without
treatment for 30 days – 400mg BID x 1 year
Necrotizing ISK
• Perforation likely eminent requiring a corneal transplant
• Use oral acyclovir to prevent graft rejection
• Zirgan should also be considered to prevent rejection
• Restasis and Avastin are new treatments to consider as
well
1. Latham , Emi. "Hyperbaric Oxygen Therapy." Medscape Reference.
WebMD LLC, 19052010. Web. 27 Apr 2012.
.
2. Onofrey B, Skorin L, Holdeman N. Ocular Therapeutics Handbook: A
Clinical Manual. 3. Philadelphia; Lippincott Williams & Wilkins, 2011.
198-204. Print.
3. Sugar, Alan. "Herpes Simplex Keratitis." UpToDate. N.p., 11/11/2011.
Web. 30 Apr 2012. .
4. Schwartz GS, Harrison AR, Holland EJ. “Etiology of immune stromal
(interstitial) keratitis.” Cornea. 1998; 17(3):278-81
5. Krachmer J, Mannis M, Holland E. Cornea. 2. 1. Philadelphia: Elsevier
Mosby, 2005. 1048-1066. Print.
6. Dr. Hetrick’s book
7. Sowka J, Gurwood A, Kabat A. “Immune Stromal (Interstital) Keratitis.”
Handbook of Ocular Disease Management. N.p.; n.d. Web. 4 March 2012.
.
8. Wang, J. “Ophthalmologic Manifestations of Herpes Simplex Keratitis.”
Medscape Reference. WebMD LLC., 18 Nov 2010. Web. 3 March 2012.
.
9. Wilhelmus KR, Gee L, Hauck WW, et al. “Herpetic Eye Disease Study. A controlled trial
of topical corticosteroids for herpes simplex stromal keratitis.” Ophthalmology.
1994;101(12):1883-95.
10. Barron BA, Gee L, Hauck WW, et al. “Herpetic Eye Disease Study. A controlled trial of
oral acyclovir for herpes simplex stromal keratitis.” Ophthalmology.
1994;101(12):1871-82.
11. Herpetic Eye Disease Study Group. “Predictors of recurrent herpes simplex virus
keratitis.” Cornea. 2001;20(2):123-8.
12. Herpetic Eye Disease Study Group. “Oral acyclovir for herpes simplex virus eye
disease: effect on prevention of epithelial keratitis and stromal keratitis.” Arch
Ophthalmol. 2000;118(8):1030-6.
13. Herpetic Eye Disease Study Group. “Acyclovir for the prevention of recurrent herpes
simplex virus eye disease.” N Engl J Med. 1998;339(5):300-6.
14. Knickelbein J, Buela K, Hendricks R. “Herpes Stromal Keratitis: Erosion of Ocular
Immune Privilege by Herpes Simplex Virus.” Future Virology, 5.6 (2010):699-708. Print.
15. Saxena S, Sinha N. Keratoplasties- Surgical techniques and complications.
Shanghai:InTech, 2012. 127-134. Print.
16. Wilhelmus KR, Dawson CR, Barron BA, et al. “Risk factors for herpes simplex virus
epithelial keratitis recurring during treatment of stromal keratitis or iridocyclitis.” Br J
Ophthalmol 1996; 80:969-72.
1-3) Latham , Emi. "Hyperbaric Oxygen Therapy." Medscape
Reference. WebMD LLC, 19052010. Web. 27 Apr 2012.
.
4-8) Photos obtained from Wainwright Memorial VAMC Walla Walla,
WA 03/24/12
9-12)Photos obtained from various cartoon monster websites
13,14)Photos obtained from Pacific Cataract and Laser Institute
Kennewick, WA 03/14/12
15)Herpes Simplex Stromal Necrotizing Keratitis- American
Academy of Ophthalmology
16)Trigeminal Nerve- wikipedia
17)Multinucleated giant cells-
18)Elvis photo-
19) Conjunctival Flap photo-
Coursebook Page 19 of 139
10

5/31/2012
Anna Griffith, O.D.
Pacific University College of Optometry
Resident in Vision Therapy, Rehabilitation and Pediatrics
TBI Case
• 33 y.o.
• Involved in 9 blasts during combat
• CC: Intermittent blur
• HPI
▫ OD>OS
▫ All distances
▫ Lasts 2 seconds - 1 minute
▫ Eyestrain on the computer after 2-3 hours
▫ Cannot see 3-D in movies, also cause nausea
• Goals
▫ Read again
▫ Return to School for Electrical Engineering
TBI Case
• Other complaints
▫ Difficulty finding things
in crowded drawers or
shelves
▫ Extreme photosensitivity,
some days much worse
than others
TBI Case: Medical History
• Brain Contusion and
Blood Clots seen on MRI
• PTSD
• HTN
• GERD
• Quitting Smoking
0.5 pack/day x 10 years
• Care giver
• Acetaminophen prn
• Diazepam
• Docusate
• Hydrocodone
10/Acetaminophen
• Mirtazapine
• Nicotine Patch and Resin
Complex
• Omeprazole
• Promethazine
• Sumatriptan
• Verapamil
TBI Case: Exam Findings
• OD: -2.50-0.75 x 030 OS: -2.50 DS
• Distance Visual Acuity
▫ OD: 20/20-1
▫ OS: 20/20-1
• Near Visual Acuity
▫ OD: 20/25
▫ OS: 20/20
• EOMs: Full, unrestricted VF: FTFC
• Pupils: PERRL-APD
• Saccades: Quick and Accurate
• Pursuits: Smooth and Accurate
TBI Case: Exam Findings
• Distance Cover Test: Ortho
• Near Cover Test: 2 Exophoria
• In-Phoropter Vertical Phoria: 1 BU OS
• Red lens test: Fusion
• Vertical Maddox Rod: (-) Vertical deviation
• Fixation Disparity:
▫ Horizontal: Type IV curve
▫ Vertical Associated Phoria: 1^BU OS
• Stereo: 30” Stereo with 1^BU OS: 20”
Coursebook Page 20 of 139
1

5/31/2012
TBI Case: Accommodative Findings
• Amplitude:
▫ OD: 5.25/4.75D
▫ OS: 5.00/4.75D
• Accuracy: MEM (+0.50)
• Facility: +/-2.00 flippers
▫ 2.00D too difficult
▫ 1.50D OD: 4.5cpm
▫ 1.50D OS: 11cpm
▫ 1.50D OU: Suppression
• Binocular Cross-Cyl: +0.75 (varied +0.25 to+1.00)
• NRA, PRA
▫ +3.50/+2.75, -1.50/-1.25
Accommodation/Vergence Relationship
• Low PRA
▫ Decreased accommodative amplitude and/or
decreased negative fusional vergence (BI)
• Low NRA
▫ Reduced ability to relax accommodation and/or
decreased positive fusional vergence (BO)
TBI Case: Vergence Findings
• Gross Convergence
▫ 18 inches
• Near Vergence Ranges
▫ Phoropter: smooth, in-instrument
• BO: 34/34/18
• BI: 24/28/15
▫ Prism bar: jump vergence, free-space
• BO: 20/14
• BI: 10/8
TBI Case: Other Testing
• Visual Midline Shift:
Negative
• DEM (Developmental Eye
Movement test) Tests for
Saccadic Dysfunction:
H/V ratio: 7 th percentile
TBI Case: Other Testing
• Motor-Free Visual Perceptual Test, Edition 3
(MVPT-3): Age equivalent: 18 years. Most
difficulty with figure ground and form constancy
TBI Case: Assessment and
Recommendations
• Assessment
▫ Accommodative Insufficiency and Infacility
▫ Gross Convergence Insufficiency (possibly
secondary to accommodative dysfunction)
▫ Decreased Visual Perceptual Skills
• Recommendations
▫ Vision therapy to improve visual efficiency and
reduce symptoms
▫ Re-evaluate vertical deviation
Coursebook Page 21 of 139
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5/31/2012
Accommodative Therapy:
Near-Far Hart Chart
• Monocular
• Push up with near chart
• Many variations
• Can also be used for
saccadic training
• Goal: Accuracy, then
speed
Accommodative Therapy:
Loose Lens Rock
• Monocular
• Target: sheet of words
or groups of letters
• Alternate viewing
between (-) and (+)
lens
• Goal: -6.00/+2.50
Accommodative Therapy:
HTS (Home Therapy System)
• Red/Blue Glasses
create monocular
fixation in a
binocular field
(MFBF)
Accommodative Therapy:
Binocular Accommodative Rock
• Binocular: Bar readers
and red/green or
polaroid glasses for
monitoring
suppression
• Use lens flipper
Accommodative Therapy:
Prolonged Reading
• Monocular or Binocular
• Bar readers
• 2 minute adaptation
period
Convergence Therapy:
Gross Convergence
• Brock String
▫ Push up
▫ Bug on a String
▫ Bead Jumps
▫ Different FOG
• Barrel Card
http://www.flickr.com/photos/xooorx/6264870613/
http://www.bernell.com/category/skeyword=barrel+card
Coursebook Page 22 of 139
3

5/31/2012
Convergence Therapy:
Smooth Vergence
• Variable Vectogram
• Variable Tranaglyph
Convergence Therapy: Smooth
Vergence
• Computer Programs
(HTS, VTS, Vision
Builder)
• Tromboning with
Stereoscope
http://www.visiontherapysolutions.net/co.php#7
http://www.bernell.com
Convergence Therapy:
Jump Vergence
• Fixed Tranaglyphs
• Fixed Tranaglyphs
• HTS, VTS, or Vision
Builder
Convergence Therapy:
Jump Vergence
• Loose Prism Rock
• Look-aways with any
vergence activity
http://www.bernell.com
• Computer Program
Jump Vergence (HTS,
VTS, Vision Builder
http://www.bernell.com
http://www.bernell.com
Convergence Therapy:
Free Space
Eccentric Circles
• Can be done in
different fields of
gaze and with
motion
Life Savers
Accommodation Progress Chart
Accomm.
Amplitude
(break /
recovery)
2/2/12 5.25/4.75D
5.00/4.75D
2/9/23 6.00/4.75 D
7.75/6.00 D
Facility +/-
2.00
(OD/OS)
7cpm/7cpm
Facility
+/-2.00
(OU)
suppression
both sides
Near Far
Rock Hart
Chart
OD/OS
3:28/not
timed
2/23/12 18cpm/18cpm 2:31/2:35
3/1/12 +/-0.75
flippers:
intermittent
suppression
3/15/12 6.5, 8cpm
5/17/12 18cpm/19cpm 9cpm 2:15/2:12
Coursebook Page 23 of 139
4

5/31/2012
Vergence Progress Chart
Developmental Eye Movements Test
Clown Vecto
2/2 BO: 4/2
BI: 2/0
Spirangle
Vecto
2/9 BO: 10/4
BI: 10/9
3/1 BO: 21/13
BI: 13/8
5/17 BO: 20/17
BI: 14/7
BO: 35/24
BI: 21/14
Quoit Vecto
BO: 2/0
BI: 2/0
BO: 2/0
BI: 2/0
BO: 25/23
BI: 13/8
BO: 29/23
BI: 11/7
Brock
String
6 inches
w/effort
7cm
Stereoscope
BO: 7
BI: 3
Vergence
Facility
8pd: 3cpm
6pd: 6cpm
8pd:
8.5cpm
• February 9 th
▫ Vertical: 77 th percentile
▫ Horizontal: 53 rd percentile
▫ H/V: 7 th percentile
▫ 1-2 errors
• March 15 th
▫ Vertical: 72 nd percentile
▫ Horizontal: 69 th percentile
▫ H/V: 47 th percentile
▫ No errors
Stereo Acuity
• Initial Evaluation: 70”
• After 2 wks of therapy: 30”
Treatment Summary
Initial Evaluation
OD Monocular Facility +/-1.50: 4.5 cpm
OS Monocular Facility +/-1.50: 11 cpm
Post Therapy
Evaluation
+/-2.00: 18 cpm
+/-2.00: 19cpm
Binocular Facility +/-0.75: unable +/-2.00: 9 cpm
• 3 months later: 20”
Near BI range 24/28/15 x/12/5
Near BO range 34/34/18 >40/30
Vergence Facility unable 8BI/BO: 8.5 cpm
NPC 18 inches 6 cm
Stereopsis 70” 20”
DEM H/V ratio 7 th percentile 47 th percentile
Subjective Improvements
Reading again
More visually aware/less blur
Feels more ready to start
school for Electrical
Engineering
Sees 3-D in movies
Treatment Summary
• Evaluations and initial treatment: Dec, Jan. 26
• 5 training sessions: Feb. 2 nd , 9 th , 23 rd , March 1 st
and 15 th
• Progress Visual Efficiency Eval: April 12 th (not
feeling well and very dim illumination needed)
• Progress: MVPT3, DEM, FD: April 19 th
• CL fit: May 3 rd
• CL check and repeat Visual Efficiency Progress
Evaluation: May 17 th
Coursebook Page 24 of 139
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5/31/2012
Special Considerations for VT patient
with TBI
• Usually takes longer
• Other factors, speech, cognitive impairment, etc.
• Mild TBI often most successful cases
• More variation in performance, good and bad
days
• Be aware of nausea
• Vision Therapy can make a difference
Traumatic Brain Injury
• 1.4 million brain injuries each year 1
• 5.3 million Americans (2% of population) need
help performing activities of daily living 2
• In combat, at least 14-20% of casualties have
TBI that require acute and long term care 3
• Mild TBI cases are not being identified. 40% of
these patients experience vision problems. 3
Biochemical Basis of Neuro-Disruption 4
Breakdown of intimate
association of cerebral
blood flow (CBF) and
cerebral glucose
metabolism (CMGL)
Cell
toxicity
Ischemia and
hypoxia
Metabolic
imbalances
Change
neuronal cell
membrane
permeability
Most Common Visual Diagnoses
Following TBI
• Convergence Insufficiency
• Strabismus
• Accommodative Insufficiency
• Accommodative Infacility
• Ocular Motility Disorders
• Visual Field Defects
• Photosensitivity
• Dry Eye
Case History
• Did you lose consciousness Did you feel heat or pressure during blast
• Did the blast affect your hearing
• Are you more sensitive to light Noise
• Blurry or double vision
• Headaches
• Balance problems
• Feel dizzy Do you feel this way when you move your eyes
• Bump into things
• Miss objects when first reach Have difficulty judging depth of stairs
• Poor concentration, memory, or attention
• Difficulty thinking or solving problems Identifying objects
• Trouble with speech
• Overstimulated Overwhelmed Do things that didn’t bother you, now do
• Change of emotions Short-tempered
• Anxious Depressed Dreams of traumatic past events Fatigue easily
• Are there things you used to be able to do and can’t anymore
• Does the floor look tilted Do walls or floor shift and move
• Cranial nerve questions
BIVSS SYMPTOM CHECKLIST
Please check the most appropriate box, or circle the item number that best matches your observations. Alll
information will be held in confidence. Circle a number below. Please rate each behavior.
How often does each behavior occur (circle a number) Never Seldom Occasionally Frequently Always
EYESIGHT CLARITY
Distance vision blurred and not clear -- even with lenses 0 1 2 3 4
Near vision blurred and not clear -- even with lenses 0 1 2 3 4
Clarity of vision changes or fluctuates during the day 0 1 2 3 4
Poor night vision / can’t see well to drive at night 0 1 2 3 4
VISUAL COMFORT
Eye discomfort / sore eyes / eyestrain 0 1 2 3 4
Headaches or dizziness after using eyes 0 1 2 3 4
Eye fatigue / very tired after using eyes all day 0 1 2 3 4
Feel “pulling” around the eyes 0 1 2 3 4
DOUBLING
Double vision -- especially when tired 0 1 2 3 4
Have to close or cover one eye to see clearly 0 1 2 3 4
Print moves in and out of focus when reading 0 1 2 3 4
Coursebook Page 25 of 139
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5/31/2012
BIVSS SYMPTOM CHECKLIST
LIGHT SENSITIVITY
Normal indoor lighting is uncomfortable – too much glare 0 1 2 3 4
Outdoor light too bright – have to use sunglasses 0 1 2 3 4
Indoors fluorescent lighting is bothersome or annoying 0 1 2 3 4
DRY EYES
Eyes feel “dry” and sting 0 1 2 3 4
“Stare” into space without blinking 0 1 2 3 4
Have to rub the eyes a lot 0 1 2 3 4
DEPTH PERCEPTION
Clumsiness / misjudge where objects really are 0 1 2 3 4
Lack of confidence walking / missing steps / stumbling 0 1 2 3 4
Poor handwriting (spacing, size, legibility) 0 1 2 3 4
PERIPHERAL VISION
Side vision distorted / objects move or change position 0 1 2 3 4
What looks straight ahead--isn’t always straight ahead 0 1 2 3 4
Avoid crowds / can’t tolerate “visually-busy” places 0 1 2 3 4
READING
Short attention span / easily distracted when reading 0 1 2 3 4
Difficulty / slowness with reading and writing 0 1 2 3 4
Poor reading comprehension / can’t remember what was read 0 1 2 3 4
Confusion of words / skip words during reading 0 1 2 3 4
Lose place / have to use finger not to lose place when reading 0 1 2 3 4
Home Training Kit $325
• 1-patch, 1-Brock String (large), 1-Marsden Ball
• R/G glasses
• 2-Lifesaver cards (Clear and Opaque)
• 10-loose lenses (+.50, +1.00, +1.50, +2.00, +2.50, -.1.00, -2.00,
-3.00, -4.00, -5.00)
• 4-flipper lenses: (+/- 1.00, +/- 1.50, +/- 2.00, +/- 2.50)
• Loose Prisms: 4, 6, 8, 12 pd
• Tranaglyphs:
6-one-piece fixed:
BC 71, BC 72 vertical
BC 51, BC 52, BC 53, BC 54
3-two-piece variable: BC 920H (horizontal mini), BC 520, BC 802
• Tranaglyph holder
• Reading Bars for suppression monitoring
Resources
• DVBIC (Defense and Veterans Brain Injury
Center)www.dvbic.org
• NORA (Neuro-Optometric Rehabilitation
Association)www.nora.cc
• Resources for returning Veterans:
http://www.oefoif.va.gov
• www.Bernell.com
• http://oep.excerpo.com/
References
1. Langlois JA, Rutland-Brown W, Thomas KE.Traumatic brain injury in the United States:
emergency department visits, hospitalizations and deaths. Atlanta GA: Centers for Disease
Control and Prevention, National Center for Injury Prevention and Control, 2004.
2. Thurmann D, Alverson C, Dunn K, Guerro J,Sniezek J. Traumatic brain injury in the United
States: a public health perspective. J Head Trauma Rehab 1999;14:602-15.
3. Traumatic Brain Injury, Veterans Health Initiative: Department of Veterans Affairs,
Employee Education System; January 2004.
4. Center for Neuro Skills. http://www.neuroskills.com/brain-injury/the-neuro-biochemicalbasis-of-post-trauma-vision-syndrome.php
5. Scheiman and Wick. Clinical Management of Binocular Vision: Heterophoric,
Accommodative, and Eye Movement Disorders
6. Griffin and Grisham. Binocular Anomalies: Diagnosis and Vision Therapy
7. NORA meeting notes. Atlanta 2011.
8. Medscape: Epidemiology and Classification of Traumatic Brain Injury
Thank you!
Coursebook Page 26 of 139
7

5/29/2012
Overview
CASE STUDY:
THE EVOLUTION AND RESOLUTION OF AN
OCULOMOTOR NERVE PALSY
PRESENTER: JESSICA DENNIS - JNDMAIL@YAHOO.COM
INSTRUCTOR: DOUGLAS DEVRIES - EMAIL
Case presentation
Differential diagnoses and assessment
Pathway and function of oculomotor nerve
Plan
Referrals
Follow ups
Additional information
Questions
Eye Care Associates of Nevada - 2285 Green Vista- Sparks, NV 89431
Ring ring
Presentation (11/14/2012)
ER doctor calls Saturday night
CC: dull eye ache/pain OS
• Stable VAs
Reports normal eye examination including
• Full EOMs, no pain/diplopia
• Pupils normal, no APD
• No AC reaction
• Normal CT scan
Initial assessments…
Follow up with Ophthalmologist Monday
Demographics-
54 year old
African American male
Medical history:
• Heart disease
• High blood pressure
• Diabetes, type II
• Insulin dependent
• Peripheral diabetic neuropathy
• Hemodialysis secondary to diabetic nephropathy
ROS:
• Hearing loss, chronic cough, arthritis, easy fatigability, depression, kidney failure
Current medications:
• Alprazolam, amlodipine, aspirin, Coreg, gabapentin, insulin, Prevacid, nitroglycerine,
Coumadin, Zovirax
Ocular history:
• Cataract extraction OU (5/2011)
Presentation (11/14/2012)
Examination (11/14/2012)
CC: “Worried implant moved”
HPI:
Constant dull ache OS
• No jaw claudication or temporal pain
• Trace photophobia
(+) diplopia for 2 days, goes away if OD covered
• Vertical and horizontal, distance and near
• Stable, constant
Slight blur/fuzzy VA OS
Reports blood glucose in the low 100’s
VA(sc)
OD: 20/20
OS: 20/25- , PH 20/25+
CVF:
full OD, OS
EOMs:
full OD
Normal primary gaze- no exotropia or hypotropia
Adduction and infraduction gaze restrictions OS, (+) diplopia
Pupils:
Aniso OS>OD in light and dim illuminations
Slow reaction to light OS
Normal near response
No APD
Hertel:
21>-----

5/29/2012
Examination (11/14/2012)
Anterior segment
Ptosis OS
Trace SPK OU
PCIOL OU
1+ PCO OS
Examination (11/14/2012)
Posterior segment
Questionable mild pallor ONH OS
Tortuous vessels OU
(+) trace cellophane changes OU
Scattered dot/blot hemes in all four quadrants OU
• possible IRMA/NVE superotemporal arcades OS
Abnormal findings…
DDx
Abnormal EOMs OS
Pupil OS
Ptosis OS
Diabetic/heart conditions…
DDx
Partial oculomotor nerve palsy
Strabismus
Decompensated phoria
Myasthenia Gravis
Grave’s
Orbital fracture
Internuclear ophthalmoplegia
Duane’s type II
Brown’s
Strabismus and Decompensated Phorias
Perform cover test in different fields of gaze
Results comitant or non-comitant
Non-comitant considered greater then 5 prism diopters
of difference between
Non-comitant generally implies cranial nerve palsies
Comitant usually indicates strabismus
Paretic or mechanical
Ductions (monocular eye movement)
Versions (binocular eye movement, physiologic H)
Ductions>Versions
Paretic
Ductions=Versions
Mechanical
Forced duction testing
Drop the suspected eye with anesthetic
Grab conjunctiva with toothless forceps near limbus and attempt to move eye in
direction opposite that mechanical restriction is thought
+ forced duction means eye did NOT move
Indicates mechanical restriction
- forced duction means eye DID move
Indicates paretic in nature
Coursebook Page 28 of 139
2

5/29/2012
History is key…
Myasthenia Gravis
Grave’s
Orbital fracture
Review
Internuclear ophthalmoplegia
Lesion of MLF
Ipsilateral adduction deficit with abducting nystagmus is
opposite eye
Duane’s type II
Adduction deficit
No globe retraction
Brown’s
Superior oblique tendon sheath syndrome
Limited elevation in adduction
Assessment
1. Left partial CN III palsy, relative pupil sparing
2. IDDM with moderate to severe NPDR OD
IDDM with likely NPDR OS
Oculomotor nerve review
Origination and pathway
Efferent pupillary pathway
OM nerve functions
Partial, complete, isolated
3. Pseudophakic OU
4. PCO OS
Origin
Oculomotor nuclear complex
http://www.neuroanatomy.wisc.edu/virtualbrain/BrainStem/21CNIII.html
Coursebook Page 29 of 139
3

5/29/2012
Origin
Pathway
http://radiologymri.blogspot.com/2010/12/oculomotor-infarct.html
http://www.medrounds.org/ocular-pathology-study-guide/uploaded_images/cwmr-768439.jpg
Pathway
Pathway
http://bestpractice.bmj.com/best-practice/monograph/956/basics/pathophysiology.html
http://legacy.owensboro.kctcs.edu/gcaplan/anat/notes/api%20notes%20m%20%20peripheral%20nerves.htm
Functions
Edinger-Westphal (Efferent pupillary pathway review)
Superior division:
levator palpebrae superioris*
superior rectus
Inferior division:
medial rectus*
inferior rectus*
inferior oblique
- preganglionic parasympathetic to ciliary ganglion
(innervation of sphincter pupillae* and ciliary muscle)
http://brains.oxfordmedicine.com/cgi/content-nw/full/12/1/med-9780198569381-chapter-002/FIG002037
Coursebook Page 30 of 139
4

5/29/2012
Types
Recall assessment
Pupil involving
Aneurysm, tumor, trauma, cavernous sinus mass, pituitary
apoplexy, herpes zoster
1. Isolated left partial CN III palsy
-relative pupil sparing
Relative pupil sparing
Ischemic microvascular disease*
Pupil sparing
Ischemic microvascular disease, GCA
Isolated
Partial or complete
2. IDDM with moderate to severe NPDR OD
IDDM with likely NPDR OS
3. Pseudophakic OU
4. PCO OS>OD
Plan
1. Order MRI of brain/orbits****
- Request CT scan
- Neuro-ophthalmic consult
2. Retina specialist consult for likely PDR
3. Yag laser OS
Treatment options for diplopia:
Patching (remember not to patch patients

5/29/2012
11/30/2012 continued
MRI w/o contrast
Examination continued…
Anisocoria OS>OD
OS down and to the left
EOMs OS
• Supraduction, infraduction, adduction restricted
• normal abduction
Negative forced ductions**
Complete ptosis OS
Maxillofacial CT scan (11/12/11) – normal
MRI (11/15/2011)
Brain
Findings
No mass effects or shift of midline structures
No hemorrhagic lesions
No evidence of acute cerebral infarction
Impression
Minimal age related cortical atrophy
Microvascular ishemic gliosis
Wedge shaped area of chronic infarction, left occipital lobe
11/30/2012 continued
12/22/2011
Assessment:
Pupillary involving left oculomotor palsy…
Diabetic (ischemic microvascular) third nerve palsies spare pupil…
Order MR angiogram of head and neck to r/o posterior communicating artery aneurysm
Left occipital infarct
HVF
Diabetic retinopathy OU
Ordered the following lab studies:
• CBC
• ESR/CRP
• ACE level
• ANA
• PRP
Trial dispense of celebrex for pain
RTC 1 month
Patient reports slight increase on inward eye movement and
complete relief of pain with celebrex
Examination:
Slightly improved motilities on supraduction and adduction
HVF 30-2:
Scattered defects
Lab results:
CBC: normal
Metabolic panel: elevated glucose level
ANA, ACE, ESR, RPR, vit B12, folate: normal
MR angiogram (12/9/2011):
Circle of Wilis: normal
Neck: normal carotid arteries
12/22/2012 continued
Assessment:
1. Marginally improved pupillary involving left
oculomotor palsy
**Importantly “no clear-cut evidence of posterior
communicating artery aneursym”
2. Left occipital lobe infarction
- No HVF defects
3. Bilateral diabetic retinopathy
RTC 1 month
03/01/2012
Missed appointments… things must be better
Yes! No double vision, pain and ptosis improved
EOMs, pupils
Examination showed full recovery of adduction,
supraduction and infraduction!
Pupils showed slight aniso (4.5 OD, 5.0 OS)
Coursebook Page 32 of 139
6

5/29/2012
Summary of Retinal Appointments
Retinal Consultation
Dr. Jarl Nielsen
Nevada Retina Associates
610 Sierra Rose Drive
Reno, NV 89511
11/15/2011 (OD 20/20, OS 20/25)
NPDR OD, Early PDR OS
12/20/2011 (OD 20/20, OS 20/40)
IVFA performed
PDR OS>OD
PRP OS performed
01/10/2012 (OD 20/20, OS 20/40)
PRP OS
1/31/2012 (OD 20/20, OS 20/30)
PRP OS
RTC for DFE OD, possible PRP
Summary of Retinal Appointments
Summary of Retinal Appointments
02/07/2012 (OD 20/20, OS 20/30)
DFE OD minimally active NVE
Stable OS
Follow up in 2-4 weeks, PRP OD
02/28/2012
PRP OD
03/20/2012
PRP OD
05/08/2012
Involuting NVE OD
No active NVE OS
RTC 1 month
04/10/2012
PRP OD
03/05/2012
Back to Eye Care Associates…
Referred back by Dr. Hershewe for possible conjunctivitis
SLE:
2+ injected nasal and temporal pinguecula
Trace to 1+ diffuse SPK
PCO OS>OD
Assessment:
Pingueculitis OD>OS
Dry eye syndrome
Plan:
Continue FML qid (as dispensed by Dr. Hershewe)
add artificial tear use
RTC for YAG OS 1 st , then OD
Coursebook Page 33 of 139
7

5/29/2012
03/14/2012
Lastly, addressing “slight blur OS”
VA post laser treatment
• OD: 20/20
• OS: 20/20-
Additional information
Possible CN III locations of involvement
Aberrant regeneration
Food for thought
And full motilities!
RTC annually
Follow up with Dr. Nielsen as scheduled
Location of palsy
Midbrain damage
All or part of nucleus may be affected
• More commonly entire nucleus
If entire nucleus
• Ipsilateral muscles involved: MR, IR IO
• Contralateral muscles involved: SR
• Both: levators
CN IV nucleus close by…
• Is contralateral superior oblique involved
Location of palsy
Intracranial
As previously discussed, posterior communicating artery
common location for aneurysm to affect oculomotor
nerve
Less common are posterior cerebral and superior
cerebellar arteries
Location of palsy
Cavernous sinus
Ipsilateral CN IV involvement possible
Ophthalmic division of V
Maxillary division of V
Eye would be out (only LR working) and facial anesthesia
would be present
Orbital
Retrobulbar tumor or inflammation
• CN VI and nasociliary nerves involved secondary to close location
in muscle cone
Eye would be down, slightly out (only SO working)
http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v1/v1c003.html
Coursebook Page 34 of 139
8

