2/16/2015 1 Steven Ferrucci, OD, FAAO Jennifer Deakins, OD, FAAO Rick Trevino, OD, FAAO Steven Ferrucci, OD, FAAO Chief, Optometry Sepulveda VA Professor, SCCO/MBKU 71 year old male Presents for routine eye exam 20/25 OU Ant seg: 1+ NSC OU Post seg: CHRPE OD Congenital Hypertrophy of the RPE RTC 1 yr Photodocumentation Unifocal lesion typically appear as flat, pigmented round lesions with distinct margins Color ranges from light brown to jet black, depending upon amount of melanin Often have areas of chorioretinal atrophy within the lesion that appear window like and allow a clear view of the underlying choroid (lacunae)
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2/16/2015
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Steven Ferrucci, OD, FAAOJennifer Deakins, OD, FAAORick Trevino, OD, FAAO
Steven Ferrucci, OD, FAAOChief, Optometry Sepulveda VAProfessor, SCCO/MBKU
71 year old male Presents for routine eye exam 20/25 OU Ant seg: 1+ NSC OU Post seg:
CHRPE OD
Congenital Hypertrophy of the RPE
RTC 1 yr Photodocumentation
Unifocal lesion typically appear as flat,
pigmented round lesions with distinct margins
Color ranges from light brown to jet black,
depending upon amount of melanin
Often have areas of chorioretinal atrophy
within the lesion that appear window like and
allow a clear view of the underlying choroid
(lacunae)
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Typical size is 2-6 mm, but may be smaller or as large as 14 DD (21 mm)
Can be located anywhere within the fundus, but about 70% in temporal half of fundus
No apparent racial predisposition, although reported more in Caucasians
May be present at birth, with reports in as young as 3 months old
Lesions are almost always stable in size, but
color may change.
Very rare instances of enlargement with time
Typically asymptomatic, and found on routine
exam, but large lesions have been shown to have
VF defects
Can also appear as multifocal CHRPE
From 3 to 30 lesions, 0.1 to 3.0 mm in size
Benign, stationary and unilateral in 85% of the cases
Often called bear tracks
Multifocal CHRPE have been associated with
Gardner’s Syndrome
Familial condition of colonic polyps that may be
precursor to colon cancer
However, these lesions are bilateral, have more
irregular borders, and are often scattered throughout
the fundus
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Deferential includes nevi and choroidalmelanoma
Nevi: nevi are rarely jet black and tend to have more indistinct borders
Melanomas tend to be greater than 2mm in thickness, where CHRPE are flat
B-scan, serial photos and frequent monitoring of assistance
Reder to GI for mutiple, odd-shaped CHRPE
Since posterior scleritis is not able to be
viewed, probably more common than
suspected
Usually only discovered if anterior scleritis is
involved or if other signs in orbit lead one to
suspect its presence
If scleritis remains posterior
severe exudative retinal detachment
retinal swelling
swelling of the disc
If scleritis extends outward, EOMs become involved
proptosis
lower lid retraction
ophthalmoplegia
Suspect if patient c/o extreme pain with no
real clinical signs seen
May have more pain on eye movement, as
well as hyperopic shift with decreased VA
B-scan can make the diagnosis
Shows thickened posterior sclera, typically > 2 mm
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Due to severity of condition requires prompt
diagnosis and urgent care
Complete physical examination by internist
and lab work is crucial
Referral to ophthalmologist is advisable
uveitic specialist if anterior scleritis
retinal specialist for posterior scleritis
Topical therapies, ie steroids, are of
questionable value
may increase pt comfort
beware long-term use
may help with diagnosis
Narcotics may provide temporary relief of
symptoms
Intensive inflammatory control is mainstay of
treatment
Mild to moderate presentations
600 mg oral ibuprofen qid or 25 mg oral
indomethacin tid for 1-2 weeks
Severe or posterior uveitis
60 to 100 mg oral prednisone for 3-5 days, then
taper
