CE in Austin

University of Houston College of Optometry

CE in Austin

Sunday Course Notes

To view notes for a specific lecture, click the lecture title on the agenda page to instantly progress to the appropriate section.

CE in Austin CourseMaster

Pat Segu, OD, FAAO

Program Location DoubleTree by Hilton Austin

6505 Interstate Highway–35 North, Austin, TX 78752

SATURDAY, OCTOBER 5th

7:00 am - 8:00 am Registration, Continental Breakfast, & Visit Exhibits

Lectures presented by Ryan Patel, OD, FAAO

8:00 am - 9:40 am Practical Ocular Pharmacology COPE ID # 64685-PH CE Broker # 20-672291 CEE Available

2 DT

9:40 am - 10:10 am Break & Visit Exhibits

10:10 am - 11:00 am Cataract Surgery Updates COPE ID # 64686-PO CE Broker # 20-672295

1 DT

Lectures presented by John McGreal, OD, FAAO

11:00 am - 12:00 pm Pain Without Stain: Managing Neuropathic Corneal Pain COPE ID # 60815-AS CE Broker # 20-672173

1 DT

12:00 pm - 1:00 pm Lunch & Visit Exhibits

1:00 pm - 2:45 pm Medicine Update For Optometry COPE ID # 64713-PH CE Broker # 20-672309 CEE Available

2 DT

2:45 pm - 3:15 pm Break & Visit Exhibits

3:15 pm - 5:00 pm Glaucoma REVISED COPE ID # 64714-GL CE Broker # 20-672313 CEE Available

2 DT

SUNDAY, OCTOBER 6th

7:00 am - 8:00 am Registration, Continental Breakfast, & Visit Exhibits

Lecture presented by Nathan Lighthizer, OD, FAAO

8:00 am - 9:45 am Grand Rounds: A String of Pearls COPE ID # 64687-AS CE Broker # 20-672297 CEE Available

2 DT

9:45 am - 10:15 am Break & Visit Exhibits

10:15 am - 12:00 pm Interpreting Retinal OCTs and Introducing OCT-Angiography COPE ID # 64696-PD CE Broker # 20-672299 CEE Available

2 DT

12:00 pm - 1:00 pm Lunch & Visit Exhibits

1:00 pm - 1:50 pm A Systemic and Ocular Approach to Uveitis COPE ID # 52187-AS CE Broker # 20-672179

1 DT

1:50 pm - 2:40 pm In-Office Electrodiagnostics for the Non-Glaucoma Patient COPE ID # 63288-PD CE Broker # 20-672181

1 DT

2:40 pm - 3:10 pm Break & Visit Exhibits

Lecture presented by Andrew Kemp, OD, FAAO

3:10 pm - 4:05 pm Clear as Mud: Managing Glaucoma Suspects in Modern Optometry

COPE ID # 60584-GL CE Broker # 20-672183

1 DT

4:05 pm - 5:00 pm 2019 Texas Professional Responsibility Course COPE ID # 60707-EJ CE Broker # 20-672185

1 PR/GEN

10/1/18

1

Grand rounds: A string of pearls

Nathan Lighthizer, O.D., F.A.A.O.Assistant Professor, NSUOCOChief of Specialty Care Clinics

Chief of Electrodiagnostics [email protected]

Case #1

Recurrent Corneal Erosions (RCE’s)

• Tendency for minor trauma to cause significant corneal epithelial disturbances

• Pathophysiology– Abnormally weak attachment between the basal

cells of the corneal epithelium and their basement membrane

• Most common causes of the weak attachment– Mechanical trauma**– Corneal dystrophy**– Corneal surgery

Recurrent Corneal Erosions

• Sx’s:–Acute, severe pain**– Photophobia **– Redness– Blepharospasm– Tearing

***Usually sx’s present first thing in the morning upon opening the eyes.***

And often this is recurrent


• Signs:– Epithelial defect may be present,

usually in the inferiorinterpalpebral area


• Signs:– If no defect is present, look for loose, irregular

epithelium(pooling of NaFl, rapid TBUT)

– Signs of corneal dystrophies (will be bilateral)

mailto:[email protected]

10/1/18

2


• Tx:– Acutely:• Lubrication**• Topical Ab (Polytrim QID, erythro or bacitracin ung)• Pain control:

– Cycloplegic (Homatropine BID)• Muro 128 drops or ung

• Bandage lens???– Alleviates pain, does not improve healing


• Tx:– After the epithelium heals (recalcitrant RCE’s):• Fresh Kote TID (15ml bottle $25)• Muro 128 ung qhs (3.5g tube $10)• Lotemax QID X 2 weeks, BID X 6 weeks• Doxycycline 20-50mg BID

– Azasite BID (2.5ml bottle $78)

**Avoid chronic long-term AT ung**


• Surgical Tx:–Anterior stromal micropuncture–Debridement of epithelium with polishing of

Bowman’s membrane with a diamond burr or excimer laser (PTK)

Case #2

Eyelid abscess vs. Preseptal Cellulitis vs. Orbital Cellulitis

• Orbital Cellulitis– All the same signs of

preseptal with– Proptosis– EOM restrictions/pain

with eye movements– Pupillary involvement

– Usually an extension from an ethmoid sinusitis

• Preseptal Cellulitis– Usually upper eyelid

swelling– Pain, tenderness,

redness

– Usually caused by adjacent infection (hordeolum, dacryocystitis)

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3

Oral Antibiotic Paradigm

Penicillins

Augmentin 875mg BID or

500mg TID

Cephalosporins

Keflex 500 mg TID

Macrolides

Zithromax“Z-pak”

Fluoro-quinolones

Levaquin or Cipro

Sulfa

Bactrim DS800/160 BID

Preventing Resistance

• Just one organism, methicillin-resistant Staphylococcus aureus (MRSA), kills more Americans every year (∼19,000) than emphysema, HIV/AIDS, Parkinson's disease, and homicide combined– most serious MRSA infections, an estimated 85%, are associated with a

healthcare exposure, but nearly 14% of the infections are community-associated.

• Almost 2 million Americans per year develop hospital-acquired infections (HAIs), resulting in 99,000 deaths the vast majority of which are due to antibiotic-resistant pathogens

• CDC: Get Smart: Know When Antibiotics Work – teaches both the provider and the patient when antibiotics should be used.

• The IDSA suggests five to seven days is long enough to treat a bacterial infection without encouraging resistance in adults, though children should still get the longer course– this is different than previous guidelines of treating infections from 10-14

days.

10/1/18

Ocular TRUST 3: Ongoing Longitudinal Surveillance of Antimicrobial Susceptibility in Ocular Isolates

• Background:• Ocular TRUST is an ongoing annual survey of nationwide

antimicrobial susceptibility patterns of common ocular pathogens. • To date, more than 1,000 isolates from ocular infections have been

submitted to an independent, central laboratory for in vitro testing.