5/29/2012
CN III aberrant regeneration
Fibers making incorrect connections
Can occur from the following
Congenital
Primary
Acquired… damage or compression
• During recovery
• NOT ISCHEMIC!!!
CN III aberrant regeneration
1. Pseudo graefe sign
levator superioris and inferior rectus
2. Eyelid dyskinesis
levator superioris and medial rectus
3. Pupil dyskinesis
parasympathetic fibers and medial rectus
Food for thought
86% of pupil involved are from aneurysms
23% of pupil involved are vascular/ischemic
14% of pupil sparing are from aneurysms
77% of pupil sparing are vascular/ischemic
Food for thought
95% of painful CN III palsies are caused by
aneurysms
80% of painful CN III palsies are ischemic/vascular
Pain not a very good differential
Kissel JT. Ann Neurol 1983
Goldstein JE, et al. Arch Ophthalmol 1960
Clinical Pearls
Questions
Case history
Investigate the double vision
• Monocular or binocular
• Vertical or horizontal
• Distance or at near
Comitant or non-comitant
Forced duction testing!
Photo document
Don’t forget imaging guidelines
Can be an ocular emergency!!
Send for proper referrals
Atypical cases… not all are textbook
Special thanks to:
Curtis Manning, MD
Paul W Hiss, MD
Douglas Devries, OD
Gerard L Hershewe, DO
Jarl Nielsen, MD
Coursebook Page 35 of 139
9

5/29/2012
Oliver
Oliver
Kuhn-Wilken,
Kuhn-Wilken,
O.D.
O.D.
Jeffery Hiett, O.D. and Irene Yang, O.D.
Drs. Jeffery Hiett and Irene Yang
Jonee Brandt, O.D. and Jason Bleazard, O.D.
Drs. Jonee Brandt American and Lake Jason VA Bleazard Hospital
American Lakewood, VA Washington Hospital
Lakewood, Washington
The Problem with
Prostaglandins
Case #1: BW
• 71 yo white male
• CC: vision OD is “like spots on a shower door” x 6 months,
gradual onset, now constant, am = pm, distance = near.
• POHx: POAG treated with TravatanZ qhs OU
cataract extraction with PCIOL (2006) and YAG OU
• PMHx: COPD
sleep apnea with CPAP cannulas
• VAs sc: OD 20/50-2 PHNI, OS 20/20-1
• Tap OD 11 mmHg, OS 13 mmHg @ 0900
• SLE: ONH: c/d ratio OD 0.65 with pallor, OS 0.30
macula: OD elevation at fovea, OS normal
Case #1: BW
• Stratus OCT:
foveal thickness
OD 541 um,
OS 214 um
Case #1: BW
• Assessment: cystoid macular edema OD
• Plan: discontinue TravatanZ
Rx dorzolamide 2% bid OU
Rx ketorolac 0.4% qid OD
Case #1: BW
Exam Date Foveal thickness OD BCVA OD IOP OD
8/19/2011 541um 20/50-2 11
8/30/2011 475um 20/40-2 15
9/13/2011 298um 20/40 17
9/27/2011 252um 20/30+1 18
10/27/2011 275um 20/40 19
CME fundus appearance
OCT
OD:10/27/2
011
CME fundus
appearance
Coursebook Page 36 of 139
1

5/29/2012
CME
Cystic spaces
on OCT:
CME can follow
ant. seg. inflammation
• Anterior uveitis
• Cataract surgery (Irvine-Gass Syndrome) or YAG
Late-phase petalloid appearance on FA:
CME can follow
post. seg. inflammation
• Retinal venous occlusions
• Epiretinal membrane
• Diabetic retinopathy
• ARMD
Edema
of
Müller
cells
Edema
of the
Edema optic
of nerve the
optic
nerve
The Prostaglandin Analogs
• First line glaucoma therapy
• Possible pro-inflammatory effect
• Relative contraindications: cataract surgery
uveitis
herpes simplex keratitis
epiretinal membrane
pregnancy
Coursebook Page 37 of 139
2

5/29/2012
The Inflammatory Cascade
The Hidden Cost of CME
• 1-2% of CE patients diagnosed with “clinical CME.”
• 20% of patients have “angiographic CME.”
0.8
LogMAR vision versus time following cataract extraction
ETDRS vision in LogMAR units
0.7
0.6
0.5
0.4
0.3
0.2
0.1
No CME
CME at 8 weeks
0
Pre-op Day 1 Day 14 Day 30 Day 60
Ursell PG, Spalton DJ, Whitcup SM, et al.
CME and cataract surgery
• The biggest risk factors:
uncontrolled diabetes or hypertension
CME following CE in the fellow eye
CE with breach of the posterior capsule
retinal venous disease
epiretinal membrane
PGs and cataract surgery
• There is no Gold Standard.
• Recommendation: cover with an NSAID
qid for 2-7 days prior to surgery.
• Do not discontinue or replace a
prostaglandin.
Management of CME
• NSAID qid
• Pred Forte qid
• Consider replacing a prostaglandin
• Referral if not improving: consider sub-
Tenon’s injection, intravitreal injection, or
vitrectomy
PGs
and
uveitis
• Uveitis is an inflammatory disease
• PGs may have a pro-inflammatory effect
• Therefore PGs are relatively
contraindicated in uveitic patients.
• Contraindication is rarely observed
Coursebook Page 38 of 139
3

5/29/2012
PGs and uveitis
Study No. of eyes Time Uveitic response
Warwar 1998 163 normals 1 year 6.4%
Smith 1999 505 normals 1 year 1.0%
Smith 1999 13 uveitics 1 year 23.1% Mostly mild cases
Chang 2008 163 uveitics 3 mos.
Markomichelakis
2008 58 uveitics 6 mos.
equal to
control
equal to
control
Control = fellow eye, non PG
glaucoma medication
Control =
dorzolamide/timolol
medication
PGs and uveitis
• Case studies describe patients in whom
uveitis occurs in the ipsilaterally treated
eye, and patients in whom the uveitis
improves after cessation and recurs after
rechallenge.
• Latanoprost may not lower IOP during a
uveitic flare.
Goldberg 2008 5,856 normals 5 years OD
laser burns OS peripheral retina, no tear
Case #2: HF
• Assessment: herpes simplex keratitis OS.
• Plan: Rx Viroptic q2h OS, acyclovir
400mg bid po, and erythromycin ung qhs
OS.
Case #2: HF
Date VA OS Assessment Current medications
10/25/07 20/200 Acute HSK OS TravatanZ qhs OU, timolol 0.5%
GFSqam OU (continued)
10/29/07 20/200 “Improving” Viroptic q2hr OS, erythromycin ung
qhs OS (continued)
11/02/07 20/200 “Improving” Viroptic 5x/day OS with taper,
acyclovir 400 mg po bid
11/09/07 4/300 “No improvement” Viroptic 5x/day OS, acyclovir 400mg
po bid (continued)
11/13/07 5/200-1 “Improving” Taper Viroptic over 4 days
11/16/07 5/200-1 “Slowly improving” Viroptic qd x 2 days then d/c
11/19/07 5/200- “Resolving” Refresh tears qid OS
11/26/07 5/250 “Resolving” no change
11/30/07 5/200 “no improvement” Replace erythro with bacitracin ung
12/3/07 5/200- “Resolving” no change
12/7/07 5/225 “Resolved” Replace baci with erythro ung qhs OU
Case #2: HF
Date VA OS Assessment Plan
12/14/07 4/160 “Resolving” TravatanZ qhs OU, timolol 0.5% GFSqam
OU, acyclovir 400 mg po bid (continued)
12/31/07 4/160 “Resolving” no change
2/5/08 5/700 Active disciform
HSK
Viroptic 5x/day OS,
acyclovir 400 mg po bid (continued)
2/8/08 2/125 “Resolving” Viroptic 5x.day OS
2/11/08 2/125 “Resolving” Viroptid qid OS
2/15/08 3/400 “Resolving” Viroptic qd OS x 1 day then d/c
2/20/08 3/350 “Improving” D/c Viroptic. D/c TravatanZ OS
2/25/08 3/350 “Improving” no change
3/4/08 5/350 “improvement” D/c TravatanZ OD
3/7/08 5/350 “continued
no change
improvement”
3/14/08 5/300 “stable” no change
Coursebook Page 39 of 139
4

5/29/2012
PGs and herpes simplex keratitis
PGs and herpes simplex keratitis
Study Patients Time HSK rate Caveat
Bean 2004 39,174 normals
on PG therapy
6 years 0.11% Only counted 1 st occurrence
Only counted if within 7
days of PG start
Lead researcher employed
by Pfizer
Research paid for by Pfizer
• Case studies: HSK reported to recur after
up to 10 years of inactivity upon
commencement of latanoprost use, and be
unresponsive to anti-viral therapy until
the latanoprost is discontinued.
• No other large studies
References
Prostaglandin take-homes
1. Cover with an NSAID prior to CE if there
are any risk factors.
2. Uveitis or HSK due to PGs is very rare.
3. Strongly consider discontinuing PGs
once CME, uveitis, or HSK occurs.
• Giuffre G. The effects of prostaglandin F2 in the human eye. Graefes Arch Clin Exp Ophthalmol
1985;222:139-41.
• Benitah, Nicole R. MD; Arroyo, Jorge G. MD. Pseudophakic Cystoid Macular Edema. International
Ophthalmology Clinics: Winter 2010 - Volume 50 - Issue 1 - pp 139-153. doi:
10.1097/IIO.0b013e3181c551da. extraction: a fluorescein funduscopic and angiographic study. Arch
Ophthalmol. 1966;76:646.
• Yanoff M, Fine BS, Brucker AJ, et al. Pathology of Human Cystoid Macular Edema. Surv Opthalmol 28
(Suppl): 505-511, 1984.
• Miyake K, Ibaraki N. Prostaglandins and Cystoid Macular Edema. Surv Opthalmol 47 (Supplement 1):
S203-S218, 2002.
• Warren K. Current Concepts in the Etiology and Treatment of Pseudophakic Cystoid Macular Edema.
Retinal Physician: http://www.retinalphysician.com/printarticle.aspxarticle=103062, 6/1/2009.
Accessed 03/06/2012.
• Ursell PG, Spalton DJ, Whitcup SM, et al. Cystoid macular edema after phacoemulsification: relationship
to blood-aqueous barrier damage and visual acuity. J Cataract Refract Surg. 1999; 25:1492-1497.
• Ngyuen, Q. The role of prostaglandin analogs in the treatment of glaucoma in the 21 st century. Int.
Ophthalmol Clin 2004;44:2:15-27.
• Arcieri ES, Santana A, Rocha FN, et al. Blood-aqueous barrier changes after the use of prostaglandin
analogues in patients with pseudophakia and aphakia. Arch Ophthalmol. 2005;123:186-192.
• Miyake K, Ota I, Maekubo K, et al. Latanoprost accelerates disruption of the blood-aquous barrier and
the incidence of angiographic cystoid macular edema in early postoperative pseudophakias. Arch
Ophthalmol. 199;117:34-40.
References
• Shrivastava A. Prostaglandins, cataract surgery and CME. Review of Ophthalmology. 07/22/2009.
• Camras CB, Bhuyan KC, Podos SM, et al. Multiple dosing of prostaglandin F2 or epinephrine on
cynomolgus monkey eyes. Invest Ophthalmol Vis Sci 1987;28:921-6.
• Arcieri ES, Pierre Filho PT, Wakamatsu TH. The effects of prostaglandin analogues on the blood aqueous
barrier and corneal thickness of phakic patients with primary open-angle glaucoma and ocular
hypertension. Eye (Lond). 2008 Feb; 22(2):179-183.
• Warner RE, Bullock JD, Ballal D. Cystoid macular edema and anterior uveitis associated with latanoprost
use: experience and incidence in a retrospective review of 94 patients. Opthalmology. 1998;105:263-268.
• Chang JK, McCluskey P, Missotten T, et al. Use of ocular hypotensive prostaglandin analogues in
patients with uveitis: does their use increase anterior uveitis and cystoid macular edema Br J
Ophthalmol. 2008 Jul;92(7):916-21.
• Goldberg I, Li XY, Selaru P, et al. A 5-year, randomized, open-label safety study of latanoprost and usual
care in patients with open-angle glaucoma or ocular hypertension. Eur J Ophthalmol. 2008;18(3):408-416.
• Wand M, Gilbert CM Liesegang Tj. Latanoprost and herpes simplex keratitis. Am J Ophthalmol
1999:127(5):602-604.
• Bean G, Reardon G, Zimmerman TJ. Association between ocular herpes simplex virus and topical ocular
hypotensive therapy. J Glaucoma. 2004;13(5):361-364.
Coursebook Page 40 of 139
5

*
Diagnosis and Management of
Posner-Schlossman Syndrome
Jonee Brandt O.D.
VA Puget Sound Health Care System: American Lake
Division
jonee.brandt@gmail.com
What is Posner-Schlossman
Syndrome
• First described in 1948 by Abraham Schlossman and Adolf Posner
who had a series of 9 patients with similar symptoms and
characteristics of both glaucoma and uveitis.
• Uncommon inflammatory eye condition, classically unilateral, with
elevated intraocular pressures and minimal inflammation.
• Recurrent
• Tends to occur in young-middle aged adults, male>female, with no
racial predilection.
• Accounts for about 4% of all anterior uveititis.
Typical Presentation
*Acute intermittent history of mild blurred vision and minimal unilateral
discomfort
*Mild conjunctival injection, minimal anterior chamber reaction, small to
medium keratitic precipitates, NO posterior synechiae, possible iris
heterochromia/sectoral atrophy, and markedly elevated IOP.
*Acute attacks will resolve spontaneously in a matter of days-weeks
*Recurrence of attacks can vary greatly from patient to patient
Differential Diagnoses
• Herpes Simplex Trabeculitis
- Viral infection of endothelial cells of TM, cellular swelling and lysis 2’ to
immune attacks
- Management: IOP control, antivirals, and concurrent topical steroid tx
- May also present with: corneal endotheliitis and 2’ edema
- (+)HSV, possible h/o keratitis
●
Differential Diagnoses
Fuch's Heterochromic Iridocyclitis
● Iris heterochromia
● Chronic mild unilateral anterior uveitis which does
NOT respond to steroid treatment
● Triad of heterochromia, cataract, and glaucoma
Differential Diagnoses
• Pigmentary Glaucoma
-Krukenberg’s spindle, iris TID’s,
pigment in TM
-glaucomatous changes to optic nerve
head
• Angle Closure/Angle
Closure Glaucoma
-closed angle on gonioscopy
-likely more severe symptoms:
including nausea/vomiting, facial
pain, haloes around lights
Coursebook Page 41 of 139
1

*
Differential Diagnoses
• Ankylosing Spondylitis
– Lower back pain
– X-Ray of sacral spinal region and
HLA-B27
• Reiter’s Syndrome
– Triad of arthritis, conjunctivitis,
urethritis
– HLA-B27
• Behcet’s Disease
– Mouth, skin, and/or genital ulcers
– Mediterranean descent
– HLA-B5
Differential Diagnoses
• Juvenile Rheumatoid
Arthritis
– Children
– Girls>Boys
– ANA
• (Granulomatous)-
Syphillis/Sarcoidosis
– RPR/VDRL if suspect syphilis (quick
nonspecific), reflect disease activity vs
FTA-ABS and MHA-TP remain
positive for life, even after active
disease
Indicated Testing
• Complete eye examination, including gonioscopy to rule out angle
closure glaucoma/pigmentary glaucoma
• As Posner Schlossman patients present with markedly elevated IOP
during these recurrent attacks monitor closely for developing
glaucomatous changes: RNFL OCT, Threshold Visual Fields
• Appropriate lab testing to rule out systemic causes of inflammation:
– CRP/ANA/HLA-B27
– HLA-B5
– PPD/Chest X-Ray to rule out TB
– CBC with differential: to determine if bacterial or viral
– RPR/VDRL, FTA-Abs, MHA-TP
Possible Etiologies
• Posner and Schlossman first theorized an infectious
etiology due to episodic nature.
• Viral favored due to intermittence of attacks
• Trabeculitis
• Elevated prostaglandin E
Possible Etiologies
Possible Etiologies
• Cytomegalovirus
– Various small scale studies have found that aqueous aspirates of PSS patients
(+)CMV
– Chee et al had first large scale study with 24/105 anterior uveitis pts (+)CMV, but
18 out of those 24 were found to have PSS. 11/18 (+)CMV reverse transciptase on
PCR, during inactive periods pts were (-)CMV
– HOWEVER, seropositivity testing reveals CMV is common in the general
population (87% seropositivity in Singapore, 60-80% in US)
●
Helicobacter Pylori
– Choi et al examined 40 PSS vs 73 normals
– 80% of PSS pts were (+)H. Pylori by ELISA, vs 56.2% normals
– Postulated theory of direct infection to the eye or that H. Pylori increases host
susceptibility for ocular inflammation, possibly through damage to blood vessels
• Herpes Simplex Virus
– 3 patients with active PSS had PCR on aqueous draws
(+)HSV, (-)CMV, (-)VZV
– Subsequent studies have failed to replicate these results
– Treatment of PSS with Acyclovir has been shown to be
ineffective
Varicella Zoster Virus
– 1985 Varicella skin testing revealed that 5/7 pts had PSS
attacks when immune response to varicella was low on skin
testing, and the other 2 with a high immune response
showed no PSS attacks in a 2 year follow up
– Small sample size
Coursebook Page 42 of 139
2

*
Is Posner Schlossman Syndrome
Benign
• CASE PP: 37 yo AM
1 st exam in 09/2007: Pt at that time reports recurrent uveitic
attacks OD x 5-6x/year and reports he felt he was having an attack at
that time: discomfort and slight blurred vision OD.
VA 20/20- OD, OS
IOP 22 OD, 14 OS mmHg
C/D ratio 0.5 H/V OD, 0.4 H/V OS
Assessment: Recurrent non-granulomatous anterior uveitis OD
Plan: Scopolamine bid, Cosopt bid, Pred Forte q2hr OD, RTC 3
weeks for follow up
Date
Acute
Attack
vs
Follow
Up
Visual Acuity
OD, OS
9/29/2007 AA 20/20‐ OD,
OS
IOP
OD, OS
Present
ocular meds
Plan
22, 14 None PF q2hr,
scop bid,
cosopt bid
OD. RTC 3
days
10/1/07 FU 20/25 OD, OS 12, 12 PF q2hr, scop
bid, cosopt
bid OD
10/5/2007 FU 20/25 OD
20/20 OS
10, 14 PF qid, Scop
bid, Cosopt
bid OD
PF qid,
continue
Scop/coso
pt bid OD
RTC 4
days
Taper PF,
d/c
Cosopt
and scop
OD
RTC 3
weeks
Additional
Recurrent
NG
Anterior
Uveitis
“”
“”
Date AA vs FU Visual
Acuity
OD, OS
1/30/12 AA 20/15,
20/20
2/10/12 FU 20/15,
20/20
3/5/12 FU with
AA:
symptoms
presented
yesterday
20/15,
20/20
3/19/12 FU 20/20 OD,
OS
IOP
OD, OS
Present ocular meds
27, 11 Self initiated PF 1day
ago OD
Plan
PF qid and Brimonidine
bid OD, RTC 10 days
8, 11 PF qid, Brim bid OD Taper PF, continue
Brim bid OD
RTC 3 weeks for
DFE/OCT
32, 12 None Begin PF qid x 2 weeks,
Brim bid OD. RTC 2
weeks.
7, 14 PF qid and Brim qd
OD
Taper PF slowly,
continue brimonidine
bid OD. Begin trial IBU
200mg po tid. F/U in 1
mo.
03/05/12
RNFL thickness OCT
Impression:
Good symmetry in a triple
hump pattern OD, OS.
No glaucomatous RNFL
thinning OD, OS.
Is Posner Schlossman Syndrome
Benign
• Case 2: NH 67 yo AAM
– 2007: OS red with 8/10 pain, photophobia, and cloudy vision. Pt
reports several occurrences over past few years. Last occurrence
3-4 mos ago and reports it usually resolves in 1 week.
• VA 20/20 OD, 20/30- OS
• Pupils: (+)APD OS
• SLE: +KP’s and 1+ cells OS
• IOP 16 OD/48 OS mmHg
• C/D 0.4 OD, 0.6 OS
• Assessment: Trabeculitis OS
• Plan: Alphagan tid OS, Levobunolol bid OS, Dorzolamide bid OS, IOP check
1 day
Date VA IOP Current ocular meds Plan
4/27/07 20/20, 20/25‐ 16, 36 Brim tid, levo bid, dorz bid, PF
qid
5/2/07 20/20, 20/25 16, 15 Brim tid, levo bid, dorz bid, PF
taper
CPM, RTC 5
days
Taper PF, RTC 2
weeks for
CEE/IOP check
6/5/07 20/20, 20/25 18, 18 Self D/C all meds Start Cosopt tx
bid OS, RTC 6
mos for
HVF/OCT/IOP
12/6/07 20/20, 20/25 18, 22 Cosopt bid OS
RTC 6 weeks
for IOP check.
***FDT at this date showed
nasal step and early inferior
arcuate defect OS. C/D 0.4
OD, 0.6 OS
LOST TO FOLLOW UP
4/10/09 20/20, 20/30‐ 19,54 D/C cosopt bid OS
C/D : 0.45 OD, 0.95 OS
***OCT today
Cosopt bid,
Brim bid, PF qid
OS
Coursebook Page 43 of 139
3

*
Date
Visual Acuity
OD, OS
IOP
OD, OS
Current Ocular
Meds
03/2011 20/20, 20/25 17, 18 Cosopt and
Brimonidine
bid OU, PF bid
OS
04/11 20/20, 20/25 20, 25 Cosopt only bid
OU
06/11 20/20, 20/40 16, 15 Cosopt bid,
Brim bid OU
Plan
CPM, D/C PF.
RTC 1 mo with
glaucoma
specialists
Reinitiate
brimonidine
bid OU. RTC 1
mo
RTC 3 mos with
GLC specialists
08/11 20/20, 20/40 16, 15 “ RTC 3 mos for
HVF/IOP
11/22/11** 20/20, 20/40 18, 35 “ Add PF qid OS,
RTC 2 days
11/24/11** 20/20, 20/40 12, 28 “+PF qid OS RTC 1 week
Date DVA IOP Current ocular meds Plan Additional
01/11/12 20/20,
20/50
02/08/12 20/20,
20/50
03/08/12 20/20,
20/50
04/10/12 20/20,
20/50
4/17/12 20/20,
20/50
05/3/12 20/20,
20/50
14, 20 Cosopt, Brim bid OU Add PF qid x 10 days
OS. Begin
Latanoprost qhs OS.
RTC 10 days
12, 13 Cosopt, Brim bid OU, RTC 4 mos HVF
Latanoprost qhs and PF
tid OS
13, 34 “” without PF OS Add PF qid OS. RTC 1
week
8, 26 Cosopt bid, Brim bid
OU, Latanoprost qhs OS
Add Rimexolone qid
OS, RTC 1 week
11, 15 “” +Rimexolone qid OS RTC for previously
scheduled F/U with
GLC specialists 2‐3
weeks
12, 16 “” RTC 2‐3 mos for HVF.
Still no improvement
of Bell’s Palsy R side.
Dx Pituitary
Microadenoma
Recent onset
Bell’s Palsy R
side
Hold HVF until
Bell’s Palsy
improved R
side.
Failed to
follow up in
GLC clinic.
04/10/2009
Impression:
OD: no glaucomatous
RNFL thinning
OS: severe RNFL
thinning S/I/T and
borderline nasal. Avg
thickness 93 OD, 43
OS
03/24/2011 HVF 24-2
OD: GHT ONL, MD -9.06dB, PSD 10.96dB. Great Reliability
OS: GHT ONL, MD -32.05dB, PSD 1.81dB. Great Reliability
Impression:
OD: Avg thickness 81 (from 93), with mild flattening of curves overall. New borderline
nasal thinning since last
OS: Avg thickness 35 (from 43), overall flattening, severe thinning.
Is Posner Schlossman Syndrome
Benign
• Retrospective review of all patients with PSS seen at Uveitis Clinic of
Singapore National Eye Center: 53 eyes of 50 patients
– Mean age at onset: 35
– 22 Female/28 Male
– Mean duration of disease: 7 years
– No patients had steroids or antiglaucoma tx between attacks
– 14/53 eyes developed glaucomatous damage 2’ to repeated attacks (26.4%)
– 11/14 eyes had normal discs/fields initially, but over a mean of 10 years had
disc/field damage
– Only predictive factor in development of glaucoma is duration of disease
– Risk of glaucoma developing after 10 years of exposure is 2.8x higher than in

*
• 9/14 glaucomatous eyes underwent glaucoma filtering surgery: 1
trabeculectomy with MMC and 8 trabeculectomy with 5-FU
• Mean post op F/U 37 mos, with a mean IOP at last visit of 10mmHg
• 1/9 required glaucoma medications, all of the rest did not
• In the year prior to surgery these 9 eyes had 3-4 iritis attacks each. After
surgery, 6 of these eyes had no further attacks. In the 3 eyes with
further attacks, 2 did not have an increase in IOP, and 1 had 15 attacks
with elevated IOP causing failure of the bleb and progression of
glaucomatous damage.
• PROBLEMS OF STUDY: followed at 6 mo intervals, with instructions
to return earlier if experiencing an attack (reliable pts)
Management
• Treatment doesn’t shorten length of attack
• During an attack inflammation responds well to
topical steroids: prednisolone acetate 1% qid
• IOP control: ocular hypotensive agents
• Careful monitoring of glaucomatous changes with
RNFL OCT and HVF
Possible Treatments
Surgical Options
• Topical Ganciclovir for possible CMV etiology
– Chee et al 10 pts with (+)CMV PSS began oral gancyclovir, oral
valgancyclovir, or intravitreal gancyclovir. All had decrease in attack
frequency and duration of inflammation.
– A follow up study found that systemic gancyclovir for 12 weeks had
cessation of episodes and normalized IOP during treatment in 91%,
topical 64%. But topical had lower recurrence rate (only 57%, vs 80%
systemic)
– Shortcoming of study: PSS recurrence can be separated by months-years.
Treatment success could have been normal time period between
exacerbations
• Not enough evidence to prove efficacy at this time
• Oral or topical NSAID Not enough research
Trabeculectomy Valve/Shunt Implantation
• No study found directly related to valve success in PSS patients
• Stavrou and Murray: 32 eyes with 20 types of uveitis found that 71.9% of eyes had
a reduction in severity of inflammation and the number of relapses after
trabeculectomy
– None of the operations failed as a result of inflammation
– Pattern of uveitis may be related to success rate
– Improved aqueous outflow may allow inflammatory mediators out of the
anterior chamber
●
●
●
●
●
●
In conclusion...
Posner Schlossman Syndrome is a recurrent unilateral mild anterior
uveitis with marked elevation in intraocular pressures.
Management of an acute attack includes ocular hypotensive agents and
topical steroids
Studies have found that 26.4% of PSS patients will develop
glaucomatous changes in the affected eye.
Most important factor in glaucoma risk analysis is duration of the disease
and likely frequency of attacks.
Importance of careful follow up including optic nerve head OCT/VF
Not enough evidence at this point to determine if filtering surgery for
IOP control or topical antivirals to prevent recurrence are viable
treatment options
References
1. Chee, S. Jap, A. Presumed Fuch’s Heterochromic Iridocyclitis and Posner-Schlossman
Syndrome. Comparison of Cytomegalovirus-Positive and Negative Eyes. American
Journal of Ophthalmology. 2008. 883-889
2. DaMata, A. et al.Management of Uveitic Glaucoma with Ahmed Glaucoma Valve
Implantation. Ophthalmology. 106. 1999. 2168-2172.
3. Green, R. Posner Schlossman Syndrome. Clinical and Experimental Optometry. 2007.
53-56
4. Jap, A. et al. Is Posner-Schlossman Syndrome Benign Ophthalmology. 2001. 913-
918.
5. Siveroj, C. et al. Diagnosis and Management of Herpetic Anterior Uveitis. 43-47.
6. Takusagawa, H. et al. Infectious Theories of Posner-Schlossman Syndrome.
International Ophthalmology Clinics. 2011. 105-115.
7. Towler, H. et al. Long-term follow up of Trabeculectomy with Intraoperative 5-FU for
Uveitis related Glaucoma. Ophthalmology. 2000. 1822-1828.
8. Stavrou, P. Murray, P. Does trabeculecomy influence the course of uveitis Ocular
Immunology and Inflammation. 1999. 103-108.
Coursebook Page 45 of 139
5

5/29/2012
Learning Objectives
Case Studies in Contact Lens Correction
for Myopic Refractive Error & Myopia Control
Kelvin So, OD
Pacific University College of Optometry
Review theories of myopia progression and treatment
options
Understand application of gas permeable (GP) and soft
contact lenses (SCL) for myopia correction and control
Review cases of Orthokeratology and Multifocal Soft
Contact Lens correction for myopia
Clinical Pearls for Orthokeratology and Multifocal Soft
Contact Lens fits
Discuss current research in GP and SCL for myopia
control
Myopia Etiology
9.2% of US children
18.5% in Asian Americans
6.6% in African Americans
80% in Taiwan
Theories of Myopia Progression
Near Work
Near-work induced accommodation causes prolate changes
shape of the globe and axial elongation
Support treatment of using progressive addition lenses
Support treatment of inhibiting accommodation or effecting
ocular physiology with the use of cycloplegic agents including
Atropine and Pirenzepine
Ostrow G, Kirkeby L. Update on myopia and myopic progression in children. International Ophthalmology Clinics 2010; 50: 87-93
Waler TW, Mutti DO. The effect of accommodation on ocular shape. Optometry and Vision Science. 2002; 70:424-430.
Smith EL III, Kee C-S. Ramamirtham R, Qiao-Grider Y, Hung L-F. Peripheral vision can influence eye growth and refractive development in
infant monkeys. Invest Ophthalmol Vis Sci 2005; 46: 3965-3972.
Theories of Myopia Progression
Peripheral Image Shell Theory
Foveal image has no effect on emmetropization
Animal studies using chicks and infant monkeys have shown
peripheral hyperopic retinal stimulus to cause axial elongation
Support treatment of shifting peripheral image shell in front of
the retina with the use of concentric multifocal optics
Waler TW, Mutti DO. The effect of accommodation on ocular shape. Optometry and Vision Science. 2002; 70:424-430.
Smith EL III, Kee C-S. Ramamirtham R, Qiao-Grider Y, Hung L-F. Peripheral vision can influence eye growth and refractive development in
infant monkeys. Invest Ophthalmol Vis Sci 2005; 46: 3965-3972.
Efficacy of Treatment Options
Progressive Addition Lenses
Limited effects in 5 years (COMET Study)
Most significant effects in children with poor accommodation
and esophoric at near (COMET II Study)
Atropine
Toxicity, photophobia, myopia rebound to normal after
treatment cessation
Pirenzepine
Limited follow-up data
Concentric Multifocal Optics
Significant slowing in axial elongation
Gwiazda J, Hyman L, Hussein M, et al. A randomized clinical trial of progressive addition lenses verses single vision lenses on the progression
of myopia in children. Invest Ophthalmol Vis Sci. 2003; 44: 1492-1500.
Walline JJ, Jones LA, Sinnott LT. Corneal reshaping and myopic progression. Br J Ophthalmol. 2009;93:1181–1185
Tong L, Huang XL, Koh AL, et al. Atropine for the treatment of childhood myopia: effect on myopia progression after cessation of atropine.
Ophthalmology. 2009;116:572–579
Coursebook Page 46 of 139
1

