Systemic Disease - Texas Optometric Associationtexas.aoa.org/Documents/TX/2015 Convention/OD...
Transcript of Systemic Disease - Texas Optometric Associationtexas.aoa.org/Documents/TX/2015 Convention/OD...
2/16/2015
1
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)
2/16/2015
2
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
2/16/2015
3
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
2/16/2015
4
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
2/16/2015
5
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
Narrow angle secondary to serous RD
Respond poorly to meds, and may require surgery
▪ Trab is best, but difficult
▪ Many need a tube instead
Cataracts
As high as 17% in 10 years
Mostly with severe and necrotizing scleritis
With long term steroid use
Cataract surgery is safe, as long as inflammation
has been quiescent for at least 3 months
Posterior involvement
Serous retinal detachment
Choroidal folds
Optic nerve involvement
Hyperopic refractive shift
With posterior scleritis
Phthisis bulbi, anterior segment ischemia, hypotony
Rare, due to serous RD or following severe scleritis
2/16/2015
6
48 yo hispanic male Sent from primary care with sudden
decreased vision right eye x 1 day Oc hx: unremarkable, last exam 3-4 years ago Med hx: HTN Meds: amlodipine
VA 20/200 OD, 20/20 OS 1+ APD OD EOMs: No pain, no diplopia, no
restriction FCF: full OU SLE: mild arcus OU
2/16/2015
7
Macula edema ONH edema temporally with leakage on FA Focal choroiditis
Tentative Diagnosis: Neuroretinitis OD Additional questions
Has flu-like symptoms x 1 mos, feeling better last few days
No camping
No cough
No travel out of country
2 cats. Doesn’t recall being scratched
Neuroretinitis
Cat scratch
Syphillis
TB
Lyme Disease
Toxoplasmosis
RPR/PPAT-TP: Syphilis Lyme Titer Quantiferon Gold: TB Bartonela Titers: Cat Scratch
Henselae
Quintana
Retina Consult Infectious disease consult
Concur with findings Bartonela most likely (Cat Scratch)
Start Doxycycline 100 mg bid
Refer to Infectious disease
2/16/2015
8
Labs ordered RPR/PPAT-TP: negative Lyme Titer: negative Quantiferon Gold: negative Bartonela Titers
▪ Henselae: 1: 1024 (reference 1:64)▪ Quintana: negative
Added by infectious diseas HIV testing: negative ACE (Sarcoid): negative HLA-B27 (Reiters): negative Histoplasmosis Abs: negative Toxoplasmosis Abs: negative
• Inflammation of the optic nerve head and surrounding retina
• Not involved with Multiple Sclerosis• Vitreous cells may be present• RAPD is present
Serous Retinal Detachment extending to the fovea
• Macular star of hard exudates• Optic nerve head swelling• Multifocal retinitis
2/16/2015
9
Several different types of plaques can
often be visualized in the retinal
vasculature
Pt is typically elderly, has HTN, CAD,
hypercholesterolemia/hyperlipidemia,
and/or atherosclerotic disease
Often totally asymptomatic and found on
routine exam
May present with amarosis fugax,
transient episodes of monocular blindness
Rarely, may report transient ischemic
attack (TIA) , which is above with
hemiparesis, parasthesia or aphasia
Three different types of plaques, but all
share strong association to significant
cardiovascular disease
Cholesterol (Hollenhorst) plaque
shiny yellow-orange in appearance
typically from the ipsilateral carotid artery
Rarely causes occlusion, unless multiple
Typically occurs at bifurcations
Mobile in nature
Calcific
Appears more whitish than HH
Classically within arteriole, not at bifurcation
Typically immobile
Often causes BRAO
Often from cardiac arethromas of heart valves
2/16/2015
10
Fibrino-platelet
Appear as dull white to gray, long plugs
Typically within arterioles, not at bifurcations
May break-up and dissolve with time
May lead to BRAO or CRAO
Often associated with carotid disease or mitral
valve insufficiency
No direct management of plaques is
needed
Management is aimed at discovering
source of embolus to decrease risk of
other emboli, occlusion, or stroke
Pts need referral to internist for complete
physical
Examination should include
Complete physical, including cardiac risk
factors and BP evaluation
Carotid ultrasound
Stress echocardiogram
Fasting BS
Lipid profiles
Cardiac enzymes
After ruling out underlying etiology, see
patient regularly, q 6 -12 mos, to evaluate
for additional plaques or other disease
associated with vascular disease
BRVO/CRVO
BRAO/CRAO
NTG
2/16/2015
11
If carotid stenosis or coronary artery disease is found treatment may include
Carotid endarterectomy
Angioplasty
Aspirin therapy
Other anti-coagulation therapy, such as coumadin
Pts with cholesterol HH emboli have 15% mortality at 1 yr, 29% by year 3, and 54% by 7 years Mostly from cardiac disease
When Anterior Uveitis Isn’t
Rick Trevino, OD, FAAO
Rosenberg School of Optometry
University of the Incarnate Word
Case Report
• 74yo WM new patient presenting on referral from PCP for a routine diabetic eye exam.
