systemic disease - texas optometric associationtexas.aoa.org/documents/tx/2015 convention/od...

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

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

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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

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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

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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

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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

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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

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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

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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

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• 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.


• 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)


• 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


• Pain

– 40% of cases

– Over 90% of patients with pain have rubeosis

– Ischemic pain is a dull constant ache in the affected eye


• 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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• 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


• 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


• 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

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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

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• 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


• 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

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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

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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

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