5/29/2012
Concentric Multifocal Optics
Orthokeratology (Ortho-K)
Over-night wear of reverse-geometry GP lens
Hydrodynamic forces compress central corneal epithelial cells,
and create mid-peripheral epithelial cells hyperplasia
Central corneal flattening corrects for myopia by placing image
at fovea while maintaining myopic peripheral image shell
Concentric Multifocal Optics
Orthokeratology (Ortho-K)
Hydrodynamic forces compress central corneal epithelial cells,
and create mid-peripheral epithelial cells hypertrophy
Choo J, Caroline P, et al. Changes in Cat Epithelium Following Overnight Lens Wear with the Paragon CRT Lens for Corneal Reshaping.
Poster presented at Pacific Univeristy. Forest Grove, Oregon.
Concentric Multifocal Optics
Orthokeratology (Ortho-K)
Orthokeratology
Effective for mild to moderate myopia correction
Conventional correction up to -6.00D, maximum correction
beyond -10.00D
Pros
No lens wear during waking hours
Durable lens with years of effective use
Parents responsible for handling lenses
Higher safety profile
Cons
Adaptation period
Potential for corneal abrasion
Reduced treatment zone size with higher myopia correction
Forister JFY et al, Prevalence of contact lens-related complications: UCLA contact lens study. Eye Contact Lens 2009 July;35(4):176-180.
Wagner H, et al (CLAY Group), Risk factors for interruption to soft contact lens wear in children and young adults, Optom Vis Sci, Aug
2011;88(8):973-980.
Concentric Multifocal Optics
Multifocal SCL
Daily wear of SCL with center-distance multifocal optics
Focused foveal image with myopic peripheral image shell
Multifocal Soft Contact Lenses
Effective for mild to high myopia correction
Correction from -0.25D to -20.00D with off-the-shelf lenses
Custom multifocal soft lenses available
Pros
Minimal adaptation period
Cons
Patient also needs to learn application and removal
Potential for infection
Potential for variable optics due to lens centration, movement,
and material
Coursebook Page 47 of 139
2

5/29/2012
Orthokeratology
Fitting Process
Corneal topography
Simulated Keratometry readings
Evaulation of corneal astigmatism
Manifest refraction
Most recent spectacle Rx
Best corrected visual acuity
Orthokeratology
Fitting Process
Consult fitting chart for appropriate lens
Order based on sliding rule
Orthokeratology
Fitting Process
Upload topography and manifest refraction data to lens fit
simulator
Adjust lens parameters to optimize fit prior to ordering lenses
Orthokeratology
Fit evaluation
“Bullseye” NaFl pattern
Approximately 0.5mm movement
Vision corrected to best spectacle corrected visual acuity
Dispense lens if all three criteria are met and patient/parent
can successfully apply and remove lens
Orthokeratology
Follow-up
One night follow-up the next morning to evaluate lens fit and
myopia correction
Tangential difference display on topographer to evaulate
centration
“Smiley face” crescent suggest high riding lens
“Frowny face” crecsent suggest low riding lens, often better visual
outcome
Axial difference display on topographer to evaluate correction
Correction over visual axis is key
Followed by one week, one month, then three months followup
schedule.
Evaluate vision and corneal integrity at each appointment
Orthokeratology
Case Study: RF
9 YOAM
Both parents myopic
Approximately 0.50D myopia progression every 6 months
Spectacle correction for myopia
Attempted Ortho-K lens dispense 1/2011, patient unable to
keep lids open for safe lens application and removal
Parents and patient practiced artificial tears instillation at home
RTC 8/2011 to attempt Ortho-K again
MRx:
OD: -6.00-0.50x180 20/20
OS: -6.25-0.75x180 20/20
Coursebook Page 48 of 139
3

5/29/2012
Orthokeratology
Case Study: RF
Topography
Orthokeratology
Case Study: RF
CRT Dual Axis Lens Simulator
Orthokeratology
Case Study: RF
CRT Dual Axis Lens Simulator
Orthokeratology
Case Study: RF
CRT Dual Axis Lens Simulator
Orthokeratology
Case Study: RF
CRT Dual Axis Lens Simulator
Orthokeratology
Case Study: RF
Initial lens ordered and dispensed 9/2011:
OD: Paragon CRT Dual Axis 8.9/550/600/35/11.0
OS: Paragon CRT Dual Axis 8.8/550/600/34/11.0
Slightly high riding lens
Lens rest on lower lid due to tight lid architecture
Expect improved centration with lid closure
Dispensed for over-night wear
Coursebook Page 49 of 139
4

5/29/2012
Orthokeratology
Case Study: RF
One-night follow-up the next morning
Slightly high correction zone (smiley face)
Uncorrected VA 20/50- OU
Good corneal integrity
Orthokeratology
Case Study: RF
One-night follow-up difference display
Continue lens wear for one week
Orthokeratology
Case Study: RF
One-week follow-up
Slightly high correction zone
Uncorrected VA 20/50- OU
Good corneal integrity
Topography shows residual myopia OU
Adjust lens parameters to increase corneal flattening using simulator
Orthokeratology
Case Study: RF
New Parameters ordered and dispensed 10/2011
OD: Paragon CRT Dual Axis 9.1/575/34/600/36/11.0
OS: Paragon CRT Dual Axis 9.0/575/34/600/36/11.0
Flattened Base Curve to increase central corneal flattening
Adjusted individual axis to improve lens centration
Flatten base curve to enhance central corneal flattening
Steepen Landing Zone Angle at one meridian to match steeper
vertical corneal meridian
Orthokeratology
Case Study: RF
Follow-up with flatter base curve dual-axis lenses
Central corneal staining with mild irritation and conj injection OD
Uncorrected VA 20/25 OU
Wider, slightly higher treatment area
Axial difference display reveal residual myopia OS
Orthokeratology
Case Study: RF
Discontinue lens wear
Moxeza ophthalmic solution 1gtt bid x 5 days OD
Nevanac ophthalmic suspension 1 gtt tid x 5 days OD
Consider Multifocal SCL at follow-up
Coursebook Page 50 of 139
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5/29/2012
Orthokeratology
Case Study: RF
Completely healed corneal abrasion with no scarring on f/u
Parent motivated to continue Ortho-K due to convenience of
no lens wear during waking hours, was educated on corneal
complications due to high myopia, agreed to try SCL.
Multi-focal Soft Lenses
Ordered and dispensed 11/2011
OD: Proclear Multifocal 8.7/-5.50/14.4/+2.50Add/D Lens 20/20
OS: Proclear Multifocal 8.7/-6.00/14.4/+2.50Add/D Lens 20/20
Tangential difference display shows centered treatment zone
Axial difference display shows full myopia correction over
visual axis, with +1.50 D add at pupil margin.
Multi-focal Soft Lenses
Increase Add to reduce peripheral myopia correction:
OD: Proclear Multifocal 8.7/-5.50/14.4/+3.00Add/D Lens 20/20
OS: Proclear Multifocal 8.7/-6.00/14.4/+3.00Add/D Lens 20/20
Multi-focal Soft Lenses
Increase Add to reduce peripheral myopia correction:
OD: Proclear Multifocal 8.7/-5.50/14.4/+3.00Add/D Lens 20/20
OS: Proclear Multifocal 8.7/-6.00/14.4/+3.00Add/D Lens 20/20
Clinical Pearls
Orthokeratology
Practice Makes Perfect
Have patient and parents practice artificial tears instillation to improve lid
manipulation and facilitate corneal de-sensitization prior to fitting.
Sleep It Off
Adaptation takes place rapidly in children, especially in over-night wear.
Take It Step by Step
When correcting high myopia, strive for lens centration first with partial
correction and SCL wear during the day, and progressively increase
corneal flattening to achieve full correction.
Be a Boy Scout (Be Prepared!)
Corneal abrasions do happen, and are easily treated with antibiotic cover,
as well as NSAID to improve comfort and control healing process. Have
these medications ready in-office.
Clinical Pearls
Multi-focal Soft Lenses
Topography over SCLs
Difference map comparing baseline topography and topography over
SCL will show effective power over visual axis, and peripheral add
Angle Lambda
Centered lens on cornea does NOT mean centered optics over visual
axis, perform corneal topography prior to fitting to predict success
Foveal Image Clarity is KEY
If lenses are decentered, it is possible that the foveal image is overplused,
consider adding minus to distance power to achieve optimal
distance vision
High Add
Start with minimum of +2.50 Add, increase to +3.00 Add if needed
Maldonado-Codina et al. Comparative clinical performance of rigid versus soft hyper Dk contact lenses used for continuous wear. Optom Vis
Sci, 2005;82(6):536-548.
Coursebook Page 51 of 139
6

5/29/2012
Research Findings
How Much Add
Peripheral image shell have increasing effectiveness with
increase in add
Ortho-K patients perform best if baseline refractive error is
high
Multi-focal soft lenses allow increase in peripheral add even in
low myopes
Case Study
JS & GS
Twins with low myopia
OD fitted with +2.50D add, OS fitted with +3.00D add
At 1 year follow-up, OD showed myopia progression in both twins
while OS stabilized
Lampa M, So K, et al. Assessing Soft Multifocal Contact Lens Centration with the Aid of Corneal Topography. Poster presented at Global
Specialty Lens Symposium. Las Vegas, NV. 2012.
Research Findings
Aspheric ortho-k lens design
Aspheric back surface to induce more mid-peripheral
steepening compared to conventional design
Attempts to induce higher mid-peripheral myopia to increase
myopia control effectiveness
Traditional OK Design
Base Curve: 8.23 mm 41.00 D.
Research Findings
Aspheric ortho-k lens design
Aspheric back surface to induce more mid-peripheral
steepening compared to conventional design
Attempts to induce higher mid-peripheral myopia to increase
myopia control effectiveness
Traditional OK Design
Base Curve: 8.23 mm 41.00 D.
Aspheric OK Design
Base Curve: 8.23 mm 41.00 D.
Aspheric OK Design
Base Curve: 8.23 mm 41.00 D.
Adjunct Therapies
Time outdoors
Sydney Myopia Study in2008 showed sig reduction in myopia
prevalent in children with more time spent outdoors. Light
intensity may play a larger role when outdoor due to
decreased image blur and increased depth of field.
Low-dose atropine
Compared to 1.0% atropine, 0.1% atropine has been reported
to have similar effects on controlling axial elongation but
without the side effects.
Rose KR, Morgan IG, Ip J, et al. Outdoor activity reduces the prevalence of myopia in children. Ophthalmology. 2008;115:1279–1285.
Cooper J. Using Atropine as A Primary or As An Adjunctive Treatment to Control Myopia. Lecture Presented at Vision by Design 2012
converence . Scottsdale, AZ. 2012.
Closing Remarks
Both ortho-keratology and multifocal soft lenses are non-pharmaceutical
options for myopia control.
Corneal topography is essential in ortho-keratology, and can greatly
enhance multi-focal soft lens fitting.
Ortho-keratology provides convenient vision correction for children
without need for daytime lens wear.
Multi-focal soft lenses can provide additional peripheral add for low
myopes, while research is underway for ortho-k lenses to provide similar
optics.
Myopia controlling optics should be standard of care for myopic patients.
Coursebook Page 52 of 139
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5/29/2012
References
Cooper J. Using Atropine as A Primary or As An Adjunctive Treatment to Control Myopia. Lecture Presented at Vision by
Design 2012 converence . Scottsdale, AZ. 2012.
Forister JFY et al, Prevalence of contact lens-related complications: UCLA contact lens study. Eye Contact Lens 2009
July;35(4):176-180.
Gwiazda J, Hyman L, Hussein M, et al. A randomized clinical trial of progressive addition lenses verses single vision lenses on
the progression of myopia in children. Invest Ophthalmol Vis Sci. 2003; 44: 1492-1500.
Hom MM, Bruce AS, Consider lid geometry when fitting RGP lenses, Ocular Surgery News, US Edition, June 1, 2000
Lampa M, So K, et al. Assessing Soft Multifocal Contact Lens Centration with the Aid of Corneal Topography. Global Contact
Lens Symposium, Las Vegas, NV. 2012.
Maldonado-Codina et al. Comparative clinical performance of rigid versus soft hyper Dk contact lenses used for continuous
wear. Optom Vis Sci, 2005;82(6):536-548.
Rose KR, Morgan IG, Ip J, et al. Outdoor activity reduces the prevalence of myopia in children. Ophthalmology.
2008;115:1279–1285.
Siatkowski RM, Cotter SA, Crockett RS, et al. Two-year multicenter, double-masked, placebo-controlled, parallel safety and
efficacy study of 2% pirenzepine ophthalmic gel in children with myopia. Ophthalmology. 2008;12:332–339.
Stapleton F, Keay L, Edwards K et al. The Incidence of Contact Lens-Related Microbial Keratitis in Australia. Ophthalmology.
2008. 115 (10): 1655-62.
Tong L, Huang XL, Koh AL, et al. Atropine for the treatment of childhood myopia: effect on myopia progression after cessation
of atropine. Ophthalmology. 2009;116:572–579.
Tan DTH, Lam DS, Chua WH, et al. One-year multicenter, double-masked, placebocontrolled, parallel safety and efficacy study
of 2% pirenzepine ophthalmic gel in children with myopia. Ophthalmology. 2005;112:84–91.
Wagner H, et al (CLAY Group), Risk factors for interruption to soft contact lens wear in children and young adults, Optom
Vis Sci, Aug 2011;88(8):973-980.
Walline JJ, Jones LA, Sinnott LT. Corneal reshaping and myopic progression. Br J Ophthalmol. 2009;93:1181–1185.
Coursebook Page 53 of 139
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5/29/2012
OVERVIEW
ENDOTHELIAL CHANGES
ASSOCIATED WITH INTRAOCULAR
LENS SURGERY
Benefits and risks.
Corneal responses.
Specular microscopy as a clinical tool.
Research study: endothelial cell
densities/structure after IOL surgeries.
Future directions.
Alison She, OD
IRIS Ophthalmology Clinic, Langley, BC
Primary Care/Ocular and refractive surgery
INTRAOCULAR LENS IMPLANTS
Benefits:
• Vision.
• Efficiency.
• Clear lens exchange.
Risks:
• Post-op side effects.
• Worst case scenarios.
SIGNIFICANCE OF THE ENDOTHELIUM
Barrier that regulates fluid uptake into cornea.
Transport nutrients into corneal tissue.
Endothelium disruption of cell membrane pumps
affects fluid balance, causing …
• corneal edema,
• haze,
• scarring.
From: Baker Eye Institute
ENDOTHELIAL HEALING
Cornea endothelium does not regenerate well after
damage.
Endothelium self-repairs by existing cells migrating
to fill gaps.
• Perimeter cells around injury site enlarge and move to
fill in damaged areas.
• Cell densities generally decrease with age.
• Natural rate of cell density decrease: 0.5%/year
If the cell density drops too low:
• affects fluid barrier stability.
Coursebook Page 54 of 139
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5/29/2012
WHAT CAUSES ENDOTHELIAL DAMAGE
DURING SURGERY
Energy from phacoemulsification
Air bubble pressure behind cornea
Turbulence from fluid and lens
fragments during surgery
SURGICAL VARIABLES
VISCOELASTIC SOLUTIONS
More
advanced
cataract
Greater
phaco
energy
Longer
surgical
time
Definition: Protective solution injected into anterior
chamber during cataract surgery.
Purpose:
• Protects endothelium from instruments and
phacoemulsification pressure.
• Maintains anterior chamber depth.
• Opens capsular space to insert IOL.
• Keeps incisions closed when instruments removed from
anterior chamber
Greater
endothelial
loss
Viscoelastic can affect surgical outcome.
PROPERTIES OF DUOVISC ®
PROVISC ® VISCOAT ® KONAN non-contact
SPECULAR MICROSCOPY
specular microscope.
Cohesive
High M.W.
Sodium hyaluronate
Dispersive
Medium M.W.
Sodium hyaluronate +
sodium chondroitin
Parameters measured:
• Cell density
• Cell morphology
Historical significance.
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SPECULAR MICROSCOPY APPLICATIONS
ENDOTHELIAL CELL COUNT NORMS
Age Average Cell Count (cells/mm 2 )
Diagnose endothelial
dystrophies
Child 3000-4000
20s 2700-3600
30s 2550-3400
Diagnose contact lens
related disorders
40s 2400-3200
50s 2250-3000
60s 2100-2800
70s 1950-2600
Monitor ocular surgery
outcomes
80s 1800-2400
Reference: KONAN microscopy manual FRM-012 Rev. A.
ENDOTHELIUM PROPERTIES
ENDOTHELIUM COMPARISONS
Hexagonality
• Cell shape.
• % cells that are six-sided.
• Normal corneas > 50-60%.
Polymegathism
• Cell size variation.
• Unit of measure: Coefficient of variation (CV).
• Normal range: 0.21-0.33.
1.0 = extremely disrupted cornea.
0 = each cell is precisely identical.
46 year old female 82 year old male
RESEARCH STUDY: CHANGES IN
ENDOTHELIAL CELLS AFTER IOL SURGERY
RESEARCH STUDY
Purpose: evaluate changes in endothelial
cell properties pre & post IOL surgery.
Parameters:
• Cell density.
• Cell hexagonality (shape).
• Cell size variation.
All surgeries at IRIS Ophthalmology
Clinic by same surgeon,
All surgeries used Duovisc ® viscoelastic
solution.
All patients fitted with foldable IOLs.
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PATIENT SELECTION
Patient age range: 46 to 82 years.
No restrictions on race or gender.
Non-candidates:
• diabetic retinopathy,
• uncontrolled diabetes mellitus,
• diagnosed endothelial dysfunction.
Patient consent for educational photos and data
collection.
METHODS
n=28 eyes of 17 patients.
• 19 eyes with cataract extraction.
• 9 eyes with clear lens exchange.
Specular microscopy taken post-op:
• 1 day.
• 1 week.
• 1 month.
• 3 months.
Cataracts removed via “stop-and-chop”
phacoemulsification.
RESULTS: CELL DENSITIES
3500
CELL DENSITY: PRE-OP TO 3 MONTHS POST-OP
20
15
CELL DENSITY: % CHANGE FROM PRE-OP
CELLS/MM²
3000
2500
2000
1500
1000
PERCENTAGE
10
5
0
-5
-10
-15
-20
-25
500
0
Pre‐op 1d post 1 wk 1 mth 3 mths
TIME AFTER SURGERY
-30
1 day post‐op 1 wk 1mth 3 mths
TIME AFTER SURGERY
HEXAGONALITY OF CELLS
70
PERCENTAGE OF HEXAGONAL CELLS
CELL VARIANCE
0.6
CELL SIZE VARIATION (POLYMEGATHISM)
PERCENTAGE
60
50
40
30
20
10
COEFFICIENT OF VARIATION
0.5
0.4
0.3
0.2
0.1
0
Pre‐op 1 day post‐op 1 wk 1 mth 3 mths
TIME AFTER SURGERY
0
Pre‐op 1 day post‐op 1 wk 1 mth 3 mths
TIME AFTER SURGERY
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RESEARCH STUDY SUMMARY
Cell density has a larger decrease at 1 day post-op
then gradually recovers over the next 90 days.
High variability at 1 week post op reflects dynamic
nature of endothelium reorganization.
Hexagonality: No statistically significant change pre
vs post surgery long-term.
Polymegathism: No statistically significant change
pre vs post surgery long-term.
FUTURE DIRECTIONS:
PHAKIC IOL SURGERY
Anterior chamber IOL
• AcrySof ® Cachet ® (Alcon)
• Surgical correction for high
refractive errors > 6 D.
Guidelines:
• Specular microscopy at
Pre-op.
6 months post-op.
1 year post-op.
FUTURE RESEARCH DIRECTIONS
Monitor at 1-2 + years post-surgery.
Evaluate systemic factors in endothelial healing:
• Diabetes.
• Inflammatory conditions (arthritis, lupus, etc).
Compare cell loss in:
• Clear lens exchange vs. cataract extraction.
• Long-term monitoring after phakic IOL surgery.
SUMMARY
REFERENCES
Mencucci, R., Ponchietti, C., Virgili, G., Giansanti, F., Menchini, U. “Corneal endothelial damage after cataract surgery:
Microincision versus standard technique.” J Cataract Refract Surg. 2006; 32:1351-1354.
Hengerer, F.H., Dick, H.B., Buchwald, S., Hütz, W.W., Conrad-Hengerer, I. “Evaluation of corneal endothelial cell loss
and corneal thickness after cataract removal with light-adjustable intraocular lens implantation: 12-month follow-up.” J
Cataract Refract Surg. 2011; 37:2095-2100.
Albert, D.M., Jakobiec, F.A. Principles and Practice of Ophthalmology. 1994. W.B. Saunders Company: Philadelphia.
Van den Bruel, A., Gailly, J., Devrieses, S., Welton, N.J., Shortt, A.J., Vrijens, F. The protective effect of ophthalmic
viscoelastic devices on endothelial cell loss during cataract surgery: a meta-analysis using mixed treatment
comparisons. Br J Ophthal. 2011; 95:5-10.
Remington, L. Clinical Anatomy of the Visual System, 2 nd Edition. 2005. Elsevier: Missouri.
Kiss, B., Findl, O., Menapace, R., Petternel, V., Wirtitsch, M., Lorang, T., Gengler, M., Drexler, W. “Corneal endothelial
cell protection with a dispersive viscoelastic material and an irrigating solution during phacoemulsification. Low cost
versus expensive combination.” J Cataract Refract Surg. 2003; 29: 733-740.
Pereira, ACA., Porfirio, F., Freitas, LL., Belfort, R. “Ultrasound energy and endothelial cell loss with stop-and-chop and
nuclear preslice phacoemulsification.” J Cataract Refract Surg. 2006; 32:1661-1666.
Gogate, P., Ambardekar, P., Kulkarni, S., Deshpande, R., Joshi, S., Deshpande, M. “Comparison of endothelial cell
loss after cataract surgery: Phacoemulsification versus manual small-incision cataract surgery. Six week results of a
randomized control trial.” J Cataract Refract Surg. 2010; 36:247-253.
Daly, L., Bourke, J. Interpretation and Uses of Medical Statistics, Fifth Edition. 2000. Blackwell Sciences: UK.
Rainer, G., Stifter, E., Luksch, A., Menapace, R. “Comparison of the effect of Viscoat ® and DuoVisc ® on Postoperative
intraocular pressure after small-incision cataract surgery.” J Cataract Refract Surg. 2008; 34:253-257
Baryanovits, P. “Stabilisation of refraction following cataract surgery.” Br J Ophthal. 1988; 72 815-819
Thomas, Craig. The Specular Microscopy Primer. KONAN Medical.
Kanski, J. Clinical Ophthalmology, 6 th Edition. 2007. Butterworth Heinemann: Toronto.
Duovisc product insert, Alcon.
THANK YOU!
QUESTIONS
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Objective
• Corneal infections are a common and sight-threatening condition which
can progress very quickly, leading to extensive corneal tissue
destruction and possible perforation.
BIC TRINH O.D
EYECARE ASSOCIATES OF NEVADA
Case Report: Persistent epithelial defect
in post-corneal graft
• Being able to recognize and appropriately treat these conditions is
critical in preserving vision. Today we will review the different etiologies,
appropriate work up and management of different corneal infections.
J.G 57 yo male
Entrance testing
• Patient
◦ 57 Y.O Hispanic Male
◦ Hx of longstanding corneal ulcer, OS
• HPI
◦ (+) mild watery discharge, photophobia, foreign body sensation
◦ No h/o contact lens wear, outdoor activity, trauma
• Gtts
◦ Durezol tid OS x 3 mo
• Oc Hx
◦ Penetrating keratoplasty OS x 20 years
• Medical Hx:
◦ Heart disease
◦ Arthritis
◦ NIDDM
◦ Elevated cholesterol
• VA (sc)
◦ OD 20/30-
◦ OS 20/100+ PH/60
• Tonometry
◦ Deferred
• MR:
◦ OD +2.75-1.00x115 20/20
◦ OS +4.00 DS 20/60
Exam
Differential diagnosis
• Anterior segment
◦ OS:
Conjunctiva: 2 + injection
Cornea:
Graft intact
1 mm epithelial defect with surrounding infiltrate, 6:00
60-70% stromal thinning
Diffuse corneal haze
Anterior Chamber
D/ 2+ mixed cell
1 mm hypopyon
Lens
3 +NSC
◦ Bacterial keratitis
Gram (-)
Pseudomonas
Gram (+)
S. Epidermis, S. Aureus,
S. Pneumoniae
◦ Herpetic eye disease
Herpes Simplex Keratitis
◦ Fungal keratitis
Fusarium, Aspergillus,
Candida
◦ Persistent epithelial defect
Toxicity
Autoimmune
Ocular surface disease
◦ Acanthomoeba
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Impression
1 day follow up
• Impression
◦ Bacterial keratitis vs. Persistent epithelial defect, OS
◦ S/p PKP, OS
• Plan
◦ Culture
◦ D/C Durezol
◦ Fortified vancomycin, fortified tobramycin q1h OS
◦ Erythromycin ung qid OS
◦ F/u 1 day
• HPI: improved pain
• Anterior segment
◦ Cornea
(+) graft edema
1mm ED, 60-70% thinning
Haze improved
◦ Anterior chamber
1+ cell
Hypopyon resolved
• Culture
◦ Gram stain: No organisms observed
◦ Media: No growth
• Impression
◦ Non-healing epithelial defect, OS
◦ Graft failure, OS
• Plan
◦ Vancomycin, Tobramycin q3h OS
◦ Erythromycin ung qid OS
Follow up
Follow up
• 5 day f/u
• 1 week f/u
• 2 week f/u
• 6 week f/u
• Anterior segment
• Anterior segment
• Anterior segment
• Anterior segment
◦ Cornea
◦ Cornea
◦ Cornea
◦ Cornea
0.6mm ED, 50% thinning
◦ Anterior chamber
• Plan
D/Q
◦ Vancomycin, Tobramycin,
Erythromycin ung qid
No ED, 50% thinning
1.5 mm V x 1.2 mm H stromal
opacity
• Plan
◦ D/C Vancomycin, Tobramycin
◦ Erythromycin ung qid OS
◦ Lotemax qid OS
1.5 mm V x 1.2 mm H stromal
opacity, 10% thinning
Microcystic edema
Pachs 777 microns
IOP 13/13
• Plan
◦ PF qid OS
Stromal opacity
Microcystic edema
IOP 14/17
• Plan
◦ Taper PF slowly
◦ Possible repeat graft with
phacoemulsification OS to
improve vision
Persistent epithelial defect
Persistent ED: Causes
• Presentation
◦ Foreign body sensation,
photophobia, corneal
hypoesthesia
◦ Central/paracentral or
inferior/inferonasal
◦ Epithelial defect with heaped
edges
◦ Underlying stromal
inflammation
◦ Resistant to maximum
therapy
Topical agents
Auto-immune
Ocular surface disease
Neurotrophic keratitis
Trauma
Aminoglycosides, trifluoridine,
antimetabolites
Sjogren’s syndrome, RA, graft-versushost
disease
Dry eye, exposure keratopathy, atopy,
rosacea, ocular pemphigoid, mooren’s
ulcer, limbal stem cell deficiency, RCE,
bullous keratopathy
Anesthetic abuse, acanthomoeba
keratitis, HSK, HZO
Underlying foreign body, local
irradiation, contact lens use
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Management
Management
• Obtain corneal culture
• Cycloplegic agent
• Treatment aimed towards surface healing and preventing stromal melt
◦ Stop/ taper medications toxic to epithelium
◦ Lubrication (non-preserved)
◦ BCL
◦ Orals
Omega-3 FA
Doxycycline
• Poor response to previous therapy
◦ Autologous serum
◦ Oral acyclovir
◦ Systemic evaluation
The use of autologous serum tears in persistent corneal epithelial defects
Eye (2004) 18, 609–614 A L Young, A C O Cheng, H K Ng, L Cheng, G Y S Leung and D S C Lam
Healing within
Current series=10
2 weeks (effective) 6 (60%)
1 month (partially effective) 0 (0%)
>1 month (ineffective) 2 (20%)
Defaulted 2 (20%)
ADEs 0 (0%)
Management
AMT with tarsorraphy
• Surgical options
◦ Punctal occlusion
◦ Total tarsorrhaphy
◦ AMT graft with tarsorraphy
◦ PKP
• Amniotic membrane graft
◦ (Amniograft® 2.5x 2.0 cm) placed in
layers
◦ Larger piece of AM placed (stromal
side down) placed over layers
◦ BCL
◦ Tarsorraphy
• ProKera
• Prospective studies
◦ Lee et al (Bascom Palmer), 1997: AMT
performed in 11 pts with PED. 10 pts
healed in 2-6wks without recurrence for 3-
15 mos
◦ Pachigolla et al (University of Texas SW),
2009: 20 eyes with ProKera implant for
avg of 25.3 days. 12 eyes noticed
increase in acuity. 5 eyes noticed PED
with removal of device
Bacterial keratitis
Bacterial keratitis
◦ S. Epidermis, S. Aureus, S.
Pneumoniae
◦ Gram (+) cocci
◦ S. Aereus binds to exposed
components of Bowman’s and
stroma
◦ Pseudomonas aeruginosa
◦ Gram (-) rod
◦ P aeruginosa binds to molecular
receptors on exposed epithelial cells
• Presentation
◦ Pain, decreased vision, redness, suppuration
◦ Sharply demarcated epithelial defect
◦ Stromal edema
◦ A/C reaction
◦ Stromal thinning/necrosis
• Risk factors
◦ Contact lens*
◦ Trauma
◦ Medications
◦ Impaired defense mechanisms
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Management
Management
• Initial therapy
◦ D/C contact lens
◦ Small (