• Ocular TRUST, now in its third year, remains the only longitudinal nationwide susceptibility surveillance program specific to ocular isolates.

Ocular Trust 3

• Antimicrobials tested represent six classes of drugs: – fluoroquinolones (ciprofloxacin, gatifloxacin, levofloxacin,

moxifloxacin); – dihydrofolate reductase inhibitors (trimethoprim); – macrolides (azithromycin);

– aminoglycosides (tobramycin); – polypeptides (polymyxin B); and

– β-lactams (penicillin).

• Staphylococci were classified as methicillin-resistant (MRSA) or methicillin-susceptible (MSSA) based on susceptibility to oxacillin.

Ocular Trust 3: Results

• most antimicrobials, except penicillin and polymyxin B, continue to be highly active against MSSA (azithromycin shows only moderate activity)

• with the exception of trimethoprim and tobramycin, less than one-third of MRSA strains are susceptible to ophthalmic antimicrobials

• susceptibility profiles remain virtually identical for the fluoroquinolones, regardless of methicillin phenotype

• S. aureus is more susceptible to the fluoroquinolones than to macrolides, as represented by azithromycin

Oral Antibiotic Paradigm

Penicillins

Augmentin 875mg BID or

500mg TID

Cephalosporins

Keflex 500 mg TID

Macrolides

Zithromax“Z-pak”

Fluoro-quinolones

Levaquin or Cipro

Sulfa

Bactrim DS800/160 BID

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4

Case #3

Acanthamoeba keratitis

• History of CL wear w/ poor lens hygiene• Often a history of hot tub/swimming

pool/swimming in the river • Symptoms:– Severe pain out of proportion to clinical picture– Redness & photophobia– All over the course of several weeks

• Signs:– Early -> Pseudodendrites– Late -> Ring-shaped stromal infiltrate

Acanthamoeba Keratitis

• Sx’s:– Severe pain**– Redness– Tearing– Decreased vision– Photophobia– Minimal discharge

These sx’s tend to develop over a period of weeks.**H/O CL hygiene problems and swimming in lenses**


• Signs:– Epithelial or subepithelial infiltrates

appearing as pseudodendrites early on– Patchy anterior stromal infiltrates can

also appear early


• Signs:– Radial keratoneuritis**• Perineural infiltrates seen during the first 1-4

weeks

–Gradual enlargement and coalescence of the infiltrates to form a ring infiltrate**• Inflammation in the cornea doesn’t look that bad**

– Corneal thinning, melting, perforation, scleritis, hypopyon


• Tx:– Topicals:

• PHMB 0.02% drops q1h• Chlorhexidine 0.02% q1h

– Fine line agents can be given separately or together• Propamidine 1% (Brolene) q1h

– Orals:• Voriconazole 200 mg BID• Itraconazole 200-400 mg QD

– Cycloplegics (homatropine BID)– Topical steroids??– Pain control– Surgery

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Fungal keratitis

• Often a history of vegetative trauma, CL wear

• H/O poor response to topical Ab’s• Symptoms:– Pain, photophobia, tearning, FB sensation

• Pain often less than what the clinical picture would indicate

• Signs:– Stromal infiltrate w/ a feathery border– Satellite lesions surrounding the primary

infiltrate

Fungal Keratitis

• Sx’s:– Gradual onset of pain– Irritation/grittiness– Photophobia – Blurred vision– Watery or mucopurulent discharge

H/O cornea infection diagnosed as bacterial**H/O vegetative trauma, CL abuse, chronic steroid

use

Fungal Keratitis

• Signs:–Gray-white stromal infiltrate with indistinct

“fluffy” or “feathery” borders/margins–Often surrounded by fingerlike satellite

lesions in the adjacent stroma

Fungal Keratitis

• Signs:– Epithelial defect overlying the ulcer• However can be quite small and sometimes is not

present– Infiltrates may progressively enlarge and extend

into deeper tissue• Necrosis, thinning and perforation can occur

Fungal Keratitis

• Tx:– Pts may require hospitalization– Topical meds:

• Natamycin 5% (for filamentous fungi)*• Amphotericin B 0.15% (for Candida)* • Both q1h around the clock initially and then tapered

over 6-12 weeks– Orals meds:

• Voriconazole 200 mg BID• Itraconazole• Fluconazole

– Cycloplegics (homatropine BID)– Surgical (PKP or DALK)

Which topical antibiotic is your “go-to” choice for a suspected MRSA infectious

bacterial ulcer?A. Zymaxid/ZymarB. PolytrimC. BesivanceD. Moxeza/Vigamo

xE. CiloxanF. TobramycinG. Vancomycin

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Bacterial Keratitis

• Tx:– Hospitalization???– No CL’s***– Pain relief– Topical Ab’s: (amount & strength depends on the

ulcer)• Besivance, Moxeza, or Zymaxid q1h around the clock for

24-48 hours & tapering according to clinical progress• Besivance (or Moxeza or Zymaxid) & Tobramycin (or

Gentamicin) q1h alternating around the clock

• Fortified Ab’s??? (large ulcers, visual axis, hypopyon)– Fortified Vancomycin, cephalosporins and/or gentamicin

Ocular Trust 3: Results

• most antimicrobials, except penicillin and polymyxin B, continue to be highly active against MSSA (azithromycin shows only moderate activity)

• with the exception of trimethoprim and tobramycin, less than one-third of MRSA strains are susceptible to ophthalmic antimicrobials

• susceptibility profiles remain virtually identical for the fluoroquinolones, regardless of methicillin phenotype

• S. aureus is more susceptible to the fluoroquinolones than to macrolides, as represented by azithromycin

Bacterial Keratitis

• Tx:– Steroids???

• Reduce inflammation, improve comfort, and minimize corneal scarring…but evidence that they improve final visual outcome is limited

• Will make herpes, fungal, acanth much worse• Epithelialization may be slowed by steroids• Can cause corneal thinning (but not usually)• DO NOT USE until clinical improvement is seen with

Ab’s alone• Pred Forte QID

– Doxycycline or Azasite???• Inhibit MMP-9

Case #4

Scleritis

• Rare disorder of inflammation & necrosis centered on the sclera

• 30-60 year olds, female > male• Bilateral 40-80% of time• Pathophysiology is poorly understood• Etiology– 50% of cases are idiopathic– 50% of cases are associated with systemic disease

• Connective tissue diseases– RA most common

• Infections– HZO, HSK, syphilis

Scleritis

• Types of Scleritis1. Diffuse anterior scleritis2. Nodular anterior scleritis3. Necrotizing anterior scleritis w/

inflammation4. Necrotizing anterior scleritis w/o

inflammation (scleromalacia perforans)5. Posterior scleritis

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Scleritis

• Symptoms– Severe, boring, deep eye pain*** (80%)• Can radiate to the forehead, brow, jaw• May awaken pt from sleep