– No ocular complaints
– Needs new eyeglasses
– Specifically denies pain or recent changes in vision
• POH: No prior eye dx or sx. LEE: 5yrs.
• MH: NIDDM x 6yrs (HbA1C: 7.2), HTN, Hyperchlesterolemia, Osteoarthritis
Case Report
Vcc• OD: 20/30• OS: 20/30• No improvement
with refraction
Ta 12/12 @ 9:20AMPERRL, No APDFROM, nontrabismicFCCF: Full OU
Case Report
SLE• LLL: Mild crusting OU• Conj: 1+ injection OU• Cornea: Few guttata OU• AC: 1+ cells, 1+ flare OD,
Clear OS• Iris: Normal OU.
No NVI OU, No synechia
• Lens: 1+ cortical, 1+ NS OU
Case Report
DFE
• CDR: 0.2 OU
• Background: Few dot/blot hemes OU
• Disc: Pink and sharp OU
• Macula: Few hard drusen OU. No CSME OU
• Vessels: Grade 2 HTN OU, No NVE/NVD
• Periphery: Few dot/blot hemes OD, clear OS
2/16/2015
12
Mid-peripheral dot/blot hemorrhages OD
Case Report
Impression
• Anterior uveitis OD
• Mild NPDR OU
• Mild cataract OU
• Refractive error
Plan
• Start PF Q1H OD
• Start Homatropine 5% BID OD
• RCT 48hrs
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
ANTERIOR POSTERIOR ORBITAL
Rubeosis Retinopathy Ophthalmoplegia
Uveitis Glaucoma Pain
Corneal decompensation
Spontaneous arterial pulsations
Hypotony
Cataract AION Ptosis
Scleral melting Neovascularization
Adapted from: Mendrinos, Surv Ophthalmol. 2010;55:2–34
2/16/2015
13
Ocular Ischemic Syndrome
• Classification
– No standardized classification system
• “Mild” and “Severe”
• Visual acuity, Neovascularization, etc
– 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+)
2/16/2015
14
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
Clinical Presentation
• Posterior Segment – Hypoperfusion retinopathy– Mid-peripheral dot/blot hemorrhages (80% cases).
• Rarely numerous, almost never confluent.
• Mimics diabetic retinopathy
– Attenuated arterioles
– Dilated (but not tortuous) veins
– Cotton-wool spots
– Neovascularization
– Macular edema
• Carotid artery imaging is the essential diagnostic test in pts with suspected OIS
Terelak-Borys, Med Sci Monit. 2012;18:138–44
Clinical Presentation
• Management
– Team approach (cardiology, vascular surgery, medicine, glaucoma, retina)
– Neovascular glaucoma
• Monitor for onset of rubeosis
• PRP usually ineffective due to choroidal insufficiency
– Anterior uveitis
• Ischemic: Monitor for progression
• Inflammatory : Steroids & cycloplegics
Key Points
• High index of suspicion in older men with “silent” anterior uveitis
• Mid-peripheral hemorrhages are not characteristic of diabetic retinopathy
• IOP may remain normal despite angle neovascularization
• Include OIS in differential diagnosis of iritis unresponsive to steroid therapy
Does Regular Aspirin Use
Cause AMD?