5/29/2012
Fungal keratitis
Fungal keratitis
• 5-10% of keratitis are fungal in
nature
• More common warmer, humid
climate
• Aspergillus, Candida, and
Fusarium
• Risk Factors
◦ Ocular trauma from plant
◦ Contact lens wear
◦ Immunosuppression
◦ Medications
◦ Penetrating keratoplasty
• Presentation
◦ Gray-white infiltrate
◦ Satellite or branching lesions
◦ A/C reaction
◦ May invade iris or posterior chamber
Fungal keratitis
Acanthamoeba
• Management
◦ Topical:
natamycin 5% suspension: effective against most cases
amphotericin B 0.15%-0.30%
◦ Oral: Effect on keratitis is limited secondary to poor penetration and systemic
side effects
ketoconazole 200-600 mg/day
fluconazole 200-400 mg/day
◦ Typical treatment time is 1 month but can be used for several months
◦ Repeat smears may be necessary
• Protozoa
• Highly resistant
• 70% of cases related to contact lens use
Acanthamoeba
Acanthamoeba
• Presentation
◦ Severe pain, photophobia, decreased vision
◦ Epithelial defect
◦ Ring shaped infiltrate
◦ Keratoneuritis
◦ A/C reaction
• Management
◦ Mechanical debridement
◦ Topical therapy (must be compounded)
Biguanides:
Chlorhexidine gluconate 0.02%(CHG) q1h
Polyhexamethylene biguanide 0.02%(PHMB) (Bacquicil) q1h
Diamidines:
Brolene
Desmodine
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Microbiology
Microbiology
• When is laboratory evaluation by culture
recommended
◦ Size
◦ Depth
◦ Chronic in nature
◦ Atypical features/ history
• How to obtain sample
◦ Topical anesthetic (proparacaine hydrocholoride)
◦ Scrape material from border as well as base of ulcer
◦ Inoculate onto solid media by streaking rows of C’s
Media/Smear
Culture
Chocolate agar
Most bacteria, Haemophilus,
Neisseria, Moraxella
Blood agar
Most bacteria, yeast, fungi
Sabourad’s agar
Non-nutrient agar
Gram stain
Most fungi, yeast
Acanthamoeba
Bacteria
Pearls
References
• Careful history
◦ Systemic history
◦ Prior ocular history
◦ Medications
• Examination
◦ Documentation of defect
◦ Observe structures around eye
◦ Take notice of unique features
• Treatment
◦ Initiate aggressive therapy
◦ Have complete list of DDx
◦ Remember guidelines for culturing
• Price F.W, Price M.O, Letko E. Curbside Consultation in Cornea and External Disease. Indianapolis,
IN: Slack Incorporated;2010: 119-130.
• Cohen EJ, Rapuano CJ. Bacteria keratitis, fungal keratitis, Acanthamoeba, herpes simplex virus,
herpes zoster virus. In Kunimoto DY, Kanitkar KD, Maker MS, Friedberg MA, Rapuano CJ, eds. The
Wills Eye Manual: Office and Emergency Room Diagnosis and Treatment of Eye Disease. 4 th ed.
Philadelphia, PA: Lippencott Williams and Wilkins. 2004:52-65.
• Sutphin JE, Dana MR, Florakis GJ. Basic and Clinical Science Course: External Disease and Cornea.
Singapore; 2007: 113-189.
• KrachmerJH, Mannis M, III. Holland EJ. Cornea: Fundamentals, Diagnosis and Management. Vol 1.
China;1997:277-307.
• Pachigolla G, Prasher P, Di Pascuale MA. Evaluation of the role of ProKera in the management of
ocular surface and orbital disorders. Eye Contact Lens. 2009 Jul;35(4):172-5.
• Lee SH, Tseng SC. Amniotic membrane transplantation for persistent epithelial defects with ulceration.
Am J Ophthalmology. 1997 Mar; 123(3):303-12.
• Seitz B, Das S, Saur R. Amniotic membrane transplantation for persistent corneal epithelial defects in
eyes after penetrating keratoplasty. Eye (London). 2009 Apr;23(4):840-8
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Chief Complaint
Blebitis
• Amy Pedersen, OD
• Portland VA Medical Center
• “Rust colored film over my eye”
– Present for 2 days, stable, (‐)pain and (‐)discharge
– Secondary Complaint
• Mild upper left lid tenderness
• Present for the past 3 days, stable
• Self treating with tobramycin QID x 2 days with no
resolution or decrease in symptoms
Ocular History
– Advanced primary open angle glaucoma OU
– S/P trabeculectomy 1991 OU ( UC Davis), revision for
leak in 1995 at PVAMC OD
– Non‐exudative age related macular degeneration
OS>OD, AREDS category 2
– Diabetes mellitus type 2 with mild non‐proliferative
diabetic retinopathy OS only
– Pseudophakia OU s/p cataract extraction at PVAMC
Medications
– Amlodipine besylate, Aspirin (81mg), Insulin (aspart),
Insulin (glargine), Lisinopril, Metoprolol succinate,
Ranitidine, Simvastatin
– Glaucoma: timolol maleate 0.5% oph soln, 1 gtt OU bid
Medical History
– Diabetes mellitus type 2, diagnosed in 1998 (Last A1C 8.1
on 09/13/11)
– Hypertension
– Hyperlipidemia
– GERD
Pertinent Findings‐ 09/16/11
• Visual Acuity: 20/25 OD, 20/30‐2 (PH: 20/25‐2) OS
• Anterior Segment
– Lids/ Lashes: 1+ MGD OU
– Cornea: temporal incisional scar OU
– Conjunctiva:
• OD: temporal pinguecula, trab scar at 12 o'clock
• OS: 1+ injection, trab scar with partial opacity at 12
o'clock with surrounding 2+ injection
– Cornea: temporal incisional scar OU
– Ant. Chamber: OD: Deep & Quiet, OS: trace cells, (‐)flare
– Iris: Normal OU, (‐)NVI
• GAT @4:31pm OD: 17mmHg OS: 8mmHg (Seidel testing
questioned pinpoint leak)
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Pertinent Findings Contd…
• Posterior Segment
– Lens: PC IOL OU
– Vitreous: OD: Clear OS: PVD; (‐)VH OU
– Optic disc:
• OD: 0.9/0.9; advanced cupping with 3+ pallor; (‐)NVD
• OS: 0.7/0.7; cupping with 2+ pallor; (‐)NVD
– Macula: scattered pinpoint drusen, trace‐1+ RPE changes ; (‐
)CSME OU
– Vitreous: OD: Clear OS: PVD; (‐)VH OU
– Vessels: Normal OU
– (+)Dot/blot heme OS inferior nasally, (‐)Dot/blot heme OD;
(+)MA's OS inferior nasal to disc, (‐)MAs OU; (‐)Hard Exudates
OU; (‐)CWS OU; (‐)IRMA OU; (‐)VB OU; (‐)NVE OU
– Posterior Pole and Periphery:
• OS: chorodial detachment ora to equator 360, (‐)vit cells
• OD: no rips, holes or tears 360 OU
Assessment/Plan
• Blebitis with choridal detachment OS, reduced pressure OS
• Instill 1gtt Vigamox OS q15min in office immediately as
loading dose
• Admit as inpatient‐ Moxifloxacin 1gtt q1h overnight
• RTC tomorrow morning in Eye Medical Retina
Follow Up #1 (9/17/11)
– Relevant Findings
• Visual Acuity: 20/25‐1 OD, 20/70‐2 (PH: 20/70‐1) OS
• Conjunctiva OS: significant superior 2‐3+ bleb injection, Seidel
positive centrally, purulent appearance
• Ant. Chamber: OS: 1+ cell with trace pigmented cell
• GAT@9:00am OD: 21 mmHg OS: 2 mmHg
• Choroidal detachment 360 degrees OS, (‐)vitreous cell and flare
– Assessment/Plan
• Blebitis OS ‐ appears to be clinically improving, with no evidence
of endopthalmitis.
• Continue Vigamox q1h during daytime, q3h at night; intiate 1gtt
atropine qd OS, timolol 0.5% bid OD only
• RTC 2 days in Eye Medical Retina
Follow Up #2 (9/19/11)
– Chief Complaint: Follow up of blebitis OS. Soreness same as before.
Feels that OS is blurry. Moxifloxacin q1h in daytime, q3‐4 h at night
OS, 1% Atropine qd OS, 0.5% timolol bid OD.
– Relevant Findings
• Visual Acuity: 20/25‐2 OD, 20/150 (PH 20/50‐2) OS
• Cornea: OS mild superior thinning and vascularization near the blebitis, some
Descemets folds, bleb has infiltration in the center, Seidel positive in center of
the bleb, 2+conj injection superiorly
• Anterior Chamber: OS rare cells
• GAT@3:33pm OD: 12 mmHg OS: 0 mmHg
• Posterior Pole & Peripheral Retina: 360 degree choroidal detachment OS
– Assessment/Plan
• Blebitis with leak OS, resolving anterior chamber reaction with hypotony and
choroidal detachment OS
• Cont Moxifloxacin q1h in the day and q3‐4h at night,1% Atropine eye drops OS
qd and 0.5% timolol bid OD
• Will schedule for bleb revision , tomorrow if possible
Bleb Revision Surgery‐ 1 day post‐op
– Relevant Findings
• VA: 20/200 OS; PH not performed
• Superior bleb revision, (‐)Seidel with intact sutures
• GAT@9:45am OS: 23 mmHg with distorted mires
– Assessment/Plan
• One day post bleb revision with patch graft OS‐ good
closure with no leaks, mild ocular HTN today
• Start Pred Forte q2‐3 hours OS and Vigamox QID OS and
Cosopt BID OS, continue timolol bid OD
1 week post‐op (9/26/11)
– Relevant Findings
• VA OD: 20/25‐ OS: 20/50‐2; PH not performed
• Conjunctivia OS‐ Seidel negative with 1 pair of nylon suture
ends that are mildly exposed, all other suture ends are
vicryls
• GAT@9:37am OD: 16 OS: 14
– Assessment/Plan
• One week post bleb revision with patch graft OS, good
closure with no leaks. Nylon suture ends cut at slit lamp.
• Improved IOP with topical Cosopt, taper Pred to QID OS, D/C
Cosopt OS; continue 0.5% timolol bid OD
• RTC 1 week
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2 week post‐op (10/3/11)
– Relevant Findings
• VA: 20/25 OD, 20/40 OS; PH not performed
• Conjunctivia OS‐ Seidel positive with slow leak along
perilimbal bleb, otherwise intact
• GAT@11:15am OD: 18 mmHg OS: 11 mmHg
– Assessment/Plan
• Bandage Contact Lens OS
• Taper Pred BID OS, restart Vigamox with bandage CL;
continue 0.5% timolol bid OD
• RTC 10/07/11
2.5 week post‐op (10/7/11)
– Relevant Findings
• VA: 20/25‐1 OS
• Conjunctivia OS‐ trace injection of superior conj with
white bled, Seidel negative even with pressure applied
• GAT@2:41pm OS: 18 mmHg
• Choroid attached 360 OS
– Assessment/Plan
• Removed Bandage Contact Lens OS
• Continue Pred Forte BID, D/C Vigmaox OS, start 0.5%
timolol qAM OS; continue 0.5% timolol bid OD
• RTC 2 weeks
1 month post‐op (10/24/11)
– Relevant Findings
• VA: 20/30 OD, 20/50 OS; PH not performed
• Conjunctivia OS‐ trace injection of superior conj with white
bleb, Seidel negative even with pressure applied
• GAT@10:55pm OD: 15mmHg OS: 16 mmHg
– Assessment/Plan
• Post bleb revision with patch graft OS, IOP trending up
though bleb is filtering, currently on 0.5% timolol qAM OS
• 5‐FU subconj OS injection today
• Increase Pred Forte to QID OS, continue 0.5% timolol qAM
OS; continue 0.5% timolol bid OD
• RTC 11/09/11 and PRN
6 week post‐op (11/9/11)
– Relevant Findings
• VA: 20/40 OS; PH not performed
• Conjunctivia OS‐ quiet with nice diffuse bleb, sutures intact,
negative Seidel
• GAT @10:00am OS: 14mmHg
– Assessment/Plan
• Post bleb revision with patch graft OS, good IOP control
(with adjunctive medical therapy‐ patient is on 0.5% timolol
qAM OS); s/p 5 FU on 10/24/11
• 5‐FU subconj OS injection today (2 nd injection)
• Continue Pred Forte to QID OS, discontinue 0.5% timolol
qAM OS to encourage filtration
• RTC 11/28/11 and PRN
9 week post‐op (11/28/11)
– Relevant Findings
• VA: 20/40 OS, PH 20/30+2
• Conjunctivia OS‐ quiet with nice diffuse bleb, sutures
intact, Seidel negative
• GAT@3:17pm OS: 16mmHg
– Assessment/Plan
• Post bleb revision with patch graft OS, good IOP control
WITHOUT glaucoma drops; s/p 5‐FU injection x 2
• 5 FU subconj OS injection today (3 rd injection)
• Continue Pred Forte QID OS
• RTC 3 weeks and PRN.
3 month post‐op (12/19/11)
– Relevant Findings
• VA: 20/40 OD, 20/40 OS; PH: not performed
• Refraction: +0.50 OD (20/25) ‐0.75 OS (20/25) +2.50 add
OU
• Conjunctivia OS‐ nicely elevated scarred bleb OS, Seidel
negative
• GAT@1:25pm OD: 15mmHg OS: 13mmHg
– Assessment/Plan
• Post bleb revision with patch graft OS, good IOP control
WITHOUT glaucoma drops; s/p 5‐FU injection x 3
• Taper Pred Forte TID OS
• Order VA issued bifocal spectacles
• RTC 4 weeks and PRN.
Coursebook Page 67 of 139
3

5/29/2012
4 month post‐op (4/30/12)
Differential Diagnoses
– Relevant Findings
• VA: 20/25 OD, 20/25 OS
• Conjunctivia OS‐ nicely elevated scarred bleb OS, Seidel
negative
• GAT@12:35pm OD: 17mmHg OS: 11mmHg
– Assessment/Plan
• Post bleb revision with patch graft OS, good IOP
control; s/p 5 FU injection x 3
• Taper Pred Forte BID OS
• RTC 2 months in glaucoma clinic and PRN
– Blebitis
– Endophthalmitis
– Episcleritis
– Conjunctivitis
– Anterior uveitis
– Ischemic bleb
– Choroidal Detachment
– Retinal Detachment
– Melanoma of ciliary
body
– Melanoma of the
choroid
Presentation
– Serious complication of trabeculectomy that
requires immediate and aggressive treatment
– “White on Red” appearance with white bleb and
surrounding conjunctival hyperemia
– Patients will typically present with mild discomfort
and redness
– May be associated with mild anterior chamber
reaction but no vitritis is present
Risk Factors
• Use of antimetabolites such as mitomycin C and 5‐
fluorouracil in surgery greatly increase the success rate
of the surgery by inhibiting fibroblast proliferation;
however, risk of infection increases because the
procedure is more likely to result in a thin avascular
bleb
• Younger age
• African American race
• Inferiorly placed blebs
• Chronic blepharitis
TRUE EMERGENCY
– Potential Complications‐ hyptonous maculopathy,
choroidal detachment, endophthalmitis
– An infected bleb with severe anterior chamber
reaction with or without hypopyon, vitritis or a
positive vitreous culture is endophthalmitis; signs
and symptoms include severe pain and reduction
of vision, redness and discharge
• If visibility is limited perform a B‐scan ultrasound to
determine the presence of vitiritis
Serous Choroidal Detachment
– Caused by hypotony
– Swelling of the suprachoroidal space limited by
firm attachment of the choroid at the vortex veins
• treat the underlying cause
– Choroid will spontaneously reattach as pressure
increases and stabilizes
– Verhoeff streaks can be present after
reattachment
Coursebook Page 68 of 139
4

5/29/2012
Bleb Revision
– Increased risk of re‐infection after initial blebitis;
significant risk of bleb revision failure
– If leak persists after treating the infection, send for
revision
• Post Bleb Revision Leak
– Bandage contact lens‐ restart topical antibiotics
for prophylactic coverage
Clinical Pearls
• Blebitis is a SERIOUS complication‐ treat immediately and
aggressively to prevent endophthalmitis (admission to hospital is
often indicated)
• Priority #1‐ Treat the Infection before addressing the hypotony: do
not send for an operation until you sterilize the area, otherwise the
infection could worsen
– Many leaks have continuous outflow and very few bacteria can swim
upstream (be more concerned if fluid is moving in and out, consider
monitoring twice a day or hospitalization
• Be a painter‐ Seidel testing with multiple stacked fluorescein strips
• Patient education is critical‐ Instruct patients with blebs to seek
help IMMEDIATELY in the event of any redness, discharge,
decreased vision or photophobia
References
• Ordan JL, Catey B, Melville MM, et al. Risk factors for development of post trabeculectomy
endophthalmitis. Br J Ophthalmol 2000:84:1349‐1353.
• Muckley ED, Lehrer RA. Late‐onset blebitis and endophthalmitis:incidence and outcomes with
mitomycin C. Optom VisSci. 2004;81:499–504.
• Soltau JB, Rothman RF, Budenz DL, Greenfield DS, Feuer W, Liebmann JM, Ritch R. Risk factors for
glaucoma filtering bleb infections. Arch Ophthalmol 2000;118:338‐42.
• Kanski, J. (2006). Clinical ophthalmology: A systemic approach, Sixth edition. New York: Butterworth
Heinemann Elsevier.
• Bartlett, J.D., & Janus,S.D. (2008). Clinical Ocular Pharmacology. St Lousi: Butterworth Heinman
Elsevier.
• Kais, P. K., & Friedman, N.J. (2004). The Massachusetts eye and ear infirmary illustrated manual of
ophthalmology, Second edition. Philadelphia: Saunders.
• Rhee, Douglas J. The fine art of managing blebitis. Review of ophthalmology online. May 2, 2011.
Coursebook Page 69 of 139
5

5/29/2012
Case Presentation
• 83 year old Caucasian male
• Presented for routine exam 9/2011
• ONH asymmetry noted
◦ FDT screening visual field performed
ERIN J. BENDER
NORTHWEST RESIDENTS CONFERENCE
JUNE 4, 2012
My Initial Visit
• Patient asymptomatic to field loss
• Systemic History:
◦ Impaired fasting glucose
• Ocular History:
◦ Past examinations reveal:
No h/o of diabetic retinopathy OU
Early lens changes OU
Presbyopia OU
Examination Results
Posterior Segment
• VA sc OD 20/20-1 OS 20/25-1
• EOMs full and smooth OU
• CF FTFC OU
• Anterior segment remarkable for 1+ NS OU
• IOP OD 15 mmHg OS 15 mmHg
• +APD OS
◦ Pt reports 50% brightness OS compared to OD
OD: Blurred disc margins with elevation,
greatest N
Macula flat and intact
Peripheral retina: scattered hard drusen
and reticular degeneration
OS: Blurred disc margins with elevation,
greatest N, SN and IN
Macula flat and intact
Peripheral retina: scattered hard drusen
and reticular degeneration
Coursebook Page 70 of 139
1

5/29/2012
Is this Papilledema
Did You KNOW
• Papilledema
◦ Increased intracranial pressure
• Pseudopapilledema
◦ Congenital anomalous disc
◦ Peripapillary myelinated NFL
◦ Crowded disc with hypermetropia
◦ OPTIC DISC DRUSEN
• “Druse” is a German word
• It means a crystal-lined hollow space in a rock
• Was widely used in the mining industry in the 16 th
century.
Clinical Presentation: Optic Disc Drusen
• Blurred disc margins
• Scalloped disc borders
• NO obscuration of surrounding vasculature
• Non-hyperemic disc, no dilated capillaries
• Multi-lobulated refractile bodies (if visible)
• Trifurcations of the blood vessels
• No elevation to surrounding NFL
Incidence
Demographic Presentation
• ~1% of general population
• Increases to ~3.4% in patients with relatives of the
same diagnosis
• Questionable AD inheritance pattern, described as
“irregular dominant fashion”
• 75 to 85% BILATERAL presentation
• Equality in sex distribution
• Caucasians higher incidence
◦ Theory: African Americans tend to have larger scleral canal
sizes as compared to Caucasians
Coursebook Page 71 of 139
2

5/29/2012
Histology
Pathophysiology
• Acellular
◦ Mucopolysaccharides
◦ Amino acids
◦ Ribonucleic and desoxyribonucleic acid
◦ Calcium
◦ Small amounts of iron
• Range from 5 to 1000 microns in diameter
• Deposits anterior to the lamina cribrosa, in 90%
behind the level of Bruch’s membrane
3 THEORIES OF FORMATION OF ODD
Congenital Dysplasia of the optic nerve head
and blood supply
Axoplasmic stasis secondary to crowded disc
Small scleral canal size
Or an amalgamation
Tso’s Theory
Development and Progression
Theory: ABNORMAL
AXONAL METABOLISM
LEADING TO
INTRACELLULAR
MITOCHONDRIAL
CALCIFICATION
Axonal rupture
Mitochondrial extrusion
into extracellular space
Calcium continues to
deposit into extracellular
mitochondria
(Ca2+ concentration
higher than within cell)
Small calcified
microbodies produced
Calcium continue to be
deposited on the surface,
forming drusen
• Labeled as “buried” in young children and adults.
Visibility increases with age secondary to axonal
atrophy and continuing calcium deposition.
• Tend to present or become “unburied” on INFERIOR
NASAL portion of ONH.
• 75% of ODD patients will develop some form of
visual field loss.
• Visual acuity tends to be well preserved.
End Stage
Associated Conditions
• Gradual worsening and compromise to vasculature
and nerve fiber layer can result in:
◦ Anterior Ischemic Optic Neuropathy
Related to mechanical forces
Patients tend to be in mid 20s or younger
Without systemic cardiovascular disease
◦ Compressive CRVO/CRAO
Secondary to impairment of blood flow
◦ Juxtapapillary Choroidal Neovascularization
Secondary to chronic ischemia
• Pseudoxanthoma elasticum
◦ Range from 1.4 to 3.6% association with ODD
◦ Elastin lines the insertion of lamina cribrosa
◦ Abnormal accumulation of polyanions with high calcium
affinity acts as triggering factor for mineralization
• Angioid streaks
◦ Theory that a common defect of abnormal mineralization
predisposes for ODD and angioid streaks
• Retinitis Pigmentosa
◦ Range from 0 to 10% association with ODD
◦ Deposits often found ADJACENT to normal sized disc
Coursebook Page 72 of 139
3

5/29/2012
Diagnostic Testing
Our Case: Visual Field 24-2
• Visual Field
◦ Typically arcuate defects on VF
◦ Enlarged blind spot (less common)
◦ Visible drusen tend to show higher mean deviation
◦ Patients tend to be unaware of visual field defect
VF defects do NOT have direct correlation
with location of drusen!!
Diagnostic Testing
Our Case: Auto fluorescent Photos
• Fluorescein Angiography
◦ Faint diffuse hyper fluorescence of ONH early with late well
defined hyper fluoresce without leakage
OD
OS
• Auto fluorescent Photography
◦ Hyper-reflective lesions within the ONH on photo
◦ Are NOT bi-refringent
◦ Higher sensitivity for detecting buried drusen than
ophthalmoscopy but lower than Bscan
Diagnostic Testing
• Optical Coherence Tomography
◦ Monitor NFL loss
◦ Eyes with buried disc drusen often do NOT show NFL loss
◦ Reveals irregular and discontinuous elevations at ONH
◦ Rounded HYPO-reflectant appearance
• B-scan ultrasonography
◦ STANDARD OF CARE
◦ Hyper reflectance at ONH that persists at low gain settings.
Coursebook Page 73 of 139
4

5/29/2012
OUR CASE:
OCT
FINDINGS
OD and OS elevated
NRR thickness
Sup and Inf NFL
loss OS
Diagnostic Testing
• Optical Coherence Tomography
◦ Monitor NFL loss
◦ Eyes with buried disc drusen often do NOT show NFL loss
◦ Reveals irregular and discontinuous elevations at ONH
◦ Rounded HYPO reflectant appearance
• B-scan ultrasonography
◦ STANDARD OF CARE
◦ Hyper fluorescence at ONH that persists at low gain settings
Our Case: Bscan
OS Bscan at Low Gain
OD at medium gain
OS at medium gain
Treatment
Papilledema versus Pseudopapilledema
• Most cases managed with serial VF testing, IOP
monitoring and NFL analysis.
• No definitive treatment. Not all cases are treated.
• Intraocular pressure lowering agents may be used
with goal of protecting the remaining NFL.
◦ If due to mechanical compression, lowering IOP may alleviate
the process.
◦ Blood flow to ONH may be improved with use of antihypertensives,
potentially reducing chance of vascular events.
• Save healthcare dollars: Diagnostic testing is
expensive and sometimes unnecessary.
• Unduly stress for the patient: Reassurance against
potential morbid outcome.
Coursebook Page 74 of 139
5

5/29/2012
MRI
To scan or not to scan
$$$$$$
36 YO WF referral with “asymptomatic
bilateral disc edema”.
Remote h/o HA and previous work-up.
Past imaging revealed pineal cyst.
Visual Field Results
Fundus Exam
Bscan Results
Bumps in the Nerve
OD: at high and low gains
OS: at high and low gains
• What is the true mechanism
◦ Is scleral size really a risk factor
• What are the genetics
• Is IOP lowering truly beneficial
• Is there an unknown modifiable risk
• Research opportunities abound…
Coursebook Page 75 of 139
6

5/29/2012
TAKE HOME POINTS
References
• Visual field defects common
◦ Often do NOT correlate with ODD location
• B – scan is standard of care
◦ Consider prior to imaging studies
• AF photography
• OCT role TBD
◦ May help in differentiating NFL defects in ODD versus
glaucoma
◦ Perhaps useful to monitor progression
1. Grippo, T. Rogers, S. Optic Disc Drusen. Glaucoma Today. 19-24. Jan/Feb 2012.
2. Antcliff, R. Spalton, D. Are Optic Disc Drusen Inherited Ophthalmology 106: 1278-1281. 1999.
3. Floyd, M. Katz, B. Measurement of Scleral Canal Using Optical Coherence Tomography in patients with Optic
Disc Drusen. Ophthalmology 139: 664-669. 2005.
4. Miller, Newman. Pseudopapilledema associated with Optic Disc Drusen. Clinical Neuro-ophthalmology. 6 th
edition, volume 1. 178-187. 2005.
5. Auw-Haedrick, C. Stauback, F. Optic Disc Drusen. Survey of Ophthalmology. 47: 515-532. Nov/Dec 2002.
6. Golnik, C. Congenital anomalies and acquired abnormalities of the optic nerve. Up to Date. 8/2011.
7. Bienfang, D. Overview and Differential diagnosis of papilledema. Up to Date. 6/2010.
8. Slotnik, S. Sherman, J. Buried Disc Drusen Have Hyporeflective Appearance on Spectral Domain Optical
Coherence Tomography. Optometry and Vision Science 89:5. May 2012.
9. Murthy, R. Storm, L. In-vivo high resolution imaging of optic nerve head drusen using spectral domain optical
coherence tomography. BMC Medical Imaging 10:11. 2010.
10. Wilkins, J. Pomeranz, H. Visual Manifestations of Visible and Buried Optic Disc Drusen. Journal of Neuroophthalmology
24. Nov 2004.
11. Katz, B. Pomeranz, H. Visual field Defects and Retinal Nerve Fiber Layer Defects in Eyes with Buried Optic
Nerve Drusen. American Journal of Ophthalmology: 141: 248-253. 2006.
12. Tatlipinar, S. Bozkurt, B. Polarimetric Nerve Fiber Analysis in Patients with Visible Optic Nerve Head Drusen.
Journal of Neuro-ophthalmology: 21: 245-249. 2001.
13. Ocakoglu, O. The investigation of Retinal Nerve Fiber layer thickness in eye with optic nerve head drusen.
Neuro-ophthalmology: 28: 205-214. 2004.
14. Kawa, P. Nowomiejska, K. Glaucoma and Drusen of the Optic Nerve Head. Neuro-ophthalmology: 33: 77-83.
2009.
15. Thurtell, M. Biousse, V. Optic Nerve Head Drusen in Black Patients. Journal of Neuro-ophthalmology: 0: 1-4.
2011.
Coursebook Page 76 of 139
7

5/29/2012
Exam of H.T.
Allison Coit
Spokane VA Resident
June 2012
• Chief Concern:
• Dozed off Friday afternoon and woke himself up when
he jammed his thumb in his right eye
• After incident noticed flash of light and snowstorm of
black floaters
• (‐)curtain over vision
• No new flashes since initial incident
• Immediately after poking eye, flushed eye out with
water
Exam…
**S/p Cataract Extraction/PCIOL OD 2 weeks ago
• DVA: w/o specs
• OD: 20/400‐
• OS: 20/50+
• Pupils: PERRL, (‐)APD
• EOMS: FULL
• CT: No Tropia
• CF: FTFC
• Anterior Segment:
• Lids: Clr OU
• Conj:
• OD: 2+ hyperemia
• OS: Clr
• Cornea: Clr OU
• AC:
• OD: 3+ pigment/cell
• OS: D/Q
• Iris: Flat OU
• Lens:
• OD: PCIOL – clear/centered
• OS: 1+ NS, Tr PSC inferior to visual Axis
Posterior Segment OD
• Vitreous: Dense
Hemorrhage
• C/D: 0.15 , distinct margins
• Macula: Flat
• Posterior Pole:
unremarkable
• A/V: 2/3
• Periphery: Flat
Assessment/Plan
Retina Evaluation
• Assessment:
• Vitreous Hemorrhage OD
• Possible Retinal Detachment
• B‐scan not working so unable to confirm
• Rebound Inflammation OD
• Plan:
• Refer to Retina Specialist
• Rx:
• Scopolamine 1gtt qpm OD and qAM tomorrow OD
• Prednisolone Acetate Q2hr OD only
• DVA: w/o specs
• OD: 5/100
• Pupils: (+)APD
• EOMS: FULL
• CT: No Tropia
• CF: FTFC
• Anterior Segment (OD )
• Lids: ClR
• Conj: Clr
• Cornea: Clr
• AC: 2‐3+ cell
• Iris: Flat
• Lens: PCIOL – clear/centered
• Gonio:
• Small hypopyon
Coursebook Page 77 of 139
1