–Diffuse red eye– Photophobia– Tearing

Scleritis

• Signs– Sectoral or diffuse inflammation of conj,

episcleral, and scleral vessels• Scleral vessels do not move at all and do not

blanch w/ phenyl

– Bluish hue to sclera***– Scleral nodules– Corneal changes (peripheral

infiltrates/keratitis)

Scleritis Scleritis

• Differential Diagnosis– Episcleritis– Uveitis

• Diagnosis– Clinical picture– If underlying systemic disease is not known, systemic

workup is indicated (refer to PCP or internist)***• CBC• ANA/RF/HLA-B27• ESR• RPR/FTA-ABS• Fasting blood sugar• ACE• C-ANCA, P-ANCA

Scleritis

• Treatment – depends on severity and type– Oral NSAIDs

• Indomethacin 25-50 mg TID• Ibuprofen 400-600 mg QID• Naproxen 250-500 mg BID

– Oral Steroids• Prednisone 60-100 mg QD X 1 week with taper down to

20 mg QD over next 2-3 weeks, slow taper after that as well

– Immunosuppressive therapy• Cyclophosphamide, methotrexate, cyclosporin

Herpes Zoster

• Nearly 1 million Americans develop shingles each year

• Ocular involvement accounts for up to 25% of presenting cases

• Over 50% incur long term ocular damage

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Herpes Zoster

***Varicella-Zoster Virus***• Herpes DNA virus that causes 2 distinct

syndromes1. Primary infection – Chicken pox (Varicella)• Usually in children• Highly contagious***• Very itchy maculopapular rash with vesicles that

crust over after ≈ 5 days• 96% of people develop by 20 years of age• Vaccine now available

Herpes Zoster

• Herpes DNA virus that causes 2 distinct syndromes

2. Reactivation – Shingles (Herpes Zoster)• More often in the elderly and immunosuppressed

(AIDS)– Systemic work-up if Zoster in someone < 40

• Can get shingles anywhere on the body• Herpes Zoster Ophthalmicus (HZO)– Shingles involving the dermatome supplied by the

ophthalmic division of the CNV (trigeminal)» 15% of zoster cases

Herpes Zoster

• Symptoms:–Generalized malaise, tiredness, fever–Headache, tenderness, paresthesias (tingling),

and pain on one side of the scalp***• Will often precede rash

– Rash on one side of the forehead– Red eye– Eye pain & light sensitivity

Herpes Zoster

• Signs:–Maculopapular rash ->

vesicles -> pustules -> crusting on the forehead

– Respects the midline***–Hutchinson sign• rash on the tip or side of the

nose***– Classically does not involve

the lower lid–Numerous other ocular signs

Herpes Zoster

• Other Eye Disease (Acute):–Acute epithelial keratitis (pseudodendrites)– Conjunctivitis– Stromal (interstitial) interstitial keratitis– Endotheliitis (disciform keratitis)–Neurotrophic keratitis

Herpes Zoster

• Other Eye Disease (Acute):– Episcleritis– Scleritis– Anterior uveitis– IOP elevation– Retinitis– Choroiditis– Neurological complications (nerve palsies)– Vascular occlusion

– Treat the complications just like as if they were primary conditions

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Herpes Zoster

• Treatment:– Treat the complications just like as if they

were primary conditions–Oral antivirals – must be started within 72

hours of symptoms**• Acyclovir 800mg 5x/day x 7-10 days• Valtrex 1000mg 3x/day X 7-10 days• Famciclovir 500mg 3x/day X 7-10 days

– Topical ointment to skin lesions to help prevent scarring• Bacitracin, erythromycin

Herpes Zoster

• Prevention:– Zostivax vaccine• Live attenuated herpes virus• Only given to people who know they had chicken

pox as a child***• Only studied in patients > 60 yo

– 51% reduction in incidence of HZ– 60% reduction in symptom severity in those who got HZ– 66.5% reduction in post-herpetic neuralgia

Shingrix Vaccine

• Shingrix is a non-live vaccine given intramuscularly in two doses.

• 38,000 patients in a phase III clinical tria• >90% efficacy sustained over 4 years

Shingrix vs. Zostivax• Shingrix:

– Efficacy in preventing shingles:– 96.6% effective in 50-59 year olds– 97.4% effective in 60-69 year olds– > 70 year olds

• 97.6% in year 1• 84.7% in years 2-4

– Efficacy in preventing PHN• 91.2% in > 50 year olds• 88.8% in > 70 year olds

–More cost effective – Lasts longer

¨ Zostivax:¡ Efficacy in preventing shingles:¡ 70% effective in 50-59 year olds¡ 64% effective in 60-69 year olds¡ > 70 year olds

ú 38%

¡ Efficacy in preventing PHNú 65.7% in 60-69 year oldsú 66.8% in > 70 year olds

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Herpes Zoster• Post-herpetic Neuralgia– Constant or intermittent pain that persists for

more than one month after the rash has healed

–Older patients with early severe pain and larger area are at greater risk

– Can be so severe that it leads to depression & suicide

– Improves with time• Only 2% of pts affected 5 years out

– Tx:• Cool compresses• Topical capsaicin ointment or lidocaine cream

Viral conjunctivitis

• Signs:– Red eye (conj hyperemia)– Watery discharge– Follicles in the inferior fornix

& conj– (+) PA node***

– Red/swollen eyelids– Petechial sub-conj hemes– SPK– SEI’s (sub-epithelial infiltrates)– Pseudomembranes/membranes

EKC

• Timecourse

Viral conjunctivitis

• Signs:– Red eye (conj hyperemia)– Watery discharge– Follicles in the inferior fornix

& conj– (+) PA node***

– Red/swollen eyelids– Petechial sub-conj hemes– SPK– SEI’s (sub-epithelial infiltrates)– Pseudomembranes/membranes

EKC conjunctivitis

• Diagnosis– Based on clinical symptoms

• Treatment:– Cool compresses– Artificial tears– “get the red out drops”

• Vasoconstrictors such as Visine– Hygiene***– Quarantine/Isolation

– Betadine 5% solution???– Zirgan???

EKC conjunctivitis

• Diagnosis– Based on clinical symptoms

• Treatment:– Cool compresses– Artificial tears– “get the red out drops”

• Vasoconstrictors such as Visine– Hygiene***– Quarantine/Isolation

– Betadine 5% solution???– Zirgan???