or more intensive immunosuppressive agents
▪ ex methotrexate
Complications from oral treatment
indomethacin
▪ GI upset
▪ can be treated with H2 blocker (tagamet) or d/c
prednisone
▪ hyperglycemia
immunosupressive agents (methotrexate)
▪ leukopenia
▪ bladder toxicity
▪ opportunistic infection
Treatment with subconjunctival or subtenons
steroids is contraindicated
could lead to perforation
Surgical treatment for defects in sclera is
rarely needed
does not really treat underlying disease
Follow-up based on severity of presentation
and opinion of specialist
Underlying medical condition should be
managed by medical specialist
Pt must be advised on possible recurrences
and followed closely
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High likelihood of systemic disease, > 50%
Rheumatoid disease most common
▪ RA, SLE, AS, PN, RP
Herpes Zoster Ophthalmicus
Syphilis
Gout
TB
Others
▪ Rieters, Wegener’s, etc
Most often :
CBC
ESR with C-reactive protein
RF
ANA
FBS
RPR/FTA-ABS
If clinical suspicion:
PPD
▪ for TB
Chest X-ray
▪ TB, sarcoid
X-ray of sacro-illiac joints and/or HLA-B27:
▪ Ankylosing spondylitis
Serum uric acid
▪ Gout
Glaucoma
As high as 13% after 10 years in some studies
Open angle due to trabeculitis, raised episcleral venous pressure or steroid use
2-DAY FOLLOW-UP VISIT• No change in symptoms or findings• IMP: Anterior uveitis OD - stable• PLAN: No change tx, RTC 48hrs
Case Report
2-WEEK FOLLOW-UP VISIT
• No change in symptoms or findings
• IMP: Anterior uveitis stable
• PLAN: Taper PF, D/C Homatropine, Labs (WNL)
4-WEEK FOLLOW-UP VISIT
• Off meds, No change in symptoms or findings
• IMP: Anterior uveitis stable
• PLAN: Carotid Duplex (Stenosis: 80% R, 60% L)
Laboratory evaluation of anterior uveitisCBC, Sed rate, CRP (nonspecific)VDRL (syphillis)ACE, serum lysozyme (sarcoid)Chest x-ray or CT scan (sarcoid, TB)PPD skin test (TB)Lyme serology (in endemic areas or h/o tick bites)
Carotid Stenosis Grading Scheme< 50% = Mild
50%-70% = Moderate>70% = Severe
Case Report
Final Diagnosis:
• Carotid artery stenosis – severe / moderate
• Ocular Ischemic Syndrome OD – mild
Final Disposition:
• Vascular consult: Pt not candidate for CEA, manage medically
• OIS stable on long-term follow-up without specific treatment
Ocular Ischemic Syndrome
• Definition
– Ocular signs and symptoms that occur as a consequence of hypoperfusion of the eye
– Published reports tend to describe severe OIS with little or no data available on mild disease• Mizener JB, Podhajsky P, Hayreh SS. Ocular ischemic syndrome.
Ophthalmology. 1997;104:859–64.
• Brown GC, Magargal LE. The ocular ischemic syndrome. IntOphthalmol. 1988;11:239–51.
Ocular Ischemic Syndrome
• Epidemiology
– Mean onset: 65yrs, rare <50yo
– Twice as common in men
– No racial predilection
– 25% of cases bilateral
– Most have known risk factors(HTN, DM, CAD, smoking)
Ocular Ischemic Syndrome
• Pathogenesis
– Ophthalmic artery insufficiency
– Ipsilateral carotid artery disease (90% cases)
– Occurs in patients with poor collateral circulation
Clinical Presentation
• Vision
– TVL occurs in 10-15% of patients
– TVL triggered by increased demand (following exposure to bright light) or decreased perfusion (postural change)
33% have 20/40 or better
33% have CF or worse
MILD MOD
SEVERE
Clinical Presentation
• Pain
– 40% of cases
– Over 90% of patients with pain have rubeosis
– Ischemic pain is a dull constant ache in the affected eye
Clinical Presentation
• Anterior Segment– Rubeosis and neovascular glaucoma
• Up to 66% of cases
• IOP may remain normal due to ciliary body decompensation (50%)
• Elevation of IOP may cause CRAO
– Anterior uveitis • Ischemic vs Inflammatory
• Mild cells/flare (≤gr 2+)
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Clinical Presentation
• Ischemic “Uveitis”– Early onset (mild OIS)
– Mimics iritis (no photophobia or ciliary flush)
– Blood-aqueous barrier beakdown due to ischemia
– Not responsive to steroids
• Inflammatory Uveitis– Late onset (advanced OIS)
– Associated with neovascular glaucoma, corneal decompensation, phthisis bulbi, etc