5/29/2012
Retina Evaluation…
• Posterior Segment ‐
OD only
• Vitreous Hemorrhage
• Vitreous: 3+ vitritis, 3‐4+
vitreous haze, clumps of
vitreous cells and a “string
of pearls”
• Retina: break at 11 o’clock
No Case of No Cataract
Surgeries Years Rate per 1000 Surgeries
Author Country Data Source Endophthalmitis
West et al United States Medicare, US 1026 447,627 1994‐2001 2.15
Taban et al United Kingdom Meta‐analysis >3,000,000 1963‐2003 1.28
Kamalaraajah et al United Kingdom
Estimations from
databases &
questionnaires ~230,000 1999‐2000 1.4
Admin and clinical
Li et al
Australia
databases 210 117,083 1980‐2000 1.79
Admin and clinical
databases 102 57,123 1995‐2000 1.79
Ng et al
Australia
National cataract
registry 112 118,151 1999‐2001 0.6
Wejde et al
Sweden
National cataract
registry 109 225,471 2002‐2004 0.48
Lundstrom et al Sweden
Krummenauer et al Germany Questionnaire 291 404,356 2000 0.72
Moshirfar et al United States 14 20,013 2003‐2005 0.7
Bascom Palmer 1984‐1989 0.7
Bascom Palmer 1990‐1994 0.9
Bascom Palmer 1995‐1999 0.6
Miller et al
Clear Corneal
Incision 6 15, 920 2000‐2004 0.5
other methods 1 0.2
Risk Factors
• Pre‐Operative
• Blepharitis/Conjunctivitis
• Lacrimal Duct Obstruction
• Contact Lens Wear
• Ocular prosthesis in fellow
orbit
• Male>Female
• >85 years old (2 nd risk group
was 20‐64 years)
• Diabetes
• Immunosuppression
• Upper Respiratory Infection
• Intraoperative
• Capsular Rupture
• Secondary IOL
• Inadequate eyelid/conjunctival
disinfection
• Prolonged surgery (>60min)
• Vitreous loss
• Prolene haptic IOLs
• Postoperative
• Wound leak/dehiscence
• Inadequate buried sutures
• Suture removal
• Presence of filtering bleb
Decreased Vision
(+)APD
Loss of red reflex
Corneal Infiltrate
Wound abnormality
Hypopyon
Pain
Corneal Edema
Fibrinoid AC response
Vitreous Inflam
Retinitis
Keratic precipitates
• External Signs
• Ciliary injection
• Chemosis
• Eyelid edema
• Orbital Infection
• Restriction of EOMs
• Proptosis
Delayed Clinical Signs/Symptoms
• Capsular plaques (89%)
• White plaque on posterior capsules
• Fungal or bacterial
• Keratic precipitates (81%)
• Hypopyon (31%)
• Small, do gonio
• Low grade uveitis (may initially respond to steroids)
• Granulomatous
• Vitritis
• Beaded fibrin strand in aqueous
• White “string of pearls” infiltrate in vitreous or aqueous
• fungal
• No pain initially (27%)
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2

5/29/2012
• Immediate (withinin 2 days of surgery)
Could be any organism!
• Pseudomonas** Streptococcus**
• Early (214 days after surgery)
Could be any organism!
Top Suspects:
•Staphylococcus (coagulase negative) &
•Staphylococcus aureus
**most virulent
Differential Diagnosis
• Delayed (>14 days after surgery)
• Most common:
• Staphylococcus
• Propionibacterium acnes
• Fungi
• Ex: Candida, Aspergillus
• Immediate
• Toxic Anterior Segment Syndrome
• Clinical Findings:
• Fibrin formation
• Corneal Edema
• Anterior Chamber inflammation
• Mid‐dilated and irregular pupil
• Low IOP
• Vs Endophthalmitis
• Usually less prominent redness
• Less pain
• Less severe anterior chamber reaction
• Little or no vitreous inflammation
Differential Diagnosis
• Early (2 14 days)
• Retained Lens Material
• Increased inflammation with time
• Amount of retained lens + amount of time in eye
• Perform gonio
Differential Diagnosis
• Early
• Proliferative Diabetic Retinopathy
• PDR greater disturbance of blood aqueous barrier
• History of Uveitis
• Greatest risk of excessive post‐op inflam and complications
when uveitis not under control
• Most specialists require 6 months of inflamm control
• Increased risk: HLA‐B27 uveities, sarcoidosis, granulomatous
uveitis, children
Coursebook Page 79 of 139
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5/29/2012
Treatment
• Intravitreal
• Ceftazidime (gram ‐, including P. aeruginosa and H. influenzae)
• 2.25mg in 0.1ml
• Vancomycin (gram +, including MRSA)
• 1.0mg in 0.1mL
• Subconjunctival
• Vancomycin
• 25mg in 0.5mL
• Ceftazidime
• 100mg in 0.5mL
• Steroids
Topical
Vancomycin
50mg in 1.0mL
Ceftazidime
100mg in 1.0mL
• Oral prednisolone 1mg/kg po Qam x 3‐5 days
• Intravitreal dexamethasone
• Topical Pred Acetate 1% q1‐2 hours
Vitrectomy
Goal:
Removing the infecting organisms and toxins
Removing vitreous membranes
Which could lead to retinal detachments
Improve distribution of antibiotics
Cons:
Increase drug toxicity
Endophthalmitis Vitrectomy
Treatment Study (EVS)
• 420 patients
• Endophthalmitis within 6 weeks of cataract surgery
or secondary IOL
• Results
• Systemic antibiotics made no difference in final visual
acuity
• VA of Hand Motion or better
• Vitrectomy made no difference in outcome
• VA of Light Perception only
• Improved outcome with immediate vitrectomy
Prophylaxis
• 5% Povidone Iodine
• Significantly decreases the risk
• Effective against bacteria, fungi, virus, protozoa, and
spores
• Surgeons place 1gtt of Betadine in eye at surgery
• Pre‐op Antibiotics
• Limit pre‐op drops to 1‐3 days to decrease risk of antibiotic
resistance
• Post‐op Subconj Antibiotics
• Inconclusive
• Not always effective because of sub‐therapeutic
intraocular concentration
Special Thanks to:
Thomas Riley, OD, FAAO
References
1. Doshi, Rishi R., J. Fernando Arevalo, Harry W. Flynn, and Emmett T. Cunningham, Jr. "Evaluating
Exaggerated, Prolonged, or Delayed Postoperative Intraocular Inflammation." American Journal of
Ophthalmology 150 (2010): 295‐304. Print.
2. Endophthalmitis Vitrectomy Treatment Group, comp. "Results of the Endophthalmitis Vitrectomy Study."
Arch Ophthalmology 113 (1995): 1479‐496. Print.
3. Hatch, Wendy V., Geta Cernat, David Wong, Robert Devenyi, and Chaim M. Bell. "Risk Factors for Acute
Endophthalmitis after Cataract Surgery: A Population‐based Study." Ophthalmology 116.3 (2009): 425‐30.
Print.
4. Kresloff, Michael S., Alessandro A. Castellarin, and Marco A. Zarbin. "Endophthalmitis." Survey of
Ophthalmitis 43.3 (1998): 193‐224. Print.
5. Lalwani, Geeta A., Harry W. Flynn Jr, Ingrid U. Scott, Carolyn M. Quinn, Audina M. Berrocal, Janet L. Davis,
Timothy G. Murray, William E. Smiddy, and Darlene Miller. "Acute‐Onset Endophthalmitis after Clear
Corneal Cataract Surgery (1996–2005)Clinical Features, Causative Organisms, and Visual Acuity
Outcomes." Ophthalmology 115.3 (2008): 473‐76. Print.
6. Moshirfar, M., V. Feiz, A. Vitale, J. Wegelin, S. Basavanthappa, and D. Wolsey. "Endophthalmitis after
Uncomplicated Cataract Surgery with the Use of Fourth‐Generation FluoroquinolonesA Retrospective
Observational Case Series." Ophthalmology 114.4 (2007): 686‐91. Print.
7. Scott, I., H. Flynnjr, W. Smiddy, J. Newton, and D. Miller. "Acute‐onset Endophthalmitis After Cataract
Surgery (2000–2004): Incidence, Clinical Settings, and Visual Acuity Outcomes After Treatment." American
Journal of Ophthalmology 139.6 (2005): 983‐87. Print.
Coursebook Page 80 of 139
4

5/29/2012
Case History
VALSALVA RETINOPATHY
Kendra Kallemeyn, OD
Roseburg, OR VAMC
65yowm presents with CC of “black spot blocking
the vision in right eye. “
Onset – sudden, 5 days ago
Activity during time of onset – was helping daughter
move an entertainment center the night before and
when he woke up in the middle of the night he could not
see out of his right eye
Change in vision does not appear to be worsening or
improving since time of onset.
No symptoms like this have been noted previously in
either eye.
Ocular History
(-) prior ocular disease, injury or surgery
LEE 4-5yrs ago at commercial practice
Patient’s wife reports he was told to get his blood
pressure checked, because “something is wrong with the
blood vessels in the eye(s).”
No follow-up appointment with PCP was made
Medical History
No prior healthcare with any VA system prior to
today
Medications
Unknown blood pressure medication
started by outside provider in ~2009
patient reports medication is NOT controlling BP
NKDA
Baseline Exam 11/1/11
Visual Acuities cc
OD: CF w/EF PHNI
OS: 20/40 PHNI
Pupils: equal, round, reactive to light, (+)APD OD
EOMs: full and smooth OU
Confrontation Fields: full to finger counting OU
Anterior Seg: unremarkable OU
Tonometry by GAT: 16/16 @ 1:21pm
BP recorded as 174/99 at check-in to ER
Coursebook Page 81 of 139
1

5/29/2012
Baseline Exam Continued…
OD
Posterior Segment
Lens: trace nuclear sclerosis OU
Vitreous: clear OU
C/D Ratio : 0.65/0.65 OD, 0.5/0.5 OS
Vessels: arterial attenuation OU, A/V crossing changes OS
Macula
• OD: 5DDx5DD subretinal and intraretinal hemorrhage
w/preretinal heme inferior
• OS: flat, mild RPE changes, (-)heme/MA
Periphery: intact 360 OU
SUBRETINAL
--green/gray
INTRARETINAL
--dark red
PRERETINAL
(Subhyaloid or sub-ILM)
--boat shape or
horizontal blood line
OS
Assessment/Plan
--arterial attenuation with
no retinal hemorrhages
Assessment
Subretinal hemorrhage OD
Plan
Refer for retinal consult; Portland VA Ophthalmology
Differential Diagnosis
Primary Diagnosis
Valsalva retinopathy
Secondary Diagnosis
Retinal Artery Macroaneurysm
Terson’s Syndrome
Trauma – Choroidal Rupture
High Altitude Retinopathy
Neovascular Macular Degeneration – CNV
Retinopathy in Blood Disorders
Purtscher Retinopathy
Hypertensive retinopathy
Diabetic retinopathy
Choroidal Melanoma
http://www.sightnation.com/eye-disorders/otherpage=3
http://www.nature.com/eye/journal/v20/n9/fig_tab/6702068f6.html#figure-title
Retinal Artery Macroaneurysm (hemorrhage)
• Aneurysmal dilation of arteriole, most commonly at bifurcation or A/V crossing, along temporal arcades
and is associated with multilayer retinal hemorrhage in 50% of cases.
• Hard exudates may also be present due to chronic leakage
• Most commonly seen with unilateral presentation in hypertensive, elderly women.
•Preretinal and vitreous hemorrhage may block underlying lesion and/or make FA difficult which can
result in misdiagnosis.
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http://savesightcentre.com/diagnostic-testing.html
http://www.sarawakeyecare.com/Atlasofophthalmology/posteriorsegment/posteriorsegmentpictur5tersonsyndrome.htm
http://www.revoptom.com
Terson’s Syndrome
• Intraocular hemorrhage (typically bilateral) associated with acute intracranial hemorrhage
• Most common cause – subarachnoid bleeding from aneurysm of the anterior communicating artery
• Mechanism -- increased intracranial pressure at the time of an acute intracranial bleed may lead to
acute obstruction of the retinal venous circulation which results in rupture of superficial retinal vessels
• Patient typically presents to ER Physician with significant systemic signs/symptoms after suffering a
spontaneous or trauma-induced subarachnoid hemorrhage
Trauma: Choroidal Rupture
• Involves the choroid, Bruch’s membrane, and RPE
• Overlying subretinal hemorrhage may obscure view of fresh rupture
• rupture will appear as a white, crescent shaped, vertical streak of exposed sclera
http://www.nejm.org/doi/pdf/10.1056/NEJMicm0909506
http://www.eyedefectsresearch.org/mac-degen.html
http://www.ncbi.nlm.nih.gov.proxy.lib.pacificu.edu:2048/pmc/a
rticles/PMC3040733/pdf/pone.0011532.pdftool=pmcentrez
http://www.rustoneyeinstitute.com/index.cfm/PageID/3788
High Altitude Retinopathy
• Acquired retinopathy which typically occurs at elevations above 16,000ft
• Delayed onset of retinal hemorrhages on descent from high altitudes is common
• Triad of dilated retinal veins, retinal hemorrhages and optic disc edema
• Part of a spectrum of conditions associated with high altitude/hypoxic conditions
• Acute Mountain Sickness, High Altitude Cerebral Edema, High Altitude Pulmonary Edema
Neovascular (Wet) Macular Degeneration: CNV
• Non-exudative (dry) Macular Degeneration
• drusen, RPE pigment changes, geographic atrophy
• Exudative (wet) Macular Degeneration
• Choroidal neovascularization (CNV)
http://www.djo.harvard.edu
www.redatlas.org
http://www.retinamaculainstitute.com/ocular-education/ocular-trauma
http://webeye.ophth.uiowa.edu
http://legacy.revoptom.com/handbook/sect7e.htm
Retinopathy in Blood Disorders
• Sickle Cell Retinopathy, Anemia, Leukemia, etc
• salmon patch intraretinal hemorrhages, black sunbursts (RPE hyperplasia), seafan
neovascularization, vitreal hemorrhage, CWS, Roth spots
Purtscher Retinopathy
• Associated with head trauma, compressive chest injuries, long bone fracture, acute
pancreatitis, retrobulbar anesthesia, or systemic disorders (ie. Lupus)
• Typically presents bilaterally with presence of CWS, peri-papillary retinal
whitening, dilated retinal venous system, and retinal hemorrhages
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http://www.mrcophth.com/retinalvasculardisorders/proliferativediabetic.html
http://www.nature.com/nrrheum/journal/v2/n8/fig_tab/ncprheum0268_F6.html
Hypertensive Retinopathy
• Arterial attenuation, vascular leakage leading to retinal edema and deposition
of hard exudates, macular star, CWS, subretinal hemorrhages, ONH swelling
http://www.rustoneyeinstitute.com/index.cfm/PageID/3796
Diabetic Retinopathy
• NPDR: multiple MA and dot/blot hemes, CWS, HE, IRMA, NVD, NVI, NVE
• progressive: mildmoderatesevere
• PDR
http://www.jhu.edu/wctb/coms/general/about-mm/coms1a.htm
http://www.sightnation.com/casephotos/choroidal-melanoma
Initial Presentation
2 weeks
2 months
Choroidal Melanoma
http://www.kellogg.umich.edu/theeyeshaveit/non-trauma/choroidal-melanoma.html
• Present with varying amounts of pigmentation or amelanotic
• If the tumor breaks through Bruch’s membrane, intrinsic blood vessels and
hemorrhages may also be visible
Valsalva Retinopathy
http://webeye.ophth.uiowa.edu/eyeforum/cases/67-Valsalva-Retinopathy-Vision-Loss-Asthma.htm
• Classically presents as a sudden loss of central vision in a healthy individual that is
caused by premacular hemorrhage secondary to Valsalva stress.
• Valsalva maneuver (stress) is defined as “increasing intrathoracic or intraabdominal
pressure against a closed glottis which slows venous return to the heart, decreases stroke
volume and subsequently increases venous system pressure”
Valsalva maneuver: pathophysiology
Causes of Valsalva Stress
2. Diminished
cardiac filling
lowers the arterial
pressure, slows the
pulse and leads to
reflex tachycardia
and peripheral
vasoconstriction.
3. Release of the
strain causes
sudden reduction
of intrathoracic
pressure, further
lowering the
blood pressure
and increasing
the cardiac
pressure.
4. Abrupt
increase in blood
pressure occurs as
blood surges
back to the heart
which induces
reflex
tachycardia.
1. Sudden
increase in
intrathoracic
pressure
decreases venous
return to the heart.
Valsalva
Retinopathy
5. As the sudden rise
in intraocular venous
pressure occurs,
retinal capillaries
spontaneously rupture
which can lean to…
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Valsalva retinopathy: Benefits of OCT
Treatment vs Observation
Valsalva retinopathy has a tendency to appear at
the macula.
Visual prognosis and treatment options depend on
the size and anatomical level of the hemorrhage.
Use of the SD-OCT can localize the hemorrhage as
sub-ILM and/or subhyaloid.
Researchers continue to
dispute if the plane of the
hemorrhage is truly sub-ILM,
subhyaloid, or if the ILM and
hyaloid membrane are in fact fused.
Why Consider Treatment
Patient may have profound vision
loss for up to 6mo if left untreated.
Longstanding macular hemorrhages
(even 10DD in area with bullous
intraretinal hemorrhage overlying
• OS: flat
Periphery: attached 360 OU
Macular OCT
OD: large subretinal elevation with large intraretinal cyst
OS: flat
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5/29/2012
Assessment/Plan:
Assessment
Subretinal hemorrhage OD – large, >10DD in area,
prominently elevated
• Given history of patient moving entertainment unit by himself this
likely represents Valsalva retinopathy
Plan
Request patient be sent to Casey Eye Institute for FA and
photos to evaluate for alternative underlying etiology.
Counseled patient only course of action is observation.
Monocular precautions.
RTC 4mo for f/u.
Follow-Up
Attempt #1 (1/23/12)
2mo f/u at Roseburg VAMC – cancelled by patient
Attempt #2 (3/27/12)
4mo f/u at Roseburg VAMC – wife reports they will not be
able to make it to any f/u appointments
*Note: Review of patient chart shows high no-show and
cancel rate for lab work and PCP appointments as well.
Chart notes or test results from Casey Eye Institute were not
available.
Valsalva Retinopathy vs Retinal Artery Macroaneurysm (RAM)
http://savesightcentre.com/diagnostic-testing.html
Dx: Valsalva Retinopathy
based on case history
OCT would typically show sub-ILM
hemorrhage
Dx: RAM
hemorrhage present at multiple layers
OCT shows subretinal and intraretinal
elevation
patient is >60yrs old and has h/o
uncontrolled hypertension
RAM “idiopathic, acquired dilation of
a major retinal arteriole typically
occurring at the first three bifurcations
or an area of A/V crossing”
Conclusions and Clinical Pearls
References
Diagnosis of Valsalva retinopathy or hemorrhage as a
complication of RAM would not change the plan or outcome in this
patient.
Multi-layer retinal hemorrhages would not benefit from Nd:YAG
membranotomy. Direct or indirect laser treatment for macroaneurysm is
controversial.
Remember to consider your patient’s occupation or recreational
demands. Is binocular vision needed as a work requirement How
is the vision in the other eye
As always, patients need to be presented with all treatment
options and educated on expected timelines for possible visual
recovery.
Al-Mujaini AS, Montana CC. Valsalva retinopathy in pregnancy: a case report. Journal of Medical Case Reports.
2008. 2:101.
De Maeyer K, et al. Sub-inner limiting membrane haemorrhage: causes and treatment with vitrectomy. British Journal
of Ophthalmology. 2007. 91:869-872.
Duane TD. Valsalva hemorrhagic retinopathy. Trans Am Ophthalmol Soc. 1972. 70: 298-313.
Kaiser, Friedman. The Massachusetts Eye and Ear Infirmary Illustrated Manual of Ophthalmology. 2 nd edition. 2004.
Kanski J. Clinical Ophthalmology, A Systemic Approach. 6 th edition, 2007.
Khan M.T., et al. Nd:YAG laser treatment for Valsalva premacular hemorrhages: 6 month follow up. Alternative
management options for preretinal premacular hemorrhages in Valsalva retinopathy. International Ophthalmology.
2008. 28:325-327.
Kwok AK, Lai TY, Chan NR. Epiretinal membrane formation with internal limiting membrane wrinkling after Nd:YAG
lasaer membranotomy in Valsalva retinopathy. American Journal of Ophthalmology. Oct 2003. 136(4):763-766.
Mumcuoglu T, Durukan A, et al. Outcomes of Nd:YAG Laser Treatment for Valsalva Retinopathy Due to Intense
Military Exercise. Ophthalmology Surgery, Lasers and Imaging. Jan/Feb 2009. Vol 40:19-24.
Sabella P, Bottoni, F, Staurenghi, G. Spectral-domain OCT evaluation of Nd:YAG laser treatment for Valsalva
retinopathy. Graefe’s Arch Clinical and Experimental Ophthalmology. 2010. 248:599-601.
Shukla D, Naresh K, Kim R. Optical coherence tomography findings in Valsalva retinopathy. American Journal of
Ophthalmology. July 2005. 140:134-136.
Tatlipinar S, et al. Optical coherence tomography features of sub-internal limiting membrane hemorrhage and
preretinal membrane in Valsalva retinopathy. Canadian Journal of Ophthalmology. 2007. 42:129-130.
Coursebook Page 86 of 139
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5/29/2012
Thank you!
Roseburg VA Eye Care Team
• Dr. Bryan Deck, OD
• Dr. Dirk Dittemore, OD
• Dr. Duva Appleman, MD
Coursebook Page 87 of 139
7

Objectives
Perioperative Vision Loss from
Non‐Ophthalmic Surgery
Brett Richardson, O.D.
Spokane VAMC
509.434.7032
• My goal for this presentation is for you to
understand that
– Non‐ophthalmic surgeries can result in
Perioperative Vision Loss (POVL)
– Altered vascular supply is the primary cause
Objectives
• I will be discussing
– Common surgeries that result in Perioperative
vision loss (POVL)
• Cardiac
• Spine
– Most common types of POVL
• Ischemic Optic Neuropathy
• Retinal Vascular Occlusion
• Cortical Blindness
Case
• 65 y.o. WM
• POHx
– Mild Hypertensive Retinopathy OU
– RPE mottling OU
• PMHx
– Malignant Hypertension (as high as 267/158)
– Hypercholesterolemia
– Coronary Artery Disease
– Myocardial Infarction with Angioplasty and stent 2007
– Renal failure
– Angioplasty and stent 2011 (2 weeks ago)
Case
• CC: “During angioplasty and stent surgery 2
weeks ago, my blood pressure shot way up
and my vision has been blurry and distorted
ever since.”
Case
• VA
– od: 20/80 ‐>> ph70, very slow
– os: 20/150 ‐>> phni, very slow
• BCVA
– od: 20/40
– os: 20/100
• PERRLA (‐) APD
• Tonometry
– od: 13
– os: 14
Coursebook Page 88 of 139

Case
• Ant Seg: Unremarkable
• Fundus
– Nerve ou: 0.4rd, (‐) pallor
– Macula: Mild Mottling OS>OD
– Vasculature ou: 2/3, mild nicking
– Posterior Pole: unremarkable ou
– Periphery: flat ou
Case
• Additional Testing
– OCT: macular
• od: 176microns centrally, normal contour
• os: 176microns centrally, normal contour
– BP: 120/72
– Visual Field
Case ‐ Visual Fields #1
Case ‐ CT Scan
• Unremarkable
Homonymous Macular Quadronopsia
Case – Follow Up
Case –Visual Fields #2
• 4 Months later
– VA
• od: 20/60+ phni
• os: 20/100 phni
– Fundus: No significant changes
• (‐) Optic Nerve Pallor
– Visual Field
Generalized Depression OU!!
Coursebook Page 89 of 139

Case – Follow Up
Case –Visual Fields #3
• 8 months later
– VA
• od:20/30
• os:20/100
– Fundus: No Significant changes
– Optic Nerve: (‐) pallor ou
– Visual Field:
Imaging
Fundus Photos
• MRI
– Chronic small right occipital infarct
– Chronic small vessel ischemic changes and chronic
lacunar infarcts
• MRA
– Unremarkable
Diagnosis
• Angioplasty with stent surgery causing
occipital lobe infarction resulting in
homonymous macular quadranopsia leading
to cortical blindness secondary to cerebral
ischemia
• CARDIAC SURGERY CORTICAL BLINDNESS
Study
• 10 Year study from 1996‐2005 by Nationwide
Inpatient Sample (NIS).
• 74 million patients
– 5.7 million relevant surgical patients
• 8 most common surgeries in U.S.
• Monitoring for Perioperative visual loss
– Ischemic Optic Neuropathy (ION)
– Retinal Vascular Occlusion (RVO)
– Cortical Blindness (CB)
Coursebook Page 90 of 139

Study
• Incidence of POVL
– Cardiac Surgery: 8.64/10,000
– Spine Surgery: 3.09/10,000
– Appendectomy: 0.12/10,000
– Total: 2.35/10,000 (all 8 surgery types)
• POVL in Cardiac Surgery
– RVO 77%
– ION 16%
– CB 8%
• POVL in Spine Surgery
– CB 49%
– ION 28%
– RVO 23%
Study
• Findings
– Highest rate of POVL is found in cardiac and spine
surgeries
– Prevalence: Males vs. Females 2:1
– ION highest in patients 50‐64 y/o
– RVO highest in patients > 65 y/o
– CB highest in patients < 18 y/o
– Highest prevalence in patients < 18 y/o (4.37/10,000)
– POVL remains unpredictable and is not related to any
particular hospital or degree of surgical experience
Literature Review Reveals:
• Ischemic Optic Neuropathy
– 3 Forms
• Perioperative, Arteritic, Non‐arteritic,
– Hypotension ION
– Anemia ION
• > 1L (average 5L)
– Hypothermia ION
• blood viscosity
• 1 o Cdecrease = 6‐7% decrease in cerebral blood flow
– Ocular Hypertension (prone position)
– Surgical Time (> 6 hours)
Literature Review Reveals:
• Central Retinal Artery Occlusion (CRAO)
– Spine Surgeries (933 cases)
• Declined Prone position venous stasis in capillary
beds
– 70% secondary to ocular trauma
• Ocular compression from head rest can raise IOP to
sufficient level to cause ischemia
Literature Review Reveals:
• Cortical Blindness
– Destruction or denervation of 1 o Visual Cortex
(Occipital Lobe) or Optic Radiations
– Highest incidence in cardiac surgery (CABG)
– Results from embolism, stroke
– Risk Factors
• HTN, DM, Renal insufficiency, Smoking, PVD, COPD
Summary
• Perioperative Vision Loss Likely to occur:
– Cardiac Surgery > Spine Surgery > all others
– ION > CRAO > Cortical Blindness
– High Risk patients
• DM, Smoking, HTN, Vascular disease
– High Risk Intraoperative Complications
• Blood loss > 5L
• Hypotension < 90 mmHg
• Long Operating Times (> 6 hours)
Coursebook Page 91 of 139

Coursebook Page 92 of 139

5/31/2012
Diabetic Teleretinal Imaging
Program:
An Assessment of the Diabetic Teleretinal Imaging Program (TRIP) at
the Portland Veterans Affairs Medical Center (PVAMC) - A Retrospective Study
Diabetes Statistics
• 24 million people in the US have DM
• 78% have retinopathy if DM >15yrs
Keely L. Hoban, O.D.
Grace L. Tsan, O.D.
Portland VA Medical Center
June 4, 2012
• 28.5 % of people with diabetes ages >40 years
have diabetic retinopathy
Burden of Diabetic Eye Disease
• #1 cause of blindness in working‐aged adults
in the US
What does this mean for
optometry
Health
Care
System
Burden
Eye Care
Providers
Patients
PVAMC Research Team
• Weon Jun, O.D., FAAO
• Keely L. Hoban, O.D.
• Steve Mansberger, M.D., MPH
• Amy L. Pedersen, O.D.
• Kevin J. Riedel, O.D.
• Grace L. Tsan, O.D.
Objectives
• Advantages and disadvantages of Diabetic Teleretinal Imaging
Program (TRIP).
• Types of clinical settings that may benefit from TRIP.
• Effectiveness of TRIP at the PVAMC.
• Identify program improvements for TRIP at the PVAMC
Coursebook Page 93 of 139
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5/31/2012
What is Telemedicine
Store‐and‐Forward Telehealth
http://www.telehealth.va.gov/
Annual vs. Biennially
DFE
TRIPDFE
Teledermatology Teleretinal Imaging Teleradiology
How does TRIP work
Four Non‐Mydriatic Images
Cavallerano AA, Conlin PR. Teleimaging to screen for diabetic retinopathy in the Veterans Health Administration. J Diabetes Sci Technol 2(1): 33-9, 2008.
Referral Guidelines for
Diabetic Eye Exam
Who may benefit from TRIP
• Target Patients:
– DM patients with low risk for retinopathy
• i.e. Newly diagnosed DM patients, patients w/ well controlled A1c
– DM patients with diabetic retinopathy that have been lost to follow‐up
• Other Uses:
– Identify co‐morbid eye conditions
• Providers:
– Hospitals
– Academic Institutions
– Group Practice Settings
Cavallerano AA, Conlin PR. Teleimaging to screen for diabetic retinopathy in the Veterans Health Administration. J Diabetes Sci Technol 2(1): 33-9, 2008.
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5/31/2012
Goals for TRIP
CASE #1
• Increase compliance with diabetic eye exams
• Improve patient education on importance of diabetic
eye exam
• Early intervention to treat and manage diabetic
retinopathy
Retrospective Chart Review
• Inclusion Criteria:
– Reviewed CPRS medical records of 200 patients from 1757
diagnosed diabetic patients
– Teleretinal imaging performed between
January 1, 2010 and January 1, 2011
• Exclusion Criteria
PVAMC TRIP Locations
Data
Vancouver
• Quality image:
90% adequate
• Male: 97%
• Average age: 64.7 yrs (std dev 10.2)
• Race:
91% Caucasian
• Avg Height/Weight: 70 inches/230 lbs
• Avg BMI: 33.8 kg/m 2 (obesity >30)
• Avg lab glucose:
155 mg/dL
• Avg HbA1c: 7.3%
• Average duration of DM: 9 yrs
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5/31/2012
Co‐morbid Conditions
• Fasting Cholesterol: 166 (normal