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Off-Label Adenoviral Treatments

• Povidone Iodine (0.4%) – Dexamethasone (0.1%)– 9 eyes of 6 patients with confirmed Adenovirus

enrolled– 8/9 enrolled showed clinical resolution by day 4– 6/6 patients with significant reduced DNA

copies by day 5– 5/6 cultures positives with no infectivity by day

5

Herpes Simplex

• Most common virus found in humans– 60-99% are infected by 20 years old

• Double stranded DNA virus–HSV type 1 (HSV-1)–HSV type 2 (HSV-2)

• Primary infection–Occurs in childhood via droplet exposure– Subclinical infection in most

• Secondary infection (recurrence)

Herpes Simplex

• Recurrent infection:– After primary infection the virus is carried to the

sensory ganglion for that dermatome (trigeminal ganglion) where a latent infection is established.

– Latent virus is incorporated in host DNA and cannot be eradicated

– Stressors (trauma, UV light, fever, hormonal changes, finals week, etc) cause reactivation of the virus and it is transported in the sensory axons to the periphery -> clinical signs/symptoms

Ocular recurrence -> 10% at one year, 50% at ten

Herpes Simplex Keratitis

• Epithelial Keratitis:– Symptoms:• Ocular irritation, redness, photophobia, watering,

blurred vision

– Signs:• Swollen opaque epithelial cells arranged in a

course punctate or stellate pattern• Central desquamation results in a dendrite***

1. Central ulceration2. Terminal end bulbs

• ***Corneal sensation is reduced***


• Epithelial Keratitis:– Symptoms:• Ocular irritation, redness, photophobia, watering,

blurred vision

– Signs:• Swollen opaque epithelial cells arranged in a

course punctate or stellate pattern• Central desquamation results in a dendrite***

1. Central ulceration2. Terminal end bulbs

• ***Corneal sensation is reduced***


• Epithelial Keratitis:– Treatment:• Zirgan (ganciclovir gel 0.15%)

– 5x/day until the dendrite disappears– 3x/day for another week

• Viroptic (trifluridine solution 1%)– 9x/day until the dendrite disappears– 5x/day for another week

• Oral antivirals (if topical not well tolerated):– Acyclovir 400 mg 5x/day X 7-10 days– Valtrex 500 mg 3x/day X 7-10 days– Famvir 250 mg 3x/day X 7-10 days

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• Epithelial Keratitis:– Treatment (con’t):• Debridement of the dendritic ulcer???• Oral antivirals???• IOP control

– Avoid prostaglandins???

• Steroids???

– Follow-up• Day 1, 4, 7


• Marginal keratitis:– Very rare

– Looks like a marginal infiltrate....but

– In HSV marginal keratitis:1. Much more pain2. Deep neovascularization3. No clear zone between

infiltrate and limbus


• Immune Stromal Keratitis (ISK):– 2% of initial ocular HSV presentations– 20-61% of recurrent disease

– 88% non-necrotizing– 7% necrotizing

– ***Can be visually devastating***


• Immune Stromal Keratitis:– Symptoms:• Gradual blurred vision• Halos• Discomfort/Pain • Redness


• Immune Stromal Keratitis:– Signs (non-necrotizing):• Stromal haze (inflammation & edema)• Neovascularization (deep)• Immune ring• Scarring and/or thinning• Intact epithelium***

– Signs (necrotizing):• All of the above• More dense infiltration• Often w/ overlying epithelial defect• Necrosis and/or ulceration• ***high perforation risk***


• Immune Stromal Keratitis:– Treatment:• Topical steroids

– Pred Forte QID-q2H– Durezol BID-QID– Lotemax QID

• Topical anti-viral cover– Viroptic (trifluridine 1%) QID– Zirgan (ganciclovir 0.15%) QID

• Topical cyclosporin (Restasis), AT’s, ung’s to facilitate epithelial healing if ulceration is present

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• Endotheliitis: AKA Disciform Keratitis–Not considered a primary form of stromal

keratitis• Stromal edema is present secondary to endothelial

inflammation

– Symptoms:• Blurred vision• Halos• Discomfort/Pain• Redness


• Endotheliitis: AKA Disciform Keratitis– Signs:• Central zone of stromal edema often with

overlying epithelial edema• KP’s underlying the edema• AC reaction• IOP may be elevated• Reduced corneal sensation• Healed lesions often have a faint ring of stromal or

subepithelial opacification and thinning


• Endotheliitis: AKA Disciform Keratitis– Treatment:• Topical steroids

– Pred Forte QID-q2H– Durezol BID-QID– Lotemax QID

• Topical anti-viral cover– Viroptic (trifluridine 1%) QID– Zirgan (ganciclovir 0.15%) TID

• Topical cyclosporin (Restasis), AT’s, ung’s to facilitate epithelial healing if ulceration is present


• Neurotrophic Keratitis:– Keratopathy occurs from loss of trigeminal

innervation to the cornea resulting in complete or partial anaesthesia

– The cornea is numb so the pt doesn’t blink

– Sx’s:• Irritation/burning/FB sensation• Redness• Tearing• Decreased vision

Neurotrophic Keratopathy• Signs:–Decreased corneal sensation***– Interpalpebral SPK– Persistent epithelial defects in which the

epithelium at the edge of the lesion appears rolled and thickened, and is poorly attached

–Advanced cases may have sterile ulceration, keratitis, and/or corneal melt • Pt may be surprisingly asymptomatic**

Neurotrophic Keratopathy

• Tx:– Find out the cause–D/C any meds that may be responsible– Lubricate, lubricate, lubricate***• Preservative free AT’s, gels, and ung’s q1h-QID

– Topical Ab drops and/or ung (Polytrim QID, etc)

– Taping the eyelids at night to ensure adequate closure

– In severe cases:• Patching, tarsorrhaphy, Botox to induce ptosis

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Neurotrophic Keratopathy

• Tx:–Healing an ulcer that won’t heal

1. Autologous serum2. Prokera– Amniotic membrane in a CL skirt

1. Also could use a scleral lens

Autologous Serum

1. Draw 40cc of blood through venipuncture2. Centrifuge for 5 minutes @ 1500 rpm3. Centrifuging will divide the blood into its

separate components4. Place 1cc of serum in each bottle5. Add 4cc of saline to make a concentration of

20% serum eye drops6. 20% serum eye drop concentration

Herpes Simplex Epithelial Keratitis

• My Regimen:– Zirgan 5x/day until the ulcer heals, then

3x/day for one week–Oral Valtrex 500 mg 3x/day for 7-10 days–Artificial tears

– L-Lysine 2 grams daily?–Debride the ulcer?