Rick Trevino, OD, FAAO
Rosenberg School of Optometry
University of the Incarnate Word
2/16/2015
15
AMD & Vascular Disease
• AMD has been linked to cardiovascular risk factors and presumed pathogenic mechanisms
• Risk factors: Smoking, obesity, exercise
• Pathogenic mechanisms: Inflammation, oxidative damage
• Agents that affect cardiovascular health might influence AMD development and progression
Aspirin
• Non-steroidal anti-inflammatory drug (NSAID)
• Pharmacologic properties:– Analgesic, antipyretic, anti-inflammatory,
antiplatelet
• Secondary prevention of CVD – Well-established benefits in preventing MI & CVA
• Primary prevention of disease– Benefits are less clearly established for prevention
of CVD, cancer, Alzheimer's disease, etc
Aspirin Use
• Aspirin is one of the most widely used medications worldwide
– 36% of adults in the US take aspirin regularly for prevention of disease
– More than 100 billion tablets consumed each year
• Adverse effects of aspirin
– Gastrointestinal hemorrhage, worsen hypertension, renal failure, aggravate asthma, hemorrhagic stroke
– 16,500 deaths annually are related to aspirin use
Aspirin & AMD
• Aspirin may have both beneficial and harmful effects on AMD
• Possible beneficial effects
– Anti-inflammatory
– Improved circulation (↓platelet aggregability)
• Possible harmful effects
– Inhibit vasodilation thereby inducing hypoxia
– Disturbed lipid oxidation
– Increased risk of hemorrhage
Aspirin & AMD
Harmful EffectFeman (1972)
Bloome (1978)
Kingham (1988)
Lewis (1988)
AREDS (2000)
Klein (2012)
de Jong (2012)
Cheung (2013)
Liew (2013)
No EffectMPS Group (1986)
MPS Group (1990)
Klein (1991)
Hirvela (1996)
Klein (2001)
Douglas (2007)
Rudnicka (2010)
Protective EffectChristen (2001)Christen (2009)
Randomized Controlled Trials
2/16/2015
16
Randomized Controlled Trials
• Christen (2001)
– Physician’s Health Study: Randomized, double-masked, placebo-controlled trial of 22,071 healthy adult men for 5yrs
• 325mg q48h
• Study terminated after 5yrs due to extreme 44% risk reduction for first MI
– Low-dose aspirin had a statistically non-significant 23% reduced risk of AMD compared to placebo
Christen, Arch Ophthalmol. 2001;119:1143-1149
Randomized Controlled Trials
• Christen (2009)
– Women’s Health Study: Randomized, double-masked, placebo-controlled trial of 39,876 healthy adult women over an average of 10 years
• 100mg q48h
– Low-dose aspirin had a non-significant 18% reduced risk of AMD compared to placebo
Christen, Ophthalmology. 2009; 116: 2386–2392
Christen WG. Ophthalmology. 2009; 116: 2386–2392
Onset of AMD in placebo group
Onset of AMD in aspirin group
18% lower risk at 10yrs
Observational Studies
Recent Observational Studies
• de Jong (2012)
– European Eye Study: 4691 participants aged 65 years and older in a population-based cross-sectional study in 7 European communities
– Frequent aspirin use was associated with increased risk of neovascular AMD, and the odds ratios rose with increasing frequency of consumption
de Jong, Ophthalmology. 2012;119:112–118
More frequentASA use
Associated with greater
AMD risk
de Jong, Ophthalmology. 2012;119:112–118
2/16/2015
17
Recent Observational Studies
• Liew (2013)
– Blue Mountains Eye Study: 2389 predominantly white participants aged 50yrs or older from a population-based cohort followed for 15yrs
– Regular aspirin use was associated with a 2.5-fold increased incidence of neovascular AMD
• No association between aspirin use and dry AMD
– Incidence of neovascular AMD: 2.2% (nonusers), 2.9% (occasional users), 5.8% (regular users)
Liew, JAMA Intern Med. 2013;173:258–264
Meta-Analyses
Aspirin use is not associated with risk of AMD
Zhu, PLoS One. 2013;8:e58821.
There is a small but statistically significant association between aspirin use and early AMD
Kahawita, Can J Ophthalmol 2014;49:35–39
Aspirin use is not associated with increase risk of AMD, but it increased the risk of neovascularization
among those who develop AMD
Ye, Invest Ophthalmol Vis Sci. 2014;55:2687–2696
There is a weak but statistically significant association between aspirin use and the risk of AMD
Li, J Clin Pharm Ther. 2014 Dec 5
2/16/2015
18
Key Points
• Inconsistent link between aspirin and AMD
• No change recommended for those taking aspirin for secondary prevention of CVD
• Educate users with strong risk factors for neovascular AMD about risk
• No evidence that discontinuation of long-term aspirin use will reduce risk of AMD
Sobrin, Am J Ophthalmol. 2013; 156: 213–217