5/31/2012
Efficiency of TRIP at PVAMC
Efficiency of TRIP at PVAMC
• Reader
(Optometrist)
Schedule
appointment
(80%)
•Eye Clinic
Redundancy
11%
6 months
Duplicate Recall
37%
1 year
Refer to eye
clinic (99%)
•Imager
(at PCP dept)
Dilated eye
exam
Eye
Exam
Teleretinal
Imaging
Teleretinal
Recall
TRIP Research Trends
Good referral into eye clinic from readers
Low redundancy by imagers
Majority of patients had no DR
Good compliance for referrals from imagers
• High teleretinal imaging recall within one year
of imaging
Suggested Program Improvements
to TRIP
• Future recall for teleretinal imaging should be based
on reader’s recommendation.
• Increase awareness of all eye care providers to check
future scheduled eye clinic appointments to reduce
duplicated eye clinic and TRIP appointments
Comparison to other VA TRIP
Comparison to Non‐VA Populations
Mansberger SL, Gleitsmann K, Gardine S, Sheppler C, Demirel S, Becker TM. The Comparative Effectiveness of Telemedicine for Providing Diabetic
Retinopathy Screening Exams: A Randomized Controlled Trial
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5/31/2012
Improved Compliance with TRIP
Sensitivity and Specificity of TRIP
Mansberger SL, Gleitsmann K, Gardine S, Sheppler C, Demirel S, Becker TM. The Comparative Effectiveness of Telemedicine for Providing Diabetic
Retinopathy Screening Exams: A Randomized Controlled Trial
Benefits of TRIP
Case #4
Increased referrals for comprehensive eye exams
Improved patient awareness and compliance
Initiated timely treatment
TRIP overcomes barriers for annual eye exams
34‐64% of patients with DM in private and public sectors have
annual eye exams, VA excels in this area
Treatment is 90% effective in preventing severe vision loss
Patient Satisfaction
• Universally Positive
• Efficient
• Less time sensitive
• More convenient for pt to be undilated
• Pt Ed, improved understanding/awareness
• Comfortable
• Improved Compliance!!
Economic Benefits
• DM vision loss = $132 billion
• Detecting proliferative diabetic retinopathy
• Averting cases of severe vision loss
• More time efficient
• Improves adherence
• TRIP may help utilize eye doctors time more
effectively
Cavallerano AA, Conlin PR. Teleimaging to screen for diabetic retinopathy in the Veterans Health Administration. J Diabetes Sci Technol 2(1): 33-9, 2008.
Cavallerano AA, Conlin PR. Teleimaging to screen for diabetic retinopathy in the Veterans Health Administration. J Diabetes Sci Technol 2(1): 33-9, 2008.
Coursebook Page 98 of 139
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5/31/2012
Practical Implications: How to Bill
Reimbursement
PCP Site
Specialist
Review
Diabetic
Screening
Encounter
• Medicare
– CPT 92227: remote imaging for detection of
retinal disease
– CPT 92228: remote imaging for monitoring and
management of active retinal disease
• Private and commercial carriers
– CPT 92250/S0625
Summary
REFERENCES
• TRIP fulfills the goals of screening low risk diabetic
patients
• Occasionally will miss some findings, or findings may
be worse or improved as it is a “static image”
• Helps patients to maintain quality of life and
independence
1. Huang ES, Basu A, O'Grady M, Capretta JC. Projecting the future diabetes population size and related costs for
the U.S. Diabetes Care 32(12):2225‐2229, 2009.
2. Diabetic Retinopathy. Preferred Practice Patterns. San Francisco: American Academy of Ophthalmology, 2008.
3. Klein R, Klein BE, Moss SE, Davis MD, DeMets DL. The Wisconsin epidemiologic study of diabetic retinopathy. III.
Prevalence and risk of diabetic retinopathy when age at diagnosis is 30 or more years. Arch Ophthalmol
102(4):527‐532, 1984.
4. Ferris FL, 3rd, Davis MD, Aiello LM. Treatment of diabetic retinopathy. N Engl J Med 341(9):667‐678, 1999.
5. Garg S, Davis R. Diabetic retinopathy screening update. Clinical Diabetes: A publication of the American
Diabetes Association 27:140‐145, 2009.
6. Conlin PR, Fisch BM, Orcutt JC, Hetrick BJ, Darkins AW. Framework for a national teleretinal imaging program to
screen for diabetic retinopathy in Veterans Health Administration patients. J Rehabil Res Dev 43(6): 741‐8, 2006.
7. Cavallerano AA, Conlin PR. Teleimaging to screen for diabetic retinopathy in the Veterans Health Administration.
J Diabetes Sci Technol 2(1): 33‐9, 2008.
8. Lin DY, Blumenkranz MS, Brothers RJ, Grosvenor DM. The sensitivity and specificity of single‐field nonmydriatic
monochromatic digital fundus photography with remote image interpretation for diabetic retinopathy
screening: a comparison with ophthalmoscopy and standardized mydriatic color photography. Am J Ophthalmol
134(2):204‐213, 2002.
9. Farley TF, Mandava N, Prall FR, Carsky C. Accuracy of primary care clinician in screening for diabetic retinopathy
using single‐image retinal photography. Ann Fam Med 6(5): 428‐34, 2008.
10. Mansberger SL, Gleitsmann K, Gardine S, Sheppler C, Demirel S, Becker TM. The Comparative Effectiveness of
Telemedicine for Providing Diabetic Retinopathy Screening Exams: A Randomized Controlled Trial
THANK YOU!
Portland VA Medical Center
&
Pacific University College of Optometry
Coursebook Page 99 of 139
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5/29/2012
Radioiodine Therapy and
Graves’ Ophthalmopathy
ZACHARY OSWALD, O.D.
RESIDENT AT
WALLA WALLA VA MEDICAL CENTER &
PACIFIC CATARACT AND LASER INSTITUTE –
KENNEWICK
MAY 29, 2012
Disclosure
• Zachary Oswald, O.D., developed this course
material and information independently without any
relevant financial interests or influence of
commercial interest.
• Consent was given by the patient to present the
photographs and personal information included in
this course.
Learning Objective
Course Outline
• By the end of this presentation, attendees will be able
to:
◦ 1. Understand, evaluate, and treat Graves’ Ophthalmopathy
with more confidence.
◦ 2. Recognize that using radioiodine therapy to treat
hyperthyroidism can cause the development or worsening
Graves’ Ophthalmopathy.
◦ 3. Better understand the process of co-management with the
other members of a patient’s health care provider team.
• Case Presentation
• Radioiodine in the treatment of hyperthyroidism
• Graves’ Ophthalmopathy Overview
• Possible Treatments of Graves’ Ophthalmopathy
• Explore contraindications and possible side effects of
oral prednisone.
• Co-management Tips
11/18/09 1 st Visit at WWVAMC
11/18/09 1 st Visit at WWVAMC
• 75 yowm
• Comprehensive Exam
• Personal Ocular History
◦ Followed as glaucoma suspect due to larger C/D ratios for 35
years, has never been prescribed glaucoma medication.
◦ 2007 Cataract Extraction at PCLI - Lewiston: phaco with pc iol
both eyes.
◦ Last eye exam was in 2007 in Lewiston, ID.
◦ Was told he had some signs of macular degeneration at last eye
exam.
◦ Wears Bifocals
• Problem List:
◦ Coronary Artery Disease
◦ Congestive Heart Failure
◦ Pulmonary Hypertension
◦ Chronic Obstructive Pulmonary Disease
◦ Dependence on supplemental oxygen
◦ Gout
◦ Dermatitis
◦ Tinnitus
◦ Sensorineural hearing loss
◦ MI 12/21/91, stopped smoking then
Coursebook Page 100 of 139
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5/29/2012
11/18/09 1 st Visit at WWVAMC
11/18/09 1 st Visit at WWVAMC
• Medications:
◦ Bosentan 125mg bid
◦ Calcium Carbonate 650mg tab qd
◦ Citalopram 20mg ½ tab qd
◦ Clopidogrel Bisulfate 75mg tab qd
◦ Colchicine 0.6mg tab qd
◦ Digoxin 0.125mg tab qd
◦ Flunisolide inhaler bid
◦ Furosemide 40mg tab bid
◦ Hydrocodone 5 / Acetaminopthen 500mg tid prn
◦ Levothyroxine 0.175mg tab qd
• Medications Continued
◦ Magnesium Oxide 400mg tab qd
◦ Potassium Chloride 10meq 2 tab bid
◦ Ranitidine HCL 150mg tab bid
◦ Sildenafil Citrate 50mg ½ tab tid
◦ Simvastatin 10mg tab qhs
◦ Sprionolactone 2 tab qAM, 1 tab afternoon
◦ Tiotropium 1 tab in inhaler qd
◦ Warfarin 5mg tab qd
11/18/09 1 st Visit at WWVAMC
11/18/09 A & P
• +1.00-2.25 x 090 20/25
• +1.00-2.25 x 090 20/20-2
• Add: 2.50 20/20
• Cover Test Distance 4^ exophoria
• ASSESSMENT:
◦ 1) Glaucoma Suspect due to larger C/D ratios (RE 0.55/0.55, LE 0.5/0.5). IOP
18mmHg RE, LE today.
◦ 2) Macular pigment changes BE
◦ 3) Pseudophakia BE with trace PCO
◦ 4) Hyperopia, Astigmatism, Presbyopia BE
• PLAN:
◦ 1&2) Fundus photos taken today. Monitor pt. in one year with a comprehensive
exam watch for changes in ONH, pressure check, and macular changes.
◦ 3) Monitor in 1 year at comprehensive exam.
◦ 4) No glasses ordered today. Pt. satisfied with vision and condition of current
glasses.
• Return to clinic in 1 year for comprehensive examination c FDT to monitor
macular pigment changes and ONH cupping.
01/20/11 Fee Basis Exam at Private Office
06/27/11 WWVAMC – Age 76
• +1.00-1.75 x 089 20/40
• +1.50-2.00 x 086 20/30-
• Add: 2.50
• BE 1-2+ PCO encroaching centrally
• YAG performed in March 2011 at PCLI – Lewiston.
• Binocular Diplopia reported as starting in February
2011.
• Veteran has been working with private doctor in
Lewiston. Last appointment with private doctor
about a week ago.
• Unsure what is causing diplopia.
• Has glasses with prism that help, but eyes still feel
like they are not working together.
• Would like to start coming to VA again because it
will be more cost effective.
Coursebook Page 101 of 139
2

5/29/2012
06/27/11 WWVAMC
06/27/11 WWVAMC
◦ Problem List same as initial visit.
◦ Medication additions since initial visit in 2009:
Albuterol 2 puffs qid prn
Bacitracin ung apply to affected area tid prn (dermatitis)
Carboxymethylcellulose 0.5% qid BE prn
Loratadine 10mg qd
Losartan Potassium 50mg ½ tab qd
Mometasone Furoate 1-2 sprays qd
Mupirocin 2% ung affected areas bid (dermatitis)
Ocular Lubricant Pres Free ung qhs BE
Nitrofurantoin 100mg cap bid
◦ Medications no longer taking since initial visit 2009:
Colchicine
Flunisolide
Simvastatin
Spironolactone
• Hab Rx from Fee Basis Dr.
◦ +1.25-2.00*088 3-4^BD 20/40+2
◦ +1.25-2.50*087 3^BU 20/50+2
◦ Base Curve
RE 6.2
LE 5.8
• EOMs
◦ Sup. right gaze, right eye appears underacting.
◦ Inf. left gaze, left eye appears underacting.
Which muscles are affected
Actions of extraocular muscles
LR
SR
IO
MR
IO
MR
SR
LR
Muscle Primary Action Secondary Tertiary
Superior Rectus Elevation Intorsion Adduction
Inferior Rectus Depression Extorsion Adduction
Medial Rectus Adduction
Inferior Oblique Excyclotorsion Elevation Abduction
Superior Oblique Incyclotorsion Depression Abduction
Lateral Rectus Abduction
IR
SO
SO
IR
Right Eye
Left Eye
06/27/11 WWVAMC
• Cover Test c older Rx (without prism):
◦ Dist: 7^BD RE neutralizes vert movement, residual 2^ BO
◦ Near: 7^BD RE, 8^ BI
• Cover Test c habitual Rx (prism):
◦ Dist: ortho vert and horiz
◦ Near: ortho vert and horiz
06/27/11 WWVAMC
• Refraction:
◦ +0.75-1.50*090 3^BD 20/25+1
◦ +1.75-2.50*081 2^BU 20/25-2 BE:20/25-2
◦ ADD: 2.50 20/25-
• Binocular Testing:
◦ Distance
Horiz Phoria: 5^ BO
Vergences: BI: x/-2/-5, BO: x/20/9
Vert Phoria: 7^ BU LE
Vergences (with 3^BO otherwise no fusion):
LE BU 9/5, BD -2/NA
◦ Near:
Horiz: 10^ BI
Vert 6^ BU LE
Coursebook Page 102 of 139
3

5/29/2012
06/27/11 WWVAMC
• Trial Framed the refraction:
◦ +0.75-1.50*090 3^BD 20/25+1
◦ +1.75-2.50*081 2^BU 20/25-2 BE:20/25-2
◦ ADD: 2.50 20/25-
• Patient reports the letters feel like they are trying to
pull apart, but 5^ BU LE was preferred to 4^ BU or
6^BU. No prism preferred horizontally.
06/27/11 WWVAMC
• Assessment:
◦ 1. Right hypertropia causing diplopia – several muscles may be
involved causing prism combinations to not totally correct the
diplopia.
◦ 2. Dry Eye Syndrome – causing some fluctuation of vision.
◦ 3. Dry AMD BE – at most is minimally affecting vision.
◦ 4. Glaucoma suspect secondary to larger c/d ratios (0.45/0.45 BE)
pressures up from before (21/19), sloping discs.
◦ 5. Bilateral pseudophakia s/p YAG BE
• Plan:
◦ 1. Ordered new bifocals.
◦ 2. Encouraged to continue artificial tears 4x day and ointment at
night.
◦ 3-5. Monitor in one year with full exam.
09/09/11 WWVAMC – Age 77
09/09/11 WWVAMC
• Vet reports that he received his new spectacles about
2 weeks ago. They function better than previous
spectacles, but he reports continued diplopia with
and without them. Sometimes in the afternoon he
sees singly. Right eye reported as much blurrier than
the left with new spectacles.
• External Exam:
◦ Patient uses oxygen by nasal cannula tank with tank set to a 5
or 6 and his lips have a blue hue (vet has pulmonary
hypertension). Right eye possibly proptotic.
• Visual Acuities
• Current Spec Rx:
◦ +1.25-1.25*092 3^BD 20/50 PH: 20/40
◦ +1.75-2.50*082 2^BU 20/25+1
◦ Add:2.25
• Refraction:
◦ RE: +0.75-2.00*092 20/25-2
09/09/11 WWVAMC
09/09/11 WWVAMC
• EOMs:
◦ Restricted RE sup/temp, LE inf/temp, Possible restriction LE
sup/temp as well. (+) forced duction test.
• Pupils: PERRL (-) APD 5-3, 2+ reaction light.
• Cover Test over new specs:
◦ Distance: 3^BD RE neutralizes vertical movement.
◦ Near: 3^BD RE neutralizes vertical movement. 6^exo after
vertical prism correction.
• Red Cap Test: = saturation BE
• Amsler Grid: BE (-) metamorphopsia, (-) scotomas
• Exophthalmometry: 22/21 @ 110 (avg is 15-17)
• SLE:
• Lids, Lashes, Adnexa: BE: edematous upper lids, 2+
dermatochalasis, 2+ MG inspissation, 1+ scalloped
lid margins, 1+ debris along lashes.
• Cornea: BE: Tr-1+ arcus 360*, 1+ diffuse SPK cent to
inf.
Coursebook Page 103 of 139
4

5/29/2012
Suspect Graves’ Ophthalmopathy
• Pertinent medical history:
◦ Veteran has a history of hyperthyroidism that was treated with
radioiodine ablation.
◦ Veteran is currently taking one 0.175mg tablet of levothyroxine
once a day for thyroid.
• Labs
◦ 05/05/08: Thyroid Stimulating Hormone (TSH) 0.85 (o.3-
6.0)
◦ 03/25/09: Free T-4: 1.7 (0.6-2.0)
TSH: 3.76 (0.3-6.0)
◦ 03/18/10: TSH: 2.10 (0.3-6.0)
◦ 08/17/11: TSH: 1.64 (0.3-6.0)
09/09/11 WWVAMC
• Assessment:
◦ 1. Binocular diplopia with right eye hypertropia.
◦ 2. Bilateral dry eye syndrome.
• Plan:
◦ 1. Ordered CT scan of both eyes from orbit to chiasm without
contrast enhancement to review in clinic to rule out Graves, Thyroid,
or compressive sources. Discussed diplopia as possibly related to
thyroid problems and possible treatment options. Dispensed and
applied 3^ BD Fresnel prism on the right lens which allowed single
vision today. Dispensed patch to use as needed to prevent diplopia.
Will call patient following review of CT results to schedule follow up
appointment.
◦ 2. Patient education. Encouraged patient to continue artificial tears 4
times a day and lubricating ointment once at night both eyes.
Monitor.
What do you notice
CT Results
09/09/2011
• Findings:
◦ “The patient has rather marked enlargement identified of the right
superior rectus muscle and the left inferior rectus muscle. There is a
lesser degree of enlargement of the right inferior rectus muscle and
the left superior rectus muscle. There is some stranding identified
surrounding the right superior rectus and left inferior rectus muscle.
This appears to infiltrate the whole muscle body itself with regards to
the right superior and left inferior rectus muscles. The remainder
appear to be infiltrating the mid body of the muscle itself.
◦ Optic nerves appear to be grossly normal. The remainder of the
extraocular muscles are normal.
◦ There is is diffuse cerebral atrophy noted. Some mild mucosal
thickening in both maxillary sinuses.
CT Results
CT Scan Coronal
• Impression:
◦ “The patient has findings most compatible with Grave’s
Ophthalmopathy.”
Coursebook Page 104 of 139
5

5/29/2012
CT Scan Coronal
Treatment Options
• Researched treatment options that would work best
for this patient.
• Decided that oral prednisone would be best with
goals of:
◦ 1. Reducing periorbital edema.
◦ 2. Reducing amount of exophthalmos.
◦ 3. Reducing diplopia.
• Who should manage this treatment plan
Co-management with PCP
Called clinical pharmacist at the VA
• We called the patient’s PCP at 12:15pm on 09/27/11 to
update her with the status of this condition and ask if she
would feel more comfortable handling the Prednisone
treatment.
• She responded that she would prefer that someone with
more experience in this field handled the treatment, and
she would be happy to coordinate follow up for systemic
side effects with Mr. Parks' primary care health team.
• Primary health team includes VA PCP, VA clinical
pharmacist, private PCP, pulmonologist, and
cardiologist.
• Asked him to review the patient’s medications and
relate any concerns with starting oral prednisone.
◦ Patient is already taking Ranitidine.
◦ No major contraindications after reviewing problem list and
medications.
Prednisone versus Prednisolone
Watch Liver Function
WWVAMC 10/12/11
• "Though prednisone and prednisolone are used in the same manner
and equally as effective, they should not be confused with each
other. Prednisone is activated by the liver into prednisolone. For
this reason and because it is more easily absorbed, prednisolone is
the drug of choice when hepatic disease or insufficiency is present."
They are both intermediate strength synthetic corticosteroids.
"Prednisone and prednisolone are synthetic members of the
glucocorticoid class of hormones. They are an intermediate acting,
broad antiinflammatory, medication. They have less activity than
dexamethasone or betamethasone, but exhibit greater activity than
hydrocortisone."
From http://patients.uptodate.com/topic.aspf…
• 77 yo WHITE MALE c Graves ophthalmopathy
(Thyroid Eye Disease = TED) presents for follow up.
• Patient reports no diplopia in straight ahead gaze
since addition of 3^BD RE fresnel prism at last
appointment, but image feels like it is "trying to pull
apart."
• Vet reports diplopia at times when looking to the
side, up, or down.
• Vet reports no pain or irritation BE. No dryness or
tearing or redness. Vet reports that sunlight is
bothersome BE.
Coursebook Page 105 of 139
6

5/29/2012
10/12/11
• EOMS: smooth pursuits. LE: restricted sup/temp,
sup, and sup/nas
◦ Diplopia reported in all field of gaze, worse with sup and
sup/left gaze.
◦ Pain Rating 0/10 in all gazes
10/12/11
• VISUAL ACUITY:
• Current Spec Rx & lens type: St 28, 3^bd Fresnel over RE
• RE:+1.25-1.25*092 3^ BD 20/50 PH: 20/40
• LE:+1.75-2.50*082 2^ BU 20/25+1
• Add:2.25
• Refraction:
• Right:+0.75-2.00*092 20/25-2
• COLOR VISION/RED CAP (RE%/LE%): Equal saturation
• AMSLER GRID: No metamorphopsia in either eye
• SLE:
• LIDS, LASHES, ADNEXA: BE: 2-3+ edematous upper lids, 2+
dermatochalasis, 2+ MG inspissation, scalloped lid margins, 1+ debris
10/12/11
10/12/11
• TONOMETRY BY iCare:
• straight ahead: 18/15
• up: 21/18
• left: 15/14
• right: 17/13
• Blood pressure 146/68 pulse measurement 68
• Weight: 212.5 lbs
• Exophthalmometry: 22/21 @ 110
• Interpalpebral distance measured vertically:
• straight ahead: 10/10 mm
• up: 12/13 mm
10/12/11 10/12/11
Coursebook Page 106 of 139
7

5/29/2012
10/12/11 Posterior Pole
WWVAMC 10/12/11
Non-VA Physicians
• ASSESSMENT(S):
• 1) Graves Ophthalmopathy (Thyroid Eye Disease) with incomitant strabismus and
• near constant diplopia, partially relieved by Fresnel prism. Veteran already
• on ranitidine.
• PLAN(S):
• 1) Veteran is unable to withstand surgical management and steroid
• immunosuppression is the best/only option - patient education. Before
• prescribing prednisone, non-VA providers will be contacted for consensus on
• treatment. 20 mg/day oral prednisone to be started for 1 week with patient
• monitoring his blood pressure, pulse, and weight - with plan to increase to 40
• mg/day if well-tolerated. Return to Walla Walla after 4 weeks of treatment;
• fasting labs: Chem, UA, CBC.
• PATIENT EDUCACTION:
• Reviewed common side effects of Prednisone with patient and his spouse
• including: osteoporosis, irritability/depression, and heartburn/GI tract
• disorders. We also discussed the increased risk of exacerbation of
• hypertension and congestive heart failure.
• Pulmonology: Spokane
• Cardiology: Spokane
• Primary Care: Lewiston
• All gave the okay for to start oral Prednisone.
• Pulmonologist said if anything, it would help his
pulmonary hypertension.
• Everyone offered to help monitor for side effects and
help with the taper when finished.
How to prescribe Prednisone (Up-to-date) 18
Started Prednisone
• “The optimal dose of prednisone is uncertain. Some
clinicians initiate therapy with a high dose, such as 100
mg/day. However, doses of 30 to 40 mg/day appear to be
as effective and have fewer side effects. Improvement
usually occurs within four weeks. About one-half of
patients have a good response to prednisone by the end
of six months; those patients with less muscle swelling
are more likely to respond [19]. However, given the many
side effects of prolonged high-dose prednisone
treatment, other treatments should be considered if the
patient does not respond in four to six weeks. IF a good
response occurs, the daily dose should be decreased to
the lowest dose at which improvement is maintained.”
• 10/18/11 20mg po once a day
• 10/25/11 40mg po once a day
Coursebook Page 107 of 139
8

5/29/2012
WWVAMC 11/21/11 – 1 month of treatment
• REASON FOR EXAM//CC:
• 77 yo WHITE MALE c Graves ophthalmopathy (Thyroid
Eye Disease = TED) presents for follow up.
• Vet reports that the double vision has gradually
improved as he has taken the prednisone and that he
feels his vision has cleared up a little bit. He feels the
prednisone is helping. Vet reports that the right eye has
become a little more fuzzy when looking through his
glasses.
• Vet reports no pain or irritation BE. No dryness or
tearing or redness. Vet reports that sunlight is
bothersome BE.
11/21/11
• EOMS: smooth pursuits. RE: sup restriction; LE:
restricted sup/temp, sup, and sup/nas
◦ With correction no diplopia straight ahead gaze or straight
right or straight left, diplopia reported sup and inf gazes.
◦ Pain Rating 0/10 in all gazes
• Tried taking Fresnel prism off right lens - vet
reported diplopia in straight ahead gaze as a
"shadow trying to pull off the letters“
• Amsler Grid:
• RE: (-) scotoma, (-) metamorphopsia
• LE: (-) scotoma, (-) metamorphopsia
11/21/11
11/21/11
• Refraction:
• Right: Plano-1.00*088 20/25-2 4^ base down
• Left: +1.25-2.50*088 20/25 3^ base up
• Vertical Vergences at distance and near: 7 right hyper
• Vet reported single vision with 7^ BD RE, Diplopia with 6^
BD
• Adjustable Maddox Rod s correction:
• Horizontal: 5-6 XP'
• Vertical: 14 right hyper
• SLE:
◦ LIDS, LASHES, ADNEXA: BE: 2-3+ edematous upper lids, 2+ dermatochalasis, 2+ MG
inspissation, scalloped lid margins, 1+ debris
◦ CONJ: Tr ping N&T BE.
• TONOMETRY BY iCare:
• straight ahead: 21/18 @ 1319
• up: 27/21
• left: 20/21
• right: 19/15
• Blood pressure 153/59 pulse measurement 61
• Weight: 210.1 lbs
• Exophthalmometry: 21/20 @ 110
• Interpalpebral distance measured vertically:
• straight ahead: 09/09 mm
• up: 07/09 mm
11/21/11
WWVAMC 11/21/11 – 1 month treatment
• DFE: SLE: +78
• DILATED PUPIL SIZE: 8 mm
• LENS: BE PCIOL s/p YAG, clear and centered
• VITREOUS: BE PVD and ant syneresis
• OPTIC NERVE C/D RATIO: RE: 0.5/0.5v; LE:
0.45/0.45v
• MACULAE: BE Flat & dry. RE>LE pigment clumps/RPE
changes, similar to photos 11/18/09
• POSTERIOR POLE (vascular arcades to mid-periphery):
intact BE
• VESSELS: A:V = 2:3,mild crossing changes
• ASSESSMENT(S):
• 1) Graves Ophthalmopathy (Thyroid Eye Disease) with incomitant
strabismus and
• diplopia relieved by prism and dry eye.
• 2) Mild dry macular degeneration, bilateral
• 3) Pseduophakia, bilateral
• 4) Glaucoma suspect due to large cup-to-disc ratios
• 5) Bilateral posterior vitreous detachment
• 6) Presbyopia, right eye simple myopic astigmatism, left eye mixed
astigmatism
Coursebook Page 108 of 139
9

5/29/2012
WWVAMC 11/21/11 – 1 month of Treatment
WWVAMC 12/19/11 – 2 months treatment
• PLAN(S):
• 1) Veteran has noticed a decrease in the frequency of diplopia. No diplopia
• noted with straight ahead gaze with the aid of prisms today, which is an
• improvement from previous exam 10/12/11. Continue oral prednisone 40mg/day.
• Veteran will continue to monitor his blood pressure, pulse, and weight. Continue
• to use artificial tears four times a day as needed both eyes. Return
• to Walla Walla clinic 12/19/11 for follow up appointment.
• 2) Patient education. Continue to use Amsler grid at home to monitor for
• distortion. Monitor.
• 3)4)5) Patient education. Monitor.
• 6) Continue to wear habitual spectacles with 3^ base down Fresnel prism on right
• lens. Right eye prescription has changed. Will wait on new glasses since amount
• of prism could change while on Prednisone. Final spectacle prescription today:
• Right: Plano-1.00*088 20/25-2 4^ base down
• Left: +1.25-2.50*088 20/25 3^ base up
• 77 yo WHITE MALE c Graves ophthalmopathy
presents for follow up appointment. Vet reports that
his right eye is still a little blurry (has the Fresnel
prism on it). Vet reports no diplopia with the glasses
and Fresnel prism on.
• Vet reports compliance taking oral Prednisone
40mg/day.
• Subjective Symptoms: Vet reports no pain or
irritation BE. No dryness, tearing, or redness. Vet
reports that sunlight is bothersome BE.
12/19/11 – 2 mos treatment
12/19/11
• External Exam, Chair Skills, Slit Lamp
◦ Improved periorbital edema BE
◦ Tr-1+ diffuse SPK
◦ Stable compared to previous exam
• Refraction:
• Right:Plano-1.25*088 20/30+1 6^ base down
• Left: +1.25-2.25*088 20/25 6^ base up
• Add: 2.50 20/25
• BINOCULAR TESTING:
• Horiz phoria @ distance: 3.5 BO
• Vertical phoria @ distance: 15 left hypo
• Horiz phoria @ near:
• Vertical phoria @ near: 9 BI
• Vertical phoria @ distance: 15 left hypo
• Adjustable Maddox Rod s correction:
• Horizontal: 5 XP'
• Vertical: 14 right hyper
12/19/11
WWVAMC 12/19/11 – 2 mos treatment
• TONOMETRY BY iCare:
• straight ahead: 18/15 @ 1044
• up: 23/18
• left: 18/15
• right: 17/16
• Blood pressure 160/60 pulse measurement 69
• Weight: 210.4 lbs
• ASSESSMENT(S):
• 1) Graves Ophthalmopathy (Thyroid Eye Disease)
with incomitant strabismus and diplopia relieved by
prism and dry eye.
• 2) Presbyopia, right eye simple myopic astigmatism,
left eye mixed astigmatism.
• Exophthalmometry: 20/20 @ 110
• Interpalpebral distance measured vertically:
• straight ahead: 09/09 mm
• up: 10/11 mm
Coursebook Page 109 of 139
10