• RTC 1 day, 4 days, 7 days


• Prophylactic Treatment:– Reduces the rate of recurrence of epithelial

and stromal keratitis by ≈ 50%• Acyclovir 400 mg BID• Valtrex 500 mg QD• Famvir 250 mg QD

• L-lysine 1 gram/day

• Frequent debilitating recurrences, bilateral involvement, or HSV infection in an only eye

Pediatric HSV Keratitis

• pediatric herpes simplex keratitis has an 80% risk of recurrence, a 75% risk of stromal disease, and a 30% rate of misdiagnosis

• •80% of children with herpes simplex keratitis develop scarring, mostly in the central cornea

• –results in the development of astigmatism

• –25% of children have more than 2 D of astigmatism, most of which is irregular

• •consider pediatric HSV when a patient

• Visual Prognosis:– 90% 20/40 or better after 12 years– 3% 20/100 or worse after 12 years

Herpes Simplex

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Case #5

Central Serous Chorioretinopathy (CSR)

• Demographics– 25-50 year old men, stressed/Type A

personalities

• Symptoms– Unilateral, blurred vision

• VA -> usually 20/20 – 20/80– Metamorphopsia

• Signs– Localized serous detachment of the neurosensory

retina in the macula

CSR

Central Serous Chorioretinopathy

• DDx:–Optic disc pit– CNVM

Central Serous Chorioretinopathy

• Med associations:– Steroids

• Nasal sprays, steroid creams, oral, injectable– Ephedra

• Ephedrine & pseudoephedrine

• Treatment:– Observation/lifestyle change– D/C steroid if possible– Possible laser therapy

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Case #6

Plaquenil Toxicity

• Antimalerials:– Chloroquine–Hydroxychloroquine (Plaquenil)

• Now used for RA, SLE, Sjogren’s, etc.

• Toxicity risk is low, but….• Lots of different screening

recommendations have been proposed

Plaquenil Toxicity

• Risk Factors:– Cumulative dose**• 1000 gram cumulative dose for Plaquenil• 6.85 years to reach that

–Daily dose–Age– Liver or kidney dysfunction– Pre-existing retinal disease or maculopathy

Plaquenil Toxicity

• Symptoms:–Asymptomatic early– Paracentral visual field defects affecting

reading– Color vision changes

• Signs:

Progression of Plaquenil maculopathy - early

Progression of Plaquenil maculopathy - moderate

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Progression of Plaquenil maculopathy - advanced Plaquenil Toxicity

• Recommended Screening Guidelines:1. Baseline exam within the first year of

starting Plaquenil• Biomicroscopy exam, 10-2 VF, Fundus photos

–After 5 years, annual screening exams• SD-OCT or• mfERG or• Fundus autofluorescence

2008 2009 2010

2012

Plaquenil Toxicity

• Recommended Screening Guidelines:1. Baseline exam within the first year of starting

Plaquenil• Biomicroscopy exam, 10-2 VF, Fundus photos• SD-OCT or mfERG or fundus autofluorescence

– After 5 years, annual screening exams• Biomicroscopy exam along with 10-2 VF and• SD-OCT or• mfERG or• Fundus autofluorescence

Fundus Autofluorescence & mfERG Plaquenil Toxicity

• Tests not recommended for screening– Fundus photography– Time-domain OCT– FA– Full-field ERG– EOG– Color vision testing–Amsler grid

10/1/18

18

Plaquenil Toxicity

• Treatment:–No medical therapy is available to treat/cure

the toxicity–D/C the med if possible• Work with the PCP

Case #7

Pseudotumor Cerebri

• AKA– Idiopathic intracranial hypertension

• Elevated intracranial pressure– Not caused by tumor, infection, or obstruction of

the ventricular system– Increased production vs. decreased absorption

• Etiology:– Idiopathic (young, obese females)– Medications

• Oral contraceptives, Tetracyclines, too much vitamin A– Trauma

Pseudotumor Cerebri

• Symptoms:–HA’s (90%)– Visual disturbances (72%)• Transient visual obscurations (TVO’s)

– Tinnitus (60%)–Diplopia (20%)– Blurred vision–Abnormal color vision–N&V

Pseudotumor Cerebri• Signs– Papilledema – hallmark sign of PTC• Increased intracranial pressure -> slowing axonal

transport -> accumulation of axonal contents in the NFL -> elevated ONH’s• Bilateral disc edema• Blurred disc margins• Obscuration of blood vessels*• Hyperemia of the disc• Venous dilation• Peripapillary hemorrhages & CWS

Pseudotumor Cerebri

• Other signs– Enlarged blind spot– 6th nerve palsy• Tends to subside as treatment is effective

10/1/18

19

Pseudotumor Cerebri

• Diagnosis:– Clean MRI/MRV– Lumbar puncture

• Elevated ICP > 250mmH20 in an obese pt> 200mmH20 in a non-obese pt

• Normal CSF composition

– No other neurological findings• Exception -> 6th nerve palsy

– SVP• Yes -> not Pseudotumor• No -> ?????

Pseudotumor Cerebri

• Treatment:–Weight Loss*• Papilledema resolution with weight loss of 6% of

total body weight–Diamox (acetazolamide)• 500 mg Sequels BID-QID• Taper as the sx’s stabilize

– Lumbar-peritoneal shunt–Optic nerve sheath decompression

Thank you for your attention!

Return to Agenda

7/9/18

1

Nate Lighthizer, O.D., F.A.A.O.Associate Professor

Assistant Dean for Clinical CareDirector of Continuing Education

Chief of Specialty Care ClinicsOklahoma College of Optometry

[email protected]

¨ Beyond (Retina) First¡ History/principles of the OCT¡ What does the normal retinal OCT look like¡ Vitreal disorders¡ Retinal/RPE disorders¡ Choroidal disorders

¨ Glaucoma¡ What does the normal ONH OCT look likeú rNFLú GCA

¡ ONH disorders

¨ 1991: 1s t scientific description of the OCT¡ Huang et al, Science. 1991; 254 (5035): 1178-1181.

¨ Original Founders:¡ David Huang, M.D., PhD¡ Dr. James Fujimoto, PhD¡ Eric Swanson, MS¡ Carmen Puliafito, M.D. ¡ Joel Schulman, M.D.

¨ Introduced commercially in the mid-1990’s

¨ 1995 OCT1 debuted at 100 axial scans per second with a resolution of 20 microns

¨ Stratus OCT – 2002¡ “Time domain”¡ 500 axial scans/second¡ 10 micron resolution

¨ “Spectral-Domain” OCT – 2007¡ “Fourier-Domain”¡ 27,000 – 40,000 axial scans/secondú Analyzes data using a spectrometerú Does not use a moving mirrorú Very fast acquisition speed

6 5 x g r e a t e r a c q u i s i t i o n s p e e d

ú 3-D imaging

*** 3.5 – 6 micron resolution ***

7/9/18

2

¨ Choroid¨ 10 layers of the retina

¡ R P E

¡ P h o t o r e c e p t o r s

¡ E L M

¡ O u t e r n u c l e a r l a y e r

¡ O u t e r p l e x i f o r m l a y e r

¡ I n n e r n u c l e a r l a y e r

¡ I n n e r p l e x i f o r m l a y e r

¡ G a n g l i o n c e l l l a y e r

¡ N e r v e f i b e r l a y e r

¡ I L M

¨ Vitreous

Vitreous

RPE

Neuro-Sensory Retina

Choroid

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3

¨ Unilateral, decreased vision ¡ Often in 60-80 year old women¡ Anyone w/ a history of trauma

¨ Symptoms:¡ Decreased vision, metamorphopsiaú 20/200 for full thickness holes

¨ Signs:¡ Red hole in the macula¡ (+) Watzke-Allen sign

¨ Stages¡ Stage 1a -> impending hole. Normal foveal

depression with yellow spot/dot in fovea.¡ Stage 1b -> Abnormal foveal depression with yellow

ring.

Stage 1b macular hole

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4

¨ Stages¡ Stage 2 -> Small full-thickness hole. 20/80 - 20/400.¡ Stage 3 -> Full-thickness hole w/ cuff of SRF. No

PVD¡ Stage 4 -> Full-thickness hole with cuff of SRF, with

complete PVD.

Stage 2 macular hole

¨ Stages¡ Stage 2 -> Small full-thickness hole. 20/80 - 20/400.¡ Stage 3 -> Full-thickness hole w/ cuff of SRF. No

PVD¡ Stage 4 -> Full-thickness hole with cuff of SRF, with

complete PVD.

Stage 3Macular hole

Stage 4 macular hole →

Small FTMH w/o tractionMedium FTMH w/o traction

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5

Large FTMH with traction

> 400 microns

¨ Treatment:¡ Stage 2 holes or beyond (full thickness macular holes)¡ Vision 20/40 or worse¡ How long has the hole been there???

¡ Vitrectomy & membrane peel¡ Face down???

¨ Prognosis:¡ 20/40 or better in up to 65% of cases

¨ Treatment:¡ Stage 2 holes or beyond (full thickness macular holes)¡ Vision 20/40 or worse¡ How long has the hole been there???

¡ Vitrectomy & membrane peel¡ Face down???

¨ Prognosis:¡ 20/40 or better in up to 65% of cases

¨ “Partial thickness macular holes”¨ Aborted macular holes

¨ “Upside down anvil” “anvil-like”¨ VA -> usually 20/40 or better¨ 4 characteristics

1 . Irregular foveal contour2 . Break in inner fovea3 . Intraretinal split4 . Intact foveal photoreceptors

¨ “Partial thickness macular holes”¨ Aborted macular holes

¨ “Upside down anvil” “anvil-like”¨ VA -> usually 20/40 or better¨ 4 characteristics

1 . Irregular foveal contour2 . Break in inner fovea3 . Intraretinal split4 . Intact foveal photoreceptors

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¨ “False hole”¨ Simulates macular hole w/o actual tissue

dehiscence ¨ Full thickness retinal tissue is still present

¡ Not an anvil

¨ VA ¡ Usually 20/20 – 20/30 unless significant ERM is

present

Vitreous

RPE


Choroid

7/9/18

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Oklahoma College of Optomet

OSODMacula Thickness : Macular Cube 512x128Signal Strength:

Exam Time:Exam Date:

Technician:Gender:DOB:ID:

Name:

7/10

9:42 AM6/25/2015

resident,Female9/22/195121674

Guevara, Viola

Serial Number: 5000-3846

Overlay: ILM - RPE Transparency: 50 %

ILM-RPE Thickness (µm)

ILM - RPE

ILM

RPE

29210.5227ILM - RPE

CubeAverage

Thickness(µm)

CubeVolume(mm³)

CentralSubfield

Thickness(µm)

Fovea: 282, 65

Doctor's SignatureSW Ver: 7.5.0.56Copyright 2014Carl Zeiss Meditec, IncAll Rights Reserved

Page 1 of 1

Comments





Name:

7/10

10:36 AM10/21/2015


Guevara, Viola




ILM - RPE

ILM

RPE

33712.1253ILM - RPE

CubeAverage

Thickness(µm)

CubeVolume(mm³)

CentralSubfield

Thickness(µm)

Fovea: 292, 62


Page 1 of 1

Comments

7/9/18

8





Name:

7/10

10:36 AM10/21/2015


Guevara, Viola




ILM - RPE

ILM

RPE

33712.1253ILM - RPE

CubeAverage

Thickness(µm)

CubeVolume(mm³)

CentralSubfield

Thickness(µm)

Fovea: 292, 62


Page 1 of 1

Comments

¨ Demographics¡ 25-50 year old men, stressed/Type A personalities

¨ Symptoms¡ Unilateral, blurred visionú VA -> usually 20/20 –20/80

¡ Metamorphopsia¨ Signs

¡ Localized serous detachment of the neurosensoryretina in the macula

¨ DDx:¡ Optic disc pit¡ CNVM

¨ Med associations:¡ Steroidsú Nasal sprays, steroid creams, oral, injectable

¡ Ephedraú Ephedrine & pseudoephedrine

¨ Treatment:¡ Observation/lifestyle change¡ D/C steroid if possible¡ Possible laser therapy

¨ Med associations:¡ Steroidsú Nasal sprays, steroid creams, oral, injectable

¡ Ephedraú Ephedrine & pseudoephedrine

¨ Treatment:¡ Observation/lifestyle change¡ D/C steroid if possible¡ Possible laser therapy

7/9/18

9

¨ Antimalerials:¡ Chloroquine¡ Hydroxychloroquine (Plaquenil)

¨ Now used for RA, SLE, Sjogren’s, etc.

¨ Toxicity risk is low, but….¨ Lots of different screening recommendations

have been proposed

¨ Risk Factors:¡ Cumulative dose**ú 1000 gram cumulative dose for Plaquenilú 6.85 years to reach that

¡ Daily dose¡ Age¡ Liver or kidney dysfunction¡ Pre-existing retinal disease or maculopathy

¨ Symptoms:¡ Asymptomatic early¡ Paracentral visual field defects affecting reading¡ Color vision changes

¨ Signs:

OD OS

7/9/18

10

¨ Recommended Screening Guidelines:1 . Baseline exam within the first year of starting

Plaquenilú Biomicroscopy exam, 10-2 VF, Fundus photos, OCT

¡ After 5 years, annual screening examsú SD-OCT orú mfERG orú Fundus autofluorescence

2008 2009 2010

2012

OD – September 2011

OS – September 2011

¨ Recommended Screening Guidelines:1 . Baseline exam within the first year of starting

Plaquenilú Biomicroscopy exam, 10-2 VF, Fundus photosú SD-OCT or mfERG or fundus autofluorescence

¡ After 5 years, annual screening examsú Biomicroscopy exam along with 10-2 VF andú SD-OCTorú mfERGorú Fundus autofluorescence

7/9/18

11

OD – September 2011

OS – September 2011

¨ Tests not recommended for screening¡ Fundus photography¡ Time-domain OCT¡ FA¡ Full-field ERG¡ EOG¡ Color vision testing¡ Amsler grid

7/9/18

12

¨ Treatment:¡ No medical therapy is available to treat/cure the

toxicity¡ D/C the med if possibleú Work with the PCP

Vitreous

RPE


Choroid

7/9/18

13

7/9/18

14

7/9/18

15

7/9/18

16

OCT Angiography: the Next Chapter in Posterior Imaging

• Images retinal microvasculature without dye injection

• Displays structure and function from a single imaging system

2002: Time Domain OCT

2006: Spectral Domain OCT

2014: OCTA

Structure & Function from One System

A New Approach to Visualizing Blood Flow

o Pa t ie n t B e n e fits

• Reduces patient burden to allow more frequent imaging

• Avoid potential side-effects of fluorescein injection

o C lin ica l B e n e fits

• Faster than a dye-based procedure

• Ultra-high resolution imaging of retinal microvasculature

• 3D visualization: segments retinal vasculature into individual layers

OCT-Angiography

How Does it Work?

7/9/18

17

Principles of OCTA

O C TA u s e s m o t io n c o n t r a s t t o d e t e c t f lo w f r o m O C T d a t a

• R a p id ly a cq u ire s m u lt ip le c ro ss-se c t io n a l im a ge s fro m a s in g le

lo ca t io n o n th e re t in a

• F lo w is th e d iffe re n ce in s ign a l b e tw e e n tw o se q u e n t ia l B -sca n s

Difference of Two OCT B-scans =

Flow Signal (Red) Overlay on OCT B-scan

Enface OCTA Generated from OCTA Volume Data

• Multiple motion-contrast frames create 3D OCTA volume

• Enface visualization of layers obtained by slicing and projecting slabs from 3D OCTA data

Deep Plexus (INL –OPL)

Superficial Plexus (ILM –IPL)Outer Retinal Zone (ONL –BM)

Choroid Capillaris

7/9/18

18

7/9/18

19

In d ic a tio n s :

A M D – d ry v s . w e t

D ia b e tic s -is th e re n e o ?

is th e ir n o n -p e rfu s io n (c a p illa ry d ro p o u t)?

V e in O c c lu s io n s

G la u c o m a p a tie n ts

n e rv e p e rfu s io n ? Nate Lighthizer, O.D., F.A.A.O.Associate Professor

Assistant Dean for Clinical CareDirector of Continuing Education

Chief of Specialty Care ClinicsOklahoma College of Optometry

[email protected]

Return to Agenda

2/16/17

1

Nathan Lighthizer, O.D., F.A.A.O.Assistant Professor

Chief of Specialty Care ClinicsChief of Electrodiagnostics Clinic

Northeastern State University Oklahoma College of Optometry

Tahlequah, [email protected]

§ Definition§ Etiology§ Signs/Symptoms§ Classification/Diagnosis§ Systemic Associations§ Lab Testing§ Treatment§ Follow-up

§ Uveitis:§ Generic, broad term referring to any

inflammation of the uvea (iris, ciliary body, and choroid)§ More precise terms include iritis and

iridocyclitis§ The inciting event -> release of chemotactic

factors/mediators that increase vascular permeability -> breakdown of the blood-aqueous barrier -> macrophages/lymphocytes/proteins = CELLS & FLARE

1 2 3 4

0% 0%0%0%

1. Trauma2. Drug abuse3. Infectious4. Autoimmune

disease

0

5

§ 3 main underlying causes are:

� reaction to trauma� autoimmune§ response to autoantigens

� response to infectious agent

¨ Patient symptoms are often very similar with all of the various etiologies¡ Can be some differences

¨ Anterior uveitis¡ pain, redness, photophobia

¨ Intermediate/Posterior uveitis¡ Floaters, mildly decreased vision from CME, etc

2/16/17

2

1 2 3

0% 0%0%

1. More symptomatic than acute uveitic pts

2. Less symptomatic3. Symptoms are

fairly equal between the two

0

5

¨ Common patient symptoms include:¡ pain – ciliary spasm¡ red eye – ciliary flush¡ tearing ¡ photophobia¡ blurred vision¡ Pupillary miosis

¨ Critical signs are cells and flare in the anterior chamber¡ Cells are lymphocytes or

macrophages and indicate active inflammation in the iris and ciliary body.

¡ Flare is a result of protein leakage.

¨ Keratic precipitates¡ collections of

inflammatory cells deposited on the endothelial surface of the cornea from the aqueous humor

¡ fresh KP’s -> white and round

¡ older KP’s -> pigmented or faded.

¡ Document size, color, distribution, and # of KP’s

¨ Accumulation of cells on the iris are referred to as iris nodules. Two types exist: ¡ Koeppe nodules are

found on the pupillaryborder and Busaccanodules are on the anterior surface.

¡ Nodules on the pupillaryborder may result in posterior synechiaebetween the iris and lens.

1 2 3

0% 0%0%

1. Higher2. Lower3. No change

0

5

2/16/17

3

¨ IOP must be monitored initially and at subsequent visits¡ usually a patient with acute uveitis will present

with low pressure likely due to infiltration of the ciliary body and reduced aqueous secretion

¡ the pressure may be elevated secondary to inflammation in the trabecular meshwork or by blockage of the angle by cells and debris

¡ in addition treatment with corticosteroids can result in glaucoma due to the patient being a steroid responder.

¨ Every patient with uveitis should have a DFE:¡ posterior inflammation (vitritis) may be

overlooked in a diagnosed case of anterior uveitis

¡ Macular area should be evaluated especially if there is any decrease in acuityú CME frequently results from anterior uveitis

and should be suspected if decreased VAú Epiretinal membranes can form and distort

the macular tissue.

1 2 3 4 5

0% 0% 0%0%0%

1. Band keratopathy2. Cataracts3. Glaucoma4. 2 &35. All of the above

0

5

¨ Cataract is a common complication of long-standing uveitis as well as chronic steroid therapy¡ most cataracts are

PSC, but cortical opacities may also be seen.

¨ CME¨ Glaucoma

¨ Band keratopathy is also seen in chronic conditions such as uveitis¡ it is the deposition of

calcium at the level of Bowman’s and in severe cases requires chelationtherapy or mechanical scraping.

§ Classification is the key to the proper diagnosis and management of the uveiticpatient

§ Most common classifications§ Anterior vs. Intermediate vs. Posterior vs. Panuveitis§ Acute vs. Chronic§ Granulomatous vs. Non-granulomatous§ Infectious vs. Autoimmune

2/16/17

4

§ 4 main questions we need answered§ Where is the inflammation located?§ Is disease acute or chronic?§ Granulomatous or non-

granulomatous?§ Unilateral or bilateral?

¨ Secondary Questions:¡ Demographics of the patient¡ Has this happened before? If so did it

respond to treatment?¡ Lung /breathing problems?¡ Rashes/skin problems?¡ Joint problems?¡ Any other systemic/autoimmune diseases?

¨ 4 answered questions -> easier diagnosis and management¡ Anterior uveitis – etiology ???¡ Acute, unilateral, non-granulomatous anterior

uveitis = Idiopathic, HLA-B27 uveitis, herpetic¡ Chronic, bilateral, granulomatous panuveitis =

sarcoidosis, syphilis, TB

¨ Most commonly encountered uveitic causes:1. Traumatic2. Post-surgical3. Anterior Idiopathic4. HLA-B27 associated uveitis5. JIA associated uveitis6. Fuch’s heterochromic iridocyclitis7. Posner-Schlossman syndrome8. Herpetic anterior uveitis9. Pars Planitis10. TB/Sarcoid/Syphilis

¨ After classification, 3 most common groups of uveitis include:

1. Acute, unilateral (or bilateral), non-granulomatousanterior uveitis

ú Idiopathic, HLA-B27, Herpetic, Behcet’s2. Chronic, bilateral (or unilateral), non-

granulomatous anterior uveitisú JIA, Fuch’s Heterochromic, Idiopathic, Herpetic

3. Chronic, bilateral (or unilateral), granulomatousanterior uveitis

ú TB, Sarcoid, Syphilis, VKH1 2 3 4

0% 0%0%0%

1) AnkylosingSpondylitis

2) Rheumatoid Arthritis

3) Reactive Arthritis (Reiter’s Syndrome)

4) Inflammatory Bowel Disease

0

5

2/16/17

5

1 2 3 4

0% 0%0%0%0

5

1. HLA-B272. ESR3. Chest X-ray4. Sacro-Iliac joint

X-ray

¨ Most common group¡ Idiopathic – most common cause of anterior uveitis¡ HLA-B27 – 2nd most common cause of anterior

uveitis – nearly 20 - 50% of acute anterior uveitis pts are HLA-B27+ú Ankylosing Spondylitisú Reactive Arthritis (Reiter’s syndrome)ú Psoriatic Arthritisú Inflammatory Bowel Disease

¡ Herpetic¡ Behcet’s

¨ Acute, rapid onset of unilateral pain and intense photophobia

¨ Moderate to severe inflammatory reaction¡ 3-4+ cells¡ Hypopyon¡ Fibrin meshwork¡ Plasmoid aqueous

¨ Aggressive treatment important¡ Average tx time = 6-10 weeks

¨ Ankylosing Spondylitis¡ Low back pain¡ Diagnosis:ú Abnormal S-I joint X-rayú Increased ESR

¡ Treatment:ú Exerciseú Oral NSAID’s

¨ Reactive Arthritis (Reiter’s syndrome)¡ “Can’t see, can’t pee, can’t climb a tree”

ú Conjunctivitis/Uveitisú Urethritisú Arthritis – lower joints

¡ Dermal skin lesions¡ Diagnosis:

ú Elevated ESR¡ Treatment:

ú NSAIDS

¨ Inflammatory Bowel Syndrome¡ Ulcerative Colitis¡ Crohn’s Disease

ú Stomach problems – diarrhea, bloody stools¡ GI referral – tx with diet change and

immunosuppresives

¨ Psoriac Arthritis¡ Arthritis upper extremities ¡ Characteristic skin lesions

2/16/17

6

¨ HSV¡ H/O unilateral red eye¡ Corneal scarring¡ Active corneal disease¡ IOP increase & iris atrophy

¨ HZO¡ Characteristic skin lesions¡ Iris atrophy

1 2 3 4

0% 0%0%0%

1. Corneal Ulcer2. Cataract3. Band

Keratopathy4. Glaucoma

0

5

1 2 3 4 5 6

0% 0% 0%0%0%0%

1. ANA (+), RF (+)2. ANA (+), RF (-)3. ANA (-), RF (+)4. ANA (-), RF (-)5. HLA-B27 (+)6. HLA-B27 (-)

0

5

¨ Most common cause¡ Juvenile Idiopathic Arthritis (JIA)

ú 80% of pediatric uveitis cases are associated with JIA

ú Slow, chronic onset; mild sx’s, many chronic signsú ANA (+) triples the risk of uveitis – base f/u’s on

thisú RF (-)ú Tx: NSAID’s, steroids, immunosuppresives

¨ ANA – very non-specific test¡ Used to confirm an autoimmune collagen

vascular diseaseú Lupus and JIAú Weaker associations: Sjogren’s, RA,

scleroderma, AS, MG¡ 15% of normals have a mildly elevated ANA

(diabetics, elderly women)

¨ RF¡ 80% of RA pts are seropositive¡ Most often JIA patients are RF negativeú ANA (+) and RF (-) -> significantly

increased risk of uveitis in a suspected JIA patient

2/16/17

7

¨ More common causes¡ Fuch’s Heterochromic Iridocyclitis

ú Low-grade chronic uveitis with iris heterochromiaú Usually unilateral – cataract & glaucomaú Uveitic eye is usually lighter in color

¡ Idiopathic¡ Herpetic

1 2 3 4 5 6

0% 0% 0%0%0%0%

1. PPD & chest X-ray

2. VDRL & FTA-ABS

3. HLA-B274. ACE5. 1, 2, & 46. All of the above0

5

¨ Most common causes¡ Sarcoid¡ Syphilis¡ TB

¨ Systemic granulomatous inflammation -> unknown etiology – Young, black, females¡ Pulmonary – 95%¡ Ocular – 60-70%¡ Skin

¨ Diagnosis¡ Serum

ú ACE, lysozyme, calcium¡ Chest X-ray, Gallium scan, biopsy of granulomas

¨ Treatment¡ Immune suppression

1 2 3 4

0% 0%0%0%0

5

1. PPD2. FTA-ABS3. VDRL4. ACE

¨ Infection with spirochete T. pallidum¡ Primary stage – Chancre¡ Secondary stage – rash palms of hands/soles of feet

ú Most ocular involvement¡ Latent and Tertiary Stage

¨ Diagnosis:¡ RPR or VDRL – general non-treponemal tests¡ FTA-ABS or MHA-TP – specific treponemal tests

¨ Treatment:¡ Penicillin

2/16/17

8

¨ Infectious disease caused by Mycobacterium tuberculosis¡ Very rare¡ Exposure/Cough/Pulmonary involvement¡ Granulomatous ant uveitis, Choroiditis, phlyctenular

keratoconjunctivitis¨ Diagnosis

¡ PPD – not useful in uveitis patients¡ Chest X-ray/Sputum culture

¨ Treatment¡ Isoniazid, Rifampicin, Ethambutol, Pyrazinamide

§ If a patient presents with a uveitis that is:§ First episode§ Unilateral§ Non-granulomatous§ Mild->