5/29/2012
WWVAMC 12/19/11 – 2 months treatment
WWVAMC 01/24/12 – 3 months treatment
• PLAN(S):
• 1) Patient education. No apparent change in the level of diplopia. Eye comfort and edema of
upper lids have both improved since oral predisone therapy began 2 months ago. Continue to
take one 20mg tablet of prednisone by mouth twice a day. If no improvement of diplopia is
noted at next exam we will discuss tapering off the prednisone. Continue to use Refresh Plus
artificial tears four times a day as needed, and ocular lubricant ointment once at night both
eyes. Veteran will call if any changes in vision or overall health. Monitor in one month.
• 2) Patient picked out a new frame today to use in case new lenses are ordered with prism
ground in at a future date. Veteran did not report any diplopia when the Fresnel prism was
removed from the right spectacle lens. The right spectacle lens in over-plussed, which causes
the patient to use his left eye for the majority of his vision, thereby, reducing the symptoms of
double vision. Fresnel prism was cleaned and placed in an envelope for Mr. Parks, so he can reapply
it if needed at a future date. Continue to use habitual prescription, full-time wear. Final
spectacle prescription today:
Right:Plano-1.25*088 20/30+1 6^ base down
Left: +1.25-2.25*088 20/25 6^ base up
Add: 2.50
• REASON FOR EXAM//CC:
• 77 yo WHITE MALE c Graves ophthalmopathy presents
for follow up appointment. Vet reports that his right eye
is still a little blurry (has the Fresnel prism on it). Vet
reports no diplopia with the glasses and Fresnel prism
on. Vet reports that he did try using the glasses without
the Fresnel prism, but experienced diplopia without it.
• Vet reports compliance taking oral Prednisone
40mg/day.
• Subjective Symptoms: Vet reports no pain or irritation
BE. No dryness or tearing or redness. Vet reports that
sunlight is bothersome BE.
01/24/12 – 3 mos treatment
01/24/12
• External Exam, Chair Skills, Slit Lamp
◦ Improved periorbital edema BE
◦ Tr-1+ diffuse SPK BE
◦ Stable compared to previous exam
• Refraction:
• Right:Plano-1.25*090 20/30+2 6^ base down
• Left: +1.00-2.00*095 20/25 6^ base up
• Add: 2.50 20/25
• Trial Frame: had patient wear this prescription for 10-15 minutes as he walked
• around the clinic and tried reading. Mr. Parks reported comfortable, clear,
• single vision.
• BINOCULAR TESTING:
• Horiz phoria @ distance: 3 BO
• Vertical phoria @ distance: 15-16 left hypo
• Horiz phoria @ near:
• Vertical phoria @ near: 6-7 BI
• Vertical phoria @ distance: 13-14 left hypo
• Adjustable Maddox Rod s correction:
• Horizontal: 4 XP'
• Vertical: 14 right hyper
01/24/12
WWVAMC 01/24/12 – 3 mos treatment
• TONOMETRY BY Tpen:
• straight ahead: 25/24 @ 1012
• up: 28/24
• left: 26/25
• right: 25/24
• Blood pressure 159/75 pulse measurement 71
• Weight: 216.5 lbs
• Exophthalmometry: 21/20 @ 110
• ASSESSMENT(S):
• 1) Graves Ophthalmopathy (Thyroid Eye Disease)
with incomitant strabismus and diplopia relieved by
prism and dry eye.
• 2) Presbyopia, right eye simple myopic astigmatism,
left eye mixed astigmatism
• Interpalpebral distance measured vertically:
• straight ahead: 09/09 mm
• up: 11/13 mm
Coursebook Page 110 of 139
11

5/29/2012
WWVAMC 01/24/12 – 3 mos treatment
Telephone Visits – 4 mos treat, 1 mo of taper
• PLAN(S):
• 1) Patient education. No apparent change in the level of diplopia. Eye
• comfort and edema of upper lids have both improved since oral predisone therapy
• began 3 months ago. Start taper of oral prednisone. Reduce from 40mg to 30mg for
• one month. Called Mr. Parks primary care physician, Dr. Celso Chavez, who will
• then see Mr. Parks for follow up to reduce travel for veteran. Then reduce to
• 20mg for one month. Return to eye clinic in 2 months for follow up with
• tonometry. Continue to use Refresh Plus artificial tears four times a day as
• needed, and ocular lubricant ointment once at night both eyes. Veteran will call
• if any changes in vision or overall health.
• 2) Order final spectacle prescription full-time wear with high-index transition
• lenses (thyroid eye disease), a rush put on the order:
• Right:Plano-1.25*090 20/30+2 6^ base down
• Left: +1.00-2.00*095 20/25 6^ base up
• Add: 2.50 20/25
• PATIENT EDUCATION:
• Reviewed common side effects of Prednisone with patient including: osteoporosis,
• irritability/depression, and heartburn/GI tract disorders. We also discussed the
• increased risk of exacerbation of hypertension and congestive heart failure.
• 02/28/11: I called veteran to see how he was doing on. He was
not home, but I spoke with his wife who said he was doing
well, but still waiting for his glasses.
• 03/01/11: I received a phone message from veteran saying
that he was in the hospital and wanted to talk with me about
the glasses that were ordered.
• 03/02/11: Veteran reported that he felt dizzy and passed out
on Wednesday of this week. He was getting ready to be
discharged from the hospital when I was speaking with him
on the phone. Veteran reports that the doctors told him that
he was low on oxygen, and they think that may be why he
passed out. He has increased his oxygen to a 7 or 8.
03/02/12 Telephone
03/14/12 Telephone
• Veteran reports that he is doing well the the prednisone
taper, and that his primary care physician has been
seeing him and ensuring that the taper is going well.
Veteran is currently down to 20mg a day and is
scheduled to reduce to 10mg a day starting March 24th.
• Veteran has an appointment scheduled at the eye clinic
on March 20th. He reported that he was not sure if he
would be up to traveling yet by that time. I told him to
call and let me know. If he can't make it, we can continue
to work with his PCP with his follow ups concerning the
tapering of the Prednisone.
• Veteran at nursing home to help with recovery.
• Veteran reports compliance with the taper of the Prednisone.
He will continue to take 20mg once a day until March 24th.
He will then start taking 10mg once a day until April 24 th .
• Veteran reports he needs a prescription written out for
Prednisone so the nursing home can continue to give it to
him.
• I suggested that veteran speak with his private primary care
doctor who signed the paperwork needed to stay at the
nursing home to see if he could provide the prescription.
Veteran spoke with his PCP and reports he was able to provide
the prescription.
04/12/12 – 6 mos treatment, 3 mos taper
04/12/12
• 77 yo MALE c Graves ophthalmopathy presents for follow up
appointment.
• Vet received his new glasses yesterday and reports that he can
see much better with them. No diplopia and clearer vision
with the spectacles.
• Current ocular medications:
◦ Refresh AT q2-4 hrs BE
◦ Ocular lubricant at night BE
◦ Prednisone 10mg po qd.
• Veteran is using a battery operated 4-wheel scooter that he
said has greatly improved his independence and mobility and
allows him to enjoy being outdoors again. Doctors
discontinued Sildenafil.
• Subjective Symptoms: Veteran reports no pain or irritation
BE. Veteran reports that his eye do not feel as puffy and that
they do not feel dry.
Coursebook Page 111 of 139
12

5/29/2012
• VISUAL ACUITY:
04/12/12
• Current Spec Rx & lens type: ST 28
• Right:Plano-1.25*090 20/30 6^ base down
• Left: +1.00-2.00*095 20/30 6^ base up
• Add: 2.50 20/25
04/12/12
• External Exam: Negative for head tilt/turn, ptosis, abnormal
symmetry, skin disorders.
• PERRL(-)APD: 5-3, 2+ RL
• EOMS:LE restricted sup/temp, RE restricted inf, (+) diplopia
sup/temp and inf gazes, Pain Rating 0/10 in all gazes.
• Cover Test cc: Distance: ortho
• Near: 3-4 exo
• Confrontation VF: Full to finger counting
• AMSLER GRID: No metamorphopsia in either eye
• Adjustable Maddox Rod c correction:
• Horizontal: ortho
• Vertical: ortho
04/12/12
• Blood pressure: 114/66 Pulse: 80
• Weight: 211.1 lbs
• Exophthalmometry: 19/19 @ 110
◦ (22/21 @ 110 on 09/09/11)
•
• Interpalpebral distance measured vertically:
• straight ahead: 10/10 mm
◦ Right eye hyper, lid at upper part of non-dilated pupil, left eye lid
2mm above upper edge of non-dilated pupil.
• up: 14/14 mm
04/12/12
• SLE:
• LIDS, LASHES, ADNEXA: RE: 1+ edematous upper lid;
LE: 1+ edematous upper lid; BE
• 1+ dermatochalasis, 1+ MG inspissation, scalloped lid
margins
• CONJ: Tr ping N&T BE.
• CORNEA: Tr-1+ arcus 360 BE, Tr diffuse SPK cent to inf
BE
• A/C: Deep & quiet without cell or flare
• IRIS: Normal, without NVI
• LENS: BE: PCIOL centered, s/p YAG
• Tears: Mid volume with breakup time >10 sec BE
04/12/12
04/12/12
• TONOMETRY BY Tpen:
• straight ahead: 15/13 @ 0934
• up: 20/14
• left: 15/15
• right: 15/14
• down: 17/17
• DFE: SLE: +78
• Stable compared to previous exams.
• (-) optic neuropathy
Coursebook Page 112 of 139
13

5/29/2012
04/12/12, 6 mos treatment, 3 mos taper
• ASSESSMENT:
• 1) Graves Ophthalmopathy (Thyroid Eye Disease) with
dry eye, incomitant strabismus, and diplopia relieved by
prism.
• PLAN:
• 1) Discussed that diplopia is stable and veteran reports
that he feels better and that new spectacles are working
great. Eye comfort and edema of upper lids have both
improved since oral prednisone therapy began. Continue
to taper prednisone. Continue to use Refresh Plus
artificial tears four times a day as needed, and ocular
lubricant ointment once at night both eyes. Veteran will
call if any changes in vision or overall health. Monitor.
Taper Schedule
• 4/24 - 5/14 7.5 mg daily (3 weeks)
• 5/15 - 6/04 5.0 mg daily (3 weeks)
• 6/11 - 6/24 4 mg daily (2 weeks)
• 6/25 - 7/08 3 mg daily (2 weeks)
• 7/09 - 7/22 2 mg daily (2 weeks)
• 7/23 - 7/30 1.5 mg daily (1 week)
• 7/30 - 8/06 1 mg daily (1 week)
• 8/07 - 8/13 0.5 mg daily (1 week)
• 8/14, 8/16, 8/18 0.5 mg every other day for 3 doses
then stop
Goals
04/12/12
9/9/11 10/13 10/18 11/21 12/19 1/24/12 4/12/12
Proptosis 22/21 22/21 Start 21/20 20/20 21/20 19/19
Tx
Prism 8^ 8^ 7^ 12^ 12^ 12^
Reduce
Periorbit
al Edema
See
photos
04/12/12 04/12/12
Coursebook Page 113 of 139
14

5/29/2012
04/12/12 Reduction in edema around eyes
10/12/11 04/12/12
Radioiodine in the treatment of Hyperthyroidism
Risk of worsening or new onset ophthalmopathy
• 69% of North American thyroid specialists chose
radioiodine for a hypothetical patient with Graves’
hyperthyroidism in a survey from 1990 1 .
• There is increasing evidence that radioiodine
therapy can cause the development or worsening of
Graves’ ophthalmopathy more often than antithyroid
drug therapy or surgery.
TRIAL
Radio
iodine
Methi
mazole
Surg
ery
Radio + Pred (3 mos) n New
Onset
Tallstedt 2 33% 10% 16% 168 13%
Traisk 3 39% 21% 313 24%
Bartalena 4 15% 4% 0% + 67% of patients who 443
already had
ophthalmopathy
improved.
Ponto 5 20% 5%
Radioiodine in the treatment of Hyperthyroidism
Lower vs. higher doses of Radioiodine
• In patients with initially mild ophthalmopathy,
worsening after radioiodine therapy may be prevented by
the concurrent administration of glucocorticoids 4 .
• An alternative option for patients with moderate to
severe eye disease is to delay treatment with radioiodine
until the eye disease has been stable for at least one
year 6 .
• In addition, radioiodine should be used with caution in
patients with risk factors for ophthalmopathy, including
smoking, or a high baseline serum concentration of
triiodothyronine 6 .
• Patients are left hypothyroid and supplements such
as Levothyroxine are then used after Radioiodine
therapy. Why not try to leave patients euthyroid after
Radioiodine treatment
◦ 1. Low-dose radioiodine therapy is more likely to result in
treatment failure, necessitating another dose in 6 to 24
months 7,8 .
◦ 2. Less than one-third of patients are euthyroid 10 years after
therapy 9 .
◦ 3. Many patients have chronic subclinical hyperthyroidism,
with its associated risks of atrial fibrillation and reduced bone
density.
Coursebook Page 114 of 139
15

5/29/2012
Graves’ Ophthalmopathy Review
Graves’ Ophthalmopathy Review
• Thyroid eye disease is a heterogeneous autoimmune
orbital reaction 10 .
• The overwhelming majority (90%) of thyroid eye
disease cases are associated with hyperthyroidism,
while the rest are either euthyroid or hypothyroid 11 .
• Approximately half of Graves’ disease patients
experience ophthalmic manifestations, with sightthreatening
disease in 3% to 5% of cases 12 .
• It is the most common orbital disorder in adults 13 .
• Different terms:
◦ Graves’ orbitopathy
◦ Thyroid-associated ophthalmopathy
◦ Thyroid-related ophthalmopathy
◦ Graves’ ophthalmopathy
◦ Thyroid eye disease
◦ Thyroid orbitopathy
◦ Endocrine exophthalmos
◦ Malignant exophthalmos
◦ Infiltrative ophthalmopathy
Risk Factors
Risk Factors
• 1. Hyperthyroidism
◦ The highest risk factor, although there is a subset of patients
who are euthyroid or hypothryroid 11 .
• 2. Smoking
◦ Once a patient has Grave’s disease, the major clinical risk
factor for developing thyroid eye disease is smoking 14 .
◦ Patients with thyroid eye disease are four times more likely to
be smokers or former smokers than never smokers 14 .
◦ The greater the number of cigarettes smoked per day, the
greater the risk 15 .
◦ Also increases the risk for progression of ophthalmopathy after
radioiodine therapy 16 .
• 3. Sex
◦ Women are five to eight times more likely to be affected by
thyroid eye disease than men, but this largely reflects the
increased incidence of Graves’ disease in women 15,19 .
◦ Once someone has Graves’ disease, his or her sex has little
effect on the risk 15 .
◦ Men older than 60 may be at increased risk may be more
severe disease 17 .
• 4. Radioiodine
Risk Factors
Graves’ Ophthalmopathy Review
• 5. Genetics
◦ Multiple genes are likely to be involved in the development of
thyroid eye diseases, and these interact with multiple
environmental risk factors 15 .
◦ An immunological predisposition is likely based on the
increased incidence in certain HLA (DR, B8, and DW) types
and recent genetic mapping of loci for Graves’ disease in some
patients to chromosome 14 11 .
This genetic localization to chromosome 14 is in the area of the
gene for the TSH receptor, but to date no mapping to the area of
the HLA region has been found 11 .
• Possible Symptoms 19 :
◦ Red eye
◦ Foreign-body sensation
◦ Tearing
◦ Decreased vision
◦ Dyschromatopsia
◦ Binocular diplopia
◦ Prominent (“bulging”) eyes
Coursebook Page 115 of 139
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5/29/2012
Graves’ Ophthalmopathy Review
Graves’ Ophthalmopathy Review
• Signs 19 :
◦ Eyelid retraction
◦ Edema
◦ Lagophthalmos
◦ Lid lag (von Graefe’s sign)
◦ Reduced blinking
◦ Superficial keratopathy
◦ Conjunctival injection
◦ Exophthalmos
◦ Limitation of extraocular movements
Supraduction most common reflecting inferior rectus involvement
• Signs 19 :
◦ Positive forced ductions
◦ Resistance to retropulsion of globe
◦ Decreased visual acuity
◦ Decreased color vision
◦ Relative afferent papillary defect
◦ Visual field defect
◦ Acute congestion of the socket and periocular tissues
Graves’ Ophthalmopathy Review
Graves’ Ophthalmopathy Review
• Werner Classification of Eye Findings 19 :
◦ No signs or symptoms.
◦ Only signs.
◦ Soft tissue involvement (signs and symptoms).
◦ Proptosis.
◦ Extraocular muscle involvement.
◦ Corneal involvement.
◦ Sight loss (optic nerve compression).
• American Thyroid Association Grading System 20 :
◦ Class I
Solely involves lid retraction and stare
◦ Class II
Soft tissue symptoms and signs (chemosis/edema)
◦ Class III
Proptosis
◦ Class IV
Decreased motility and/or diplopia
◦ Class V and Class VI
Corneal exposure symptoms/signs
◦ Class VI
Optic neuropathy
Treatment of Graves’ Orbitopathy
Treatment of Graves’ Orbitopathy
• Treatment of patients has 3 components:
◦ Reversal of hyperthyroidism, if present
◦ Symptomatic treatment
◦ Treatment with a glucocorticoid, and/or orbital irradiation,
and/or orbital decompression surgery to reduce inflammation
in the periorbital tissues.
• Symptomatic Treatment
◦ Sunglasses
◦ Prisms for diplopia
◦ Artificial Tears and Ointments
◦ Lid taping or moisture chamber goggles at nighttime
Wiley X sunglasses with gasket.
◦ Punctal occlusion
◦ Avoid “dry eye environments”
◦ Avoid sleeping on face
◦ Raising the head of the bed at night
◦ Cold packs
◦ Smokers should stop smoking
◦ Selenium 100mcg twice daily 18
Coursebook Page 116 of 139
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5/29/2012
Selenium 21
Treatment of Graves’ Orbitopathy
• “Graves' disease (GD) and ophthalmopathy (GO) are
organ-specific autoimmune-inflammatory disorders
characterized by a complex pathogenesis.
• The inflammatory process is dominated by an imbalance
of the antioxidant-oxidant mechanism, increased
production of radical oxygen species (ROS), and
cytokines which sustain the autoimmune process and
perpetuate the disease.
• Recently, selenium, which is a powerful antioxidant, has
been successfully applied in patients with mild GO,
slowing the progression of disease, decreasing the clinical
activity score, and appreciably improving the quality of
life.”
• Glucocorticoid Therapy
◦ Primary treatment for moderate to severe Graves’
◦ Oral
◦ Intravenous
◦ Retrobulbar or subconjunctival injections have been found to
be less effective, but can be used if oral or intravenous routes
are contraindicated 20 .
◦ Should monitor liver function and watch for possible side
effects such as hyperglycemia and increased blood pressure.
Contraindications and possible side effects of
Prednisone from Micromedex.
Contraindications and possible side effects of
Prednisone from Micromedex.
• Common
• Cardiovascular:
• Hypertension
◦ All corticosteroids cause sodium retention which results in FLUID RETENTION.
◦ Older patients or those with a history of hypertension are more likely to develop HIGH BLOOD
PRESSURE during treatment with corticosteroids.
• Dermatologic:
• Acne, Ecchymosis, Atrophic condition of skin, Impaired healing.
• Endocrine metabolic:
• Body fluid retention, Decreased body growth, Hypernatremia
• Gastrointestinal:
• Gastrointestinal perforation, Gastrointestinal ulcer, Pancreatitis, Superinfection
• Immunologic:
• Superinfection: At higher risk for infection
• Musculoskeletal: Osteoporosis
• Psychiatric: Depression, Euphoria
• -Serious
• Endocrine metabolic:
• Cushing's syndrome, Hyperglycemia, Primary
adrenocortical insufficiency
• Ophthalmic:
• Cataract (2.5-60% incidence), Glaucoma (more likely
after 1 year or more of therapy), increased IOP (decreases
the outflow), central serous retinopathy, optic nerve
damage
• Respiratory:
• Pulmonary tuberculosis, abscess of lung, aspergillosis,
interstitial pneumonia, pulmonary nocardiosis.
Prednisone Possible Drug Interactions
Prednisone Possible Drug Interactions
• Acenocoumarol
Alatrofloxacin
Alcuronium
Aldesleukin
Alfalfa
Amobarbital
Amphotericin B Liposome
Anthrax Vaccine Adsorbed
Aprobarbital
Asparaginase
Aspirin
Atracurium
Bacillus of Calmette and Guerin Vaccine,
Live
Balofloxacin
Bupropion
Butabarbital
Butalbital
Carbamazepine
Cinoxacin
Ciprofloxacin
Cisatracurium
Clarithromycin
Clinafloxacin
• Cyclosporine
Desogestrel
Dicumarol
Dienogest
Diphtheria Toxoid, Adsorbed
Doxacurium
Drospirenone
Echinacea
Enoxacin
Estradiol Cypionate
Estradiol Valerate
Ethinyl Estradiol
Ethynodiol Diacetate
Etonogestrel
Fleroxacin
Fluconazole
Fluindione
Flumequine
Fosphenytoin
Gallamine
Gatifloxacin
Gemifloxacin
Grepafloxacin
Haemophilus B Vaccine
• Hepatitis A Vaccine, Inactivated
Hexafluorenium
Hydrochlorothiazide
Indinavir
Influenza Virus Vaccine
Isoniazid
Itraconazole
Ketoconazole
Levofloxacin
Levonorgestrel
Licorice
Lomefloxacin
Lyme Disease Vaccine (Recombinant
OspA)
Ma Huang
Measles Virus Vaccine, Live
Medroxyprogesterone Acetate
Meningococcal Vaccine
Mephobarbital
Mestranol
Metocurine
• Mivacurium
Montelukast
Moxifloxacin
Mumps Virus Vaccine, Live
Nateglinide
Neostigmine
Nimodipine
Norelgestromin
Norethindrone
Norfloxacin
Norgestimate
Norgestrel
Ofloxacin
Pancuronium
Pefloxacin
Pentobarbital
Pertussis Vaccine
Phenobarbital
Phenprocoumon
Phenytoin
Pipecuronium
Plague Vaccine
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5/29/2012
Prednisone Possible Drug Interactions
Warfarin/Aspirin (Micromedex)
• Pneumococcal Vaccine, Diphtheria
Conjugate
Pneumococcal Vaccine Polyvalent
Poliovirus Vaccine, Live
Primidone
Prulifloxacin
Pyridostigmine
Quetiapine
Rabies Vaccine
Rifampin
Rifapentine
Ritonavir
Rocuronium
Rosoxacin
Rotavirus Vaccine, Live
Rubella Virus Vaccine, Live
Rufloxacin
Saiboku-To
• Secobarbital
Smallpox Vaccine
Somatropin
Sparfloxacin
Succinylcholine
Telaprevir
Temafloxacin
Tetanus Toxoid
Tosufloxacin
Tretinoin
Trovafloxacin Mesylate
Tuberculin
Tubocurarine
Typhoid Vaccine
Varicella Virus Vaccine
Vecuronium
Warfarin
Yellow Fever Vaccine
• “Summary: The concomitant use of corticosteroids
and anticoagulants has been associated with both
enhanced and diminished anticoagulant effects.
Monitoring of coagulation indices is recommended
when prednisone is co-administered with an
anticoagulant, such as warfarin.”
Treatment of Graves’ Orbitopathy
Treatment of Graves’ Orbitopathy
• External orbital radiation
◦ The role of orbital radiotherapy is controversial 15 .
◦ Effective in up to 70% of patients 11 .
◦ Has been used in the treatment of Graves’ Orbitopathy for more than
90 years 20 .
◦ Used for anti-inflammatory effects and radiosensitivity of activated
orbital T-cells and fibroblasts 20 .
◦ A common cumulative dose of radiation is 20 Gy per eye,
fractionated over a 2-week period 20 .
◦ Known complications are fortunately rare, but may include radiation
retinopathy and cataract 20 .
◦ Also theoretic concerns of cancer induction which is estimated at
0.39% 20 .
◦ Can be used as adjunct to steroids, decompression, or both for
recalcitrant disease 20 .
◦ Contraindicated in diabetic patients with pre-existing retin0pathy 15 .
• Surgical interventions are deferred until a 9-12 month
stable interval is recorded, except in cases of optic
neuropathy or extreme proptosis causing severe
exposure keratopathy 19 .
• Surgery (order is stepwise posterior to anterior):
◦ Orbital decompression surgery
Traditional indications for decompression involved predominantly
optic neuropathy and severe exposure keratopathy 10 .
◦ Fat decompression surgery
Removal of intraconal fat reduces congestive orbitopathy, proptosis,
and may improve preoperative diplopia 10 .
◦ Strabismus surgery
◦ Eyelid reconstruction as indicated
Optic Neuropathy 19
Treatment of Graves’ Orbitopathy
• “Immediate treatment with oral steroids (prednisone
100mg po qd for 2-14 days).
• The use of external beam irradiation (15-30Gy) is
controversial and falling out of favor.
• Orbital decompression for compressive optic
neuropathy should be performed by an oculplastic
surgeon. A balanced approach with decompression
of the medial and lateral orbital walls is most
commonly employed. Removal of the inferior wall is
avoided if possible due to higher incidence of
induced diplopia.”
• Rituximab 18
◦ A number of reports have indicated that some patients with
severe GO may respond dramatically to B cell depletion
induced by Rituximab, which is a monoclonal antibody
directed against the B cell CD20 molecule.
◦ Rituximab induces a fall in TSH receptor antibody levels and
depletion of B cells in the retro orbital tissues, not just the
periphery.
◦ Currently undergoing larger trials; preliminary results from
these trials suggest efficacy in some, but not all, patients.
◦ Used in cases of lymphomas, leukemia, transplant rejection
and some autoimmune disorders.
Coursebook Page 118 of 139
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5/29/2012
Treatment of Graves’ Orbitopathy
Prognosis 19
• Somatostatin analogs 18
◦ “Have been explored as potential therapy for GO, based upon
the observations that orbital fibroblasts have somatostatin
receptors and the activity of orbitopathy correlates with
activity on octreotide scintigrams.”
• “Diplopia and ocular surface disease are common;
6% develop optic nerve disease. Despite surgical
rehabilitation, which may require multiple
procedures, patients are often left with functional
and cosmetic defects.”
Quality of Life and Occupational Disability in
Endocrine Orbitopathy
Quality of Life and Occupational Disability in
Endocrine Orbitopathy
• Background
◦ “In endocrine orbitopathy (EO), disfiguring proptosis and
diplopia impair patients quality of life both at home and at
work.”
• Methods
◦ “From late 2006 to the beginning of 2008, 250 outpatients in
an interdisciplinary thyroid and eye clinic filled out a
questionnaire about their quality of life, occupational
disability, and use of psychotherapy. 400 physicians who
referred their EO patients to the clinic also participated in a
survey on these issues.”
• Patient Results
◦ 45% of the patients complained of restrictions in their daily
activities.
◦ 38% reported impaired self-perception.
◦ 36% were on sick leave because of EO.
◦ 28% were disabled.
◦ 5% had retired early.
◦ 3% had lost their jobs.
◦ 21% underwent psychotherapy.
Quality of Life and Occupational Disability in
Endocrine Orbitopathy
Co-management Tips
• Physician results
◦ 75% stated that they were taking care of temporarily disabled
patients.
◦ 34% stated that they were taking care of permanently disabled
patients.
◦ 38% stated that they were treating EO patients who were
undergoing psychotherapy.
• Golden Rule: “Do unto others as you would have
them do unto you.”
• Take the time to fully understand the case and
prepare for questions the other health care
professional might ask.
• Have the patient’s chart with you during all
communication with others.
• Always look for opportunities to learn something
new and build relationships with others.
Coursebook Page 119 of 139
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5/29/2012
Sources
Sources
• 1. Wartofsky L, Glinoer D, Solomon B, et al. Differences and
similarities in the diagnosis and treatment of Graves’ disease
in Europe, Japan, and the United States. Thyroid 1991; 1:129.
• 2. Tallstedt L, Lundell G, Torring O, et al. Occurrence of
ophthalmopathy after treatment for Graves’ hyperthyroidism.
The Thyroid Study Group. N Engl J Med 1992; 326:1733.
• 3. Traisk F, Tallstedt L, Abraham-Nordling M, et al. Thyroidassociated
ophthalmopathy after treatment of Graves’
hyperthyroidism with antithyroid drugs or iodine-131. J Clin
Endocrinol Metab 2009; 94:3700.
• 4. Bartalena L, Marcocci C, Bogazzi F, et al. Relation between
therapy for hyperthyroidism and the course of Graves’
ophthalmopathy. N Engl J Med 1998; 338:73.
• 5. Ponto KA, Zang S, Kahaly GJ. The tale of radioiodine and
Graves’ orbitopathy. Thyroid 2010 Jul; 20(7):785-93.
• 6. Mariotti S, Martino E, Francesconi M, et al. Serum thyroid
autoantibodies as a risk factor for development of
hypothyroidism after radioactive iodine therapy for single
thyroid ‘hot’ nodule. Acta Endocrinol (Copenh) 1986; 113:500.
• 7. Rapoport B, Caplan R, DeGroot LJ. Low-dose sodium
iodide I 131 therapy in Graves disease. JAMA 1973; 224:1610.
• 8. Goolden AW, Stewart JS. Long-term results from graded
low dose radioactive iodine therapy for thyrotoxicosis. Clin
Endocrinol (Oxf) 1986; 24:217.
• 9. Sridama V, McCormick M, Kaplan EL, et al. Long-term
follow-up study of compensated low-dose 131I therapy for
Graves’ disease. N Engl J Med 1984; 311:426.
Sources
Sources
• 10. Bothun, ED, Scheurer RA, Harrison AR, et al. Update
on thyroid eye disease and management. Clinical
Ophthalmology 2009; 3:543-51.
• 11. Burch HB, Wartofsky L. Graves’ ophthalmopathy:
current concepts regarding pathogenesis and
management. Endocr Rev. 1993; 14(6):747-93.
• 11. Liu, GT, Volpe NJ, Galetta SL. Thyroid-associated
ophthalmopathy. Neuro-ophthalmopathy: Diagnosis
and Mangement. Philadelphia: Saunders, 2001. 661-72.
Print.
• 12. Bartalena L, Pinchera A, Marcocci C. Management of
Graves’ ophthalmopathy: reality and perspectives.
Endocr Rev 2000;21(2):168-99.
• 13. Ponto KA, Pitz S, Pfeiffer N, et al. Quality of life and
occupational disability in endocrine orbitopathy. Dtsch
Arztebl Int 2009; 106(17):283-9.
• 14. Vestergaard, P. Smoking and thyroid disorders—a
meta-analysis. Eur J Endocrinol 2002; 146:153-61.
• 15. Cawood T, Moriarty P, O’Shea D. Recent
developments in thyroid eye disease. BMJ 2004;
329:385-90.
• 16. Bartalena L, Marcocci C, Tanda ML, et al. Cigarette
smoking and tretment outcomes in Graves
ophthalmopathy. Ann Intern Med 1998; 129:632-5.
Sources
• 17. Perros P, Crombie AL, Matthews JN, Kendall-Taylor P. Age and
gender influence the severity of thyroid-associated ophthalmopathy:
a study of 101 patients attending a combined thryroid-eye clinic.
Clin Endocrinol (Oxf) 1993; 38:367-72.
• 18. Davies TF. Treatment of graves’ orbitopathy (ophthlamopathy).
www.uptodate.com 20 Jun 2011.
• 19. Friedman NJ, Kaiser PK, Pineda R. Thyroid-related
ophthalmopathy. The Massachusetts Eye and Ear Infirmary
Illustrated Manual of Ophthalmology. Saunders 2009. 15-19.
• 20. Griepentrop GJ, Garrity JA. Update on the medical treatment of
Graves’ ophthalmopathy. Int J of Gen Med 2009; 2:263-9.
• 21. Duntas, LH. The evolving role of selenium in the treatment of
graves’ disease and ophthalmopaty. J Thyroid Res 2012; Published
online 2012 January 19. doi: 10.1155/2012/736161.
Coursebook Page 120 of 139
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5/29/2012
ACNE ROSACEA
LONG TERM COMPLICATIONS OF OCULAR
ROSACEA
Kevin Riedel, O.D.
Portland VA Medical Center
Optometry Resident, PGY-1
Pacific University NW Resident’s Conference
June 4, 2012
• Idiopathic, chronic dermatologic
condition
• Characterized by erythema of
the skin
• Primarily affecting skin of the
cheeks, forehead, chin, and
nose
• Signs/symptoms vary
DERMATOLOGIC FEATURES
• Subtype 1
• “Erythematotelangiectatic”
• Often asymptomatic
• Characterized by flushing (erythema) and telangiectasia
DERMATOLOGIC FEATURES
• Subtype 2
• “Papulopustular”
• Often asymptomatic, but can have burning sensation of the
skin especially during exacerbations
• Characterized by papules and pustules
DERMATOLOGIC FEATURES
• Subtype 3
• “Phymatous”
• ‘Phyma’ – Greek for swollen or bulbous mass
• More likely to be symptomatic
• Classically characterized by extreme sebaceous gland
hypertrophy and rhinophyma
Coursebook Page 121 of 139
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5/29/2012
Gnathophyma
Metophyma
Otophyma
TRIGGERS
• Environmental factors can cause an outbreak of symptoms (taken from survey of
1,066 patients by the National Rosacea Society)
• Sun exposure (81%)
• Emotional stress (79%)
• Hot weather (75%)
• Wind (57%)
• Strenuous exercise (56%)
• Alcohol consumption (52%)
• Hot bath/shower (51%)
• Others: spicy foods, hot beverages, cigarette smoke, caffeine
EPIDEMIOLOGY
• More common in:
• Adults (acne vulgaris more common
in adolescents)
• Women, however usually more
severe in men (phymatous rosacea
seen less often in females)
• Fair skin (less common in darkly
pigmented races)
• Northern European descent
• Irish
• English
• Scandanavian
• Dutch
• German
TREATMENT
• Topical antibiotics
• Usually erythromycin or metronidazole
• Oral tetracyclines
• Tetracycline or doxycycline
• Surgical treatment
• Typically for severe phymatous rosacea that does not respond to
oral/topical therapy
• Electrosurgery
• Laser (CO2)
• Dermabrasion
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5/29/2012
BEFORE
AFTER
PATHOPHYSIOLOGY – THEORIES
• Climate exposure
• Chemical/food exposure
• Microbial trigger
• Impaired iron metabolism
• Affects of reactive oxygen species and free radical exposure
• Vascular endothelial growth factor and other angiogenic factors
• Antimicrobial peptides
PATHOPHYSIOLOGY – THEORIES
• Climate exposure
• Chemical/food exposure
• Microbial trigger
• Impaired iron metabolism
• Affects of reactive oxygen species and free radical exposure
• Vascular endothelial growth factor and other angiogenic factors
• Antimicrobial peptides
CLIMATE EXPOSURE
• Harsh ultraviolet exposure can cause damage to superficial
blood vessels and connective tissue in the dermis
• This theoretically can lead to chronic increased vascular
permeability and dermatitis
• Could explain why rosacea is typically seen on sun exposed
areas
• Sunlight is believed to be a possible trigger of outbreaks
PATHOPHYSIOLOGY – THEORIES
• Climate exposure
• Chemical/food exposure
• Microbial trigger
• Impaired iron metabolism
• Affects of reactive oxygen species and free radical exposure
• Vascular endothelial growth factor and other angiogenic factors
• Antimicrobial peptides
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CHEMICAL/FOOD EXPOSURE
• Spicy food, hot beverages, & alcohol known to cause
exacerbations
• Medications can also cause exacerbations
(topical/intranasal steroids, high dose vitamin B6/B12,
amiodarone)
• No evidence that these are the underlying cause of the
disease
PATHOPHYSIOLOGY – THEORIES
• Climate exposure
• Chemical/food exposure
• Microbial trigger
• Impaired iron metabolism
• Affects of reactive oxygen species and free radical exposure
• Vascular endothelial growth factor and other angiogenic factors
• Antimicrobial peptides
MICROBIAL TRIGGER
• Demodex (parasitic mites that live in & around human hair follicles)
• Prefer skin of nose and cheeks
• Some research shows that helper T-cell infiltration occurs adjacent
to known Demodex infestation in patients with rosacea
• Demodex is also found in many healthy individuals without rosacea
Bonnar E, Eustace P, Powell FC. The Demodex mite population in rosacea. J Am Acad Dermatol. Mar
1993;28(3):443-8.
• Helicobacter pylori (bacterium associated with peptic ulcer disease)
• Incidentally, patients with rosacea have been found to have higher
incidence of serological evidence of H. pylori
PATHOPHYSIOLOGY – THEORIES
• Climate exposure
• Chemical/food exposure
• Microbial trigger
• Impaired iron metabolism
• Affects of reactive oxygen species and free radical exposure
• Vascular endothelial growth factor and other angiogenic factors
• Antimicrobial peptides
IMPAIRED IRON METABOLISM
• Iron catalyzes conversion of hydrogen peroxide to free radicals, which
cause tissue injury
• Unmetabolized iron is stored as ferritin
• “Oxidative stress and ferritin expression in the skin of patients with
rosacea.” J Am Acad Dermatol. Feb 2009
• Amount of ferritin in histological skin analysis significantly higher in
patients with rosacea
• Higher ferritin was associated with more advanced stages of rosacea
Tisma VS, Basta-Juzbasic A, Jaganjac M, et al. Oxidative stress and ferritin expression in the skin of patients with
rosacea. J Am Acad Dermatol. Feb 2009;60(2):270-6
PATHOPHYSIOLOGY – THEORIES
• Climate exposure
• Chemical/food exposure
• Microbial trigger
• Impaired iron metabolism
• Affects of reactive oxygen species
• Vascular endothelial growth factor and other angiogenic factors
• Antimicrobial peptides
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5/29/2012
REACTIVE OXYGEN SPECIES
• Released early in inflammatory process by
neutrophils
• Cause tissue damage and cause the release of
inflammatory mediators from damaged cells
PATHOPHYSIOLOGY – THEORIES
• Climate exposure
• Chemical/food exposure
• Microbial trigger
• Impaired iron metabolism
• Affects of reactive oxygen species and free radical exposure
• Vascular endothelial growth factor and other angiogenic
factors
• Antimicrobial peptides
VEGF & ANGIOGENESIS
• Studies show increased VEGF expression in skin with
rosacea lesions vs. skin without rosacea lesions (within
the same patient)
• “Therapeutic response of rosacea to dobesilate”. Eur J
Med Res. Oct 18 2005
• Topical dobesilate (used in Europe) improved
erythema and telangiectasia in rosacea
Cuevas P, Arrazola JM. Therapeutic response of rosacea to dobesilate. Eur J Med Res.
Oct 18 2005;10(10):454-6.
PATHOPHYSIOLOGY – THEORIES
• Climate exposure
• Chemical/food exposure
• Microbial trigger
• Impaired iron metabolism
• Affects of reactive oxygen species and free radical exposure
• Vascular endothelial growth factor and other angiogenic factors
• Antimicrobial peptides
ANTIMICROBIAL PEPTIDES
• Part of the innate immune response
• Cathelicidin
• Abnormally high levels in rosacea patients vs.
normals
• Stimulates angiogenesis and modulates expression
of VEGF
• When injected into mice it induces inflammation,
erythema, and telangiectasia
Schauber J, Gallo RL. Antimicrobial peptides and the skin immune defense system. J Allergy
Clin Immunol. Aug 2008;122(2):261-6
OCULAR ROSACEA (SUBTYPE 4)
• Meibomian glands are sebaceous glands and
are often affected by acne rosacea
• Ocular rosacea is very common (prevalent in up
to 50% of patients with rosacea) and very
commonly ignored by patients and their doctors
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5/29/2012
FEATURES OF OCULAR ROSACEA
• Mild ocular rosacea
• Signs
• Meibomian gland dysfunction
• Lid margin telangiectasia
• Reduced tear stability
(decreased TBUT)
• Symptoms
• Can be asymptomatic
• **Fluctuating vision**
• Mild foreign body sensation
FEATURES OF OCULAR ROSACEA
• Moderate ocular rosacea
• Signs
• Recurrent hordeola &
chalazia
• Corneal disruptions
• Non-central punctate
epithelial erosions
• Conjunctival hyperemia
• Symptoms
• Constant blurred vision
• Persistent epiphoria
• **Burning sensation**
FEATURES OF OCULAR ROSACEA
• Severe ocular rosacea
• Signs
• Severe keratitis
• Coalescent PEE affecting central
cornea
• Corneal ulcers
• Corneal edema
• Corneal neovascularization
• Symptoms
• Blurred vision
• Eye pain
TREATMENT OF OCULAR ROSACEA
• Mild stages
• Preservative free artificial tears QID/PRN
• Eyelid hygiene -- VERY important part of the management
• Avoidance of triggers
• Avoidance of over-the-counter medications that dry out mucous membranes
• Decongestants
• Anti-histamines
• Avoidance of over-the-counter eye drops with preservatives
• Visine and other ocular decongestants
• Artificial tears with preservative
EYELID HYGIENE
• What is a warm compress
• Temperature Not warm…you want HOT
• Duration Needs to be at least 5 minutes, if not 10-15
• Digital massage is essential – breaks up stagnant material in meibomian
glands
• Lid scrubs
• Commercial preparations vs. baby shampoo
• Either works fine, but warm compress with digital massage is more
important
• Better for anterior blepharitis, in ocular rosacea the disease process
is occurring in the meibomian glands
TREATMENT OF OCULAR ROSACEA
• Moderate Stages
• Night-time lubrication
• Celluvisc or lubricating
ointment qHS
• Eyelid hygiene
• Topical steroids for
symptomatic exacerbations
• Lotemax or
fluorometholone
• Topical cyclosporine for longterm
control of inflammation
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TREATMENT OF OCULAR ROSACEA
• Moderate Stages
• Low dose oral doxycycline
• Start 50-100mg bid then taper
to as low as 50mg qd or qod
• Judicious use of punctal plugs
• Must treat lid
disease/inflammation first or
else you are keeping a pool of
inflammatory tears on the
ocular surface
• Consider referral to dermatologist
depending on individual
presentation and symptomology
NOTES ON DOXYCYCLINE
• Not appropriate for pregnant/breastfeeding women or for children
• Use with caution in patients on chronic anticoagulation (coumadin)
• Increases the INR, an indicator of increased bleeding risk
• Primary care physician or clinical pharmacist should always be consulted
• Use caution in liver/kidney disease
• Consult with primary care physician in patients with complicated medical
histories
• Instructions
• Take on empty stomach
• Take separate from dairy products, calcium supplements, & iron supplements
• Side effects
• Photosensitivity
• GI upset/diarrhea
ANTI-INFLAMMATORY PROPERTIES OF
DOXYCYCLINE
• Inhibits interleukin-1 in cultured human corneal epithelium
Solomon, A et al. Invest Ophthalmol Vis Sci. 2000 Aug;41(9):2544-57.
• Inhibits MMP-13 & MMP-8 in vitro
Smith GN Jr et al. Arthritis Rheum. 1999 Jun;42(6):1140-6.
• Accepted treatment for dermatologic manifestations of rosacea for many
years
RESTASIS & OCULAR ROSACEA
• Cyclosporine is an immunosuppressant that is used systemically to combat
rejection in organ transplants
• Reduces inflammation by inhibition of T-lymphocyte activation and migration
• Topical cyclcosporine (Restasis) BID shown to be more effective than
artificial tears BID in some studies
• Statistically significant improvement in Schirmer scores, symptoms
(OSDI questionaire), tear breakup time, & corneal staining scores.
Schechter B. Adv Ther (2009) 26(6)
TREATMENT OF OCULAR ROSACEA
• Severe Stages
• Consider referral to corneal specialist
• May need corneal transplantation if corneal neovascularization
or ulcer causing central corneal scarring
TREATMENT OF OCULAR ROSACEA
• Emerging Therapy – Anti-VEGF agents
• Commonly used for retinal conditions
• Choroidal neovascularization
• Diabetic macular edema
• Cystoid macular edema associated with retinal vascular
occlusions
• Now being used in subconjunctival injection by
ophthalmologists to induce recession of neovascular vessels
in the cornea and increase chances of successful corneal
grafts
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5/29/2012
FUNCTIONAL TREATMENT FOR ADVANCED
CASES
• Modest magnification
• Increased add power with proper education
• Low power hand held magnifiers
• Low power Optivisor for hands-free near
tasks
• **Glare Control**
• These patients will be VERY light sensitive
• Wrap-around tint
• Gray/Plum for bright days
• Amber/Yellow for cloudy days
Benayoun Y et al. “Effects of Subconjunctival Bevacizumab on Corneal
Neovascularization: Results of a Prospective Study.” Cornea, online ahead of print 2012.
CASE PRESENTATION – A LESSON TO BE
LEARNED
• 9/23/2011 – Portland VAMC Optometry Clinic
• 57yo white male, presenting for consult from PCP for baseline
DM exam (recently diagnosed)
• CC: Decreased vision and eye pain, both gradually progressing
for 3 months
• Eyes feel very dry and scratchy, and pain is constant and sharp,
especially on blink
• Vision “foggy”, like “looking through water”
• LEE: August 2010
OCULAR HISTORY
• Chronic dry eye syndrome secondary to ocular rosacea and ectropion
• Chronic ocular allergies
• Refractive error & presbyopia
• Ocular Medications
• PFAT several times daily
• Cromolyn sodium QID OU
• FML once daily OU (ran out several months ago)
MEDICAL HISTORY
• Recently diagnosed type 2 diabetes mellitus
• Last A1c: 13.4
• Patient taking metformin, reports recent improvement in home blood glucose levels since
starting
• Depression/anxiety associated with post-traumatic stress disorder
• Chronic allergies
• HTN/HLD/CAD
• Systemic medications
• Oral doxycycline (for ocular rosacea)
• Oral antihistamine qd
• Oral anti-depressant
• Metformin
• Lisinopril/Simvastatin/Metoprolol
INITIAL FINDINGS
• Visual Acuity (with correction)
OD: 20/200 PH 20/150
OS: 20/100+2 PH 20/70
• Pupils ERRL, no APD noted OD or OS
• Visual field FTFC OD & OS
• EOM intact OU, no additional pain on movement
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5/29/2012
ANTERIOR SEGMENT FINDINGS
CORNEA OS 20/100 (20/70 BCVA)
• External: (+)flushed cheeks & prominent blood vessels on cheeks/forehead/nose
• Lids/Lashes:
• Significant meibomian gland stasis on digital expression
• Severe lid margin telangiectasia
• Generalized erythema with prominent eyelid fullness
• Very poor lower eyelid snapback
• Conjunctiva: significant, diffuse conjunctival injection 360
• Cornea
CORNEA OD 20/200 (20/150 BCVA)
ASSESSMENT:
1. Extensive Corneal Neovascularization OD>OS related to multifactorial ocular surface
disease
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5/29/2012
TREATMENT
• Pred Forte QID OU
• Cyclosporine BID OU
• PFAT q1hr OU
• Celluvisc qHS OU
• Eyelid hygiene BID OU
• d/c Cromolyn sodium
• Oral NSAID for pain
• Avoid oral antihistamine
• Referral to Cornea Clinic
LESSONS
• Something that is common and often relatively benign (like
ocular rosacea) with the right circumstances & factors can
cause vision loss and blindness
• Early treatment is key because advanced ocular rosacea is very
challenging to control
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5/29/2012
Benjamin Taylor, OD
White City VA SORCC
• 59 year old Caucasian male presented to clinic for his
annual diabetic eye exam
• Patient complaints were:
• 1. Blurred vision at distance
• 2. For the last year he has been noticing “stars” in his
peripheral vision 2‐3 times a week, greater in the left eye.
He reported that this generally lasted for 5‐10 minutes
but never lasted more than an hour and then would just
fade away.
• Type II Diabetes
• Last A1c‐‐>6.7
• Congestive Heart Failure
• Patient has pacemaker
• Chronic Obstructive Pulmonary Disease
• Sleep Apnea
• Anemia secondary to kidney failure
• Hyperlipidemia
• Cholesterol‐‐>205
• LDL‐‐>could not be accurately calculated because triglycerides were
greater than 400
• HDL‐‐>29
• Triglycerides‐‐>674
• Hyperuricemia
• Albuterol
• Carvedilol
• Digoxin
• Furosemide
• Glipizide
• Hydralazine HCl
• Omeprazole
• Simvastatin
• Valsartan
• Warfarin—patient reported starting this just two months
earlier
• Visual Acuities without Correction
• OD: 20/40
• OS: 20/25+2
• Pupils: errl, (‐)apd ou
• EOM’s: full/no restrictions
• CVF: ftfc od, os
• Cover Test: orthophoria at 6m
• Refraction
• OD: +0.50‐1.50x079 VA: 20/20
• OS: plano‐1.00x085 VA: 20/20‐1
• Add +2.50 20/20 OU
• Slit lamp findings
• Lids/Lashes: Mild Meibomian capping
• Conjunctiva: Pinguecula OU
• Cornea: Clear OU
• Anterior Chamber: Deep and Quiet OU
• Iris: Normal OU, (‐)NVI OU
• Lens: 1+ NS OU, trace ACC OU
• Intraocular Pressure
• OD: 15mmHg
• OS: 16mmHg
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5/29/2012
• C/D Ratio
• OD: 0.45v/0.40h
• OS: 0.35 round, flame shaped hemorrhage on inferior temporal rim
• Blood Vessels
• Mild tortuosity, (‐)venous engorgement
• Posterior Pole
• OD: one blot heme inf/temp at the edge of arcades
• OS: two large blot hemes superior to the macula within 1DD with
foveal thickening. Extensive blot hemes all 4 quadrants throughout
the arcades.
• Macular thickening OU per OCT
• Periphery
• OD: few scattered mid‐peripheral blot hemes
• OS: extensive mid‐peripheral blot hemes all 4 quadrants
• (‐)holes, tears, retinal detachments OU
• Assessment/Differentials
• Central Retinal Vein Occlusion OS
• Diabetic Retinopathy with possible CSME
• Asymmetric OS>OD
• Carotid Occlusive Disease secondary to greater hemorrhaging
in the left eye
• Warfarin induced retinopathy OS
• Since patient recently started this medication 2 months earlier
• Plan
• Patient was sent to lab for ProtimeINR
• Ordered Carotid Doppler Ultrasound
• Also placed consult to Portland VAMC for fluorescein
angiography
• ProtimeINR came back slightly low at 1.9
• Carotid Ultrasound results were estimated to have 90‐
99% stenosis for both the right and left internal
carotid arteries
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5/29/2012
• Patient then decided not to pursue further optometric
testing until the stenosis was addressed
• VA Physician referred patient to local Vascular
Surgeon
• Patient chose to pursue
bilateral carotid
endarterectomy done by
a local vascular surgeon
in Medford. The left side
first on 11/16/2011 then
the right on 12/28/2011.
http://www.primehealthchannel.com/carotid‐endarterectomy.html
• After endarterectomies patient was referred to local
Ophthalmologist in Medford for a fluorescein
angiography
• Results are as follows:
Taken 1/11/2012 Taken 10/31/2011
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5/29/2012
• Window defect associated
with pigmentary change in
drusen
• One fine microaneurysm
without leakage
• The left side had multiple
microaneurysms in the
temporal macula and
periphery without
significant leakage.
• There was also blockage
from dot and blot
hemorrhages.
• There was no significant
filling delay of the choroid
or retina for either eye.
• Probable ocular ischemic syndrome, left eye
• Non‐proliferative diabetic retinopathy, left eye greater
than right
• History of carotid occlusive disease status post
bilateral carotid endarterectomy
• Cataracts
• The patient was placed under observation and was
scheduled for follow up with Ophthalmology in 3
months.
• Patient was seen again on 4/23/2012 and the findings
below were described by the Ophthalmologist:
• The right retinal periphery has one or two small
intraretinal hemorrhages. In the left periphery, there
are several intraretinal hemorrhages in each of the four
quadrants of the periphery. This represents a significant
decrease in hemorrhages from when I last saw him in
January.
• Epidemiology
• Average age of 65 years, rare before 50
• Men affected 2x more than women
• No racial predilection
• Bilateral involvement in approximately 22% of cases
• 7.5 cases per 1 million people per year
• May be an underestimation as OIS may be misdiagnosed as
other vascular diseases
• 29% of patients with Symptomatic carotid occlusion
manifest retinal vascular changes that are usually
Asymptomatic, and 1.5% of them per year will progress
to symptomatic OIS
• Pathogenesis
• OIS develops primarily in patients
with poor collateral circulation
between the internal and external
carotid arteries or between the two
internal carotid arteries
• People with well developed
collateral circulation may not
develop OIS even with total
occlusion of the internal carotid
artery
• Those with poor collateral
circulation can develop OIS with
less than 50% stenosis of the
internal carotid artery
http://medicaldictionary.thefreedictionary.com/_/viewer.aspxpath=mosbyC
AM&name=500069‐fx30.jpg
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• Symptoms: patients may have the following
complaints
• Vision Loss
• Can be described as loss of vision anywhere from suddenly to
gradually over the course of a month
• Pain
• Patients will sometimes describe it as a dull, constant ache in
the affected eye. Dull pain also felt over the orbit, upper face,
and temple. This pain may worsen when patient is upright.
• Lying down either can relieve or lessen the pain.
• Episcleral Injection
http://www.aafp.org/afp/2002/0915/p991.html
• Corneal Edema
• Rubeosis Iridis
• Can lead to:
• Hyphema
• Neovascular Glaucoma
http://arapaho.nsuok.edu/~fulk/kanski.html
• Iridocyclitis
• Lead to anterior or
posterior synechiae
• Other Anterior Segment findings:
• Corneo‐scleral Melting
• Iris Atrophy
• Fixed semi‐dilated or sluggish pupil
• Uveal Ectropion
• Asymmetric Cataract
http://disorders.eyes.arizona.edu/disorders/corneal‐dystrophycongenital‐endothelial‐1
http://www.musculoskeletalnetwork.com/rheumatoidarthritis/content/article/1145622/1517642
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• Cherry Red Spot
• Neovascularization of the disc
http://content.lib.utah.edu/cdm4/item_viewer.phpCISOROO
T=/EHSL‐WFH&CISOPTR=850
http://www.southcoasteye.com/whatsnew.html
• Choroidal Neovascular
Membrane
• Cholesterol Emboli
• Hollenhorst Plaque
http://www.kenteyesurgery.co.uk/a‐z‐of‐eyes‐view.php/amd‐‐
‐age‐related‐macular‐degeneration
• Dilated Retinal Veins
• Narrowed Retinal Arteries
http://www.aao.org/theeyeshaveit/optic‐fundus/hollenhorstplaque.cfm
http://content.lib.utah.edu/cdm4/item_viewer.phpCISOROOT=/EHSL‐
WFH&CISOPTR=524
• Other Posterior Segment Findings
• Retinal hemorrhages
• More prominent in the mid‐periphery
• Microaneurysms
• Macular capillary telangiectasia
• Retinal arteriovenous communication
• Cotton‐wool spots
• Neovascularization elsewhere
• Vitreous Hemorrhage
• Spontaneous Retinal Arterial Pulsations
• Anterior Ischemic Optic Neuropathy
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• Differential Diagnosis
• Diabetic Retinopathy and Central Retinal Vein
Occlusion are the two most likely conditions to be
confused with OIS
• One way to differentiate is light digital pressure on the eyelid.
Doing this on eyes with OIS will induce retinal arterial
pulsations. (Ophthalmodynamometry)
• Diabetic retinopathy may coexist with OIS.
• It is recommended that those patients with unilateral
retinopathy or large asymmetry of retinopathy be examined
for carotid occlusive disease
• Systemic Associations
• A study by Mizener et al in 1988 of 32 patients showed
the following associated systemic diseases
• Diabetes mellitus (56%)
• Hypertension (50%)
• Coronary Artery Disease (38%)
• Previous Cerebral Infarction or Transient Ischemic Attack
(31%)
• The study also showed that OIS was the initial
manifestation of carotid occlusive disease in 69% of the
patients.
• Other Systemic Associations with OIS:
• Giant Cell Arteritis
• Aortic Arch Syndrome
• Takayasu Arteritis
• Diagnosis techniques
• Fluorescein Angiography
• Indocyanine Green Angiography
• Electroretinography
• Visual‐Evoked Potentials
• Ophthalmodynamometry
• Ocular Plethysmography
• Imaging Methods
• Carotid Duplex Ultrasound
• Color Doppler Imaging of Retrobulbar Vessels
• Magnetic Resonance Angiography
• Carotid Arteriography
• Fluorescein Angiography
• Delayed choroidal filling time
• Staining of the retinal vessels
• Indocyanine Green Angiography
• Delayed choroidal filling time
• Slow filling of the watershed zones of the choroid
• Electroretinography
• The a wave corresponds to photoreceptor activity
• The b wave corresponds to bipolar cells
• OIS results in decreased amplitude of a and b waves
• Visual‐Evoked Potentials
• Recovery time after photostress is prolonged in patients
whom have severe carotid artery stenosis
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• Ophthalmodynamometry
• Used to estimate the pressure in the
Ophthalmic Artery, approximately at the
origin of the Central Retinal Artery.
• Apply pressure to globe to increase IOP, when
artery pulsations are observed this reflects
the ophthalmic artery diastolic pressure.
• In OIS the Central Retinal Artery perfusion
pressure is low meaning less pressure is
necessary for artery pulsations to appear.
• Ocular Plethysmography
• Measures indirectly the Ophthalmic Artery pressure by
recording variations in the size and volume of the eye or
ocular pulsations
• http://bjo.bmj.com/content/87/3/361.2.full
• Imaging Methods
• Carotid Duplex Ultrasound
• Probably will be most ordered diagnostic test by Optometrist
when OIS is suspected
• Color Doppler Imaging of Retrobulbar Vessels
• Magnetic Resonance Angiography
• Carotid Arteriography
• Management
• Carotid Endarterectomy
• http://www.youtube.com/watchv=8rPwO‐093Lo
• Carotid Artery Stenting
• http://www.youtube.com/watchv=6nyNLQUUmOQ&feature=related
• Study from the New England Journal of Medicine called the CREST trial
• 4 year rate of stroke or death was 6.4% with stenting and 4.7% with
endarterectomy.
• The overall results of this study showed that stenting and endarterectomy were
associated with similar primary composite outcomes
• Periprocedural stroke
• Myocardial infarction
• Death and subsequent ipsilateral stroke
• Stroke was more likely after stenting and myocardial infarction was more likely
after endarterectomy. Also worth noting was that younger patients had slightly
fewer problems after stenting and older patients had fewer problems after
endarterectomy
• Management Continued
• Treatment is directed toward control of anterior segment
inflammation, retinal ischemia, increased IOP and
neovascular glaucoma
• Topical Therapy
• Steroid
• Cycloplegic
• Beta blockers
• Alpha Agonists
• Prostaglandins should be avoided because they can increase ocular
inflammation
• When neovascular glaucoma develops surgery or
cycloablation is often needed
• Trabeculectomy with antimetabolites
• Aqueous shunt implants or diode laser cyclophotocoagulation
• Management Continued
• Panretinal Photocoagulation may be effective in some
patients with ocular neovascularization caused from carotid
occlusive disease
• PRP caused regression of iris neovascularization in 36% of the
treated eyes
• Intravitreal Anti VEGF has been used to treat iris
neovascularization and macular edema
• 2 cases reported by Amselem et al of Intravitreal Avastin injection
when carotid endarterectomy was contraindicated
• One week after injection there was a regression of NVI in both cases
and at three months there was no NVI
• One case had a recurrence of NVI at 4 months and was reinjected
and at seven months remained without NVI
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5/29/2012
• Conclusion
• Signs and symptoms of carotid artery occlusive disease
may occur before cerebrovascular and cardiovascular
complications. As a result, optometrists may be the first
to deal with patients suffering from carotid artery
occlusive disease and should be aware of the clinical
presentation of OIS.
• Amselem L, Montero J, et al. Intravitreal Bevacizumab (Avastin) Injection in Ocular
Ischemic Syndrome. American Journal of Ophthalmology 2007;144:122‐124.
• Brott T, Hobson R, et al. Stenting versus Endarterectomy for Treatment of Carotid‐Artery
Stenosis. The New England Journal of Medicine 2010;363(1):11‐23
• Brown GC, Magargal LE. The ocular ischemic syndrome. Clinical, fluorescein
angiographic and carotid angiographic features. Int Ophthalmol. 1988;11 (4):239‐51
• Cohen R, Padilla J, et al. Carotid artery occlusive disease and ocular manifestations:
Importance of identifying patients at risk. Optometry (2010)81, 359‐363.
• Ferguson G, Eliasziw M, et al. The North American Symptomatic Carotid
Endarterectomy Trial: Surgical Results in 1415 patients. Stroke, Journal of the American
Heart Association 1999, 30: 1751‐1758.
• Groschel K, Ernemann U, et al. Incidence and risk factors for medical complications after
carotid artery stenting. Journal of Vascular Surgery 2005; 42: 1101‐1107.
• McCullough H, Reinert C, et al. Ocular findings as predictors of carotid artery occlusive
disease: Is carotid imaging justified Journal of Vascular Surgery 2004; 40: 279‐286.
• Mendrinos E, Machinis T, Pournaras C. Ocular Ischemic Syndrome. Survey of
Ophthalmology 2010; 55(1): 2‐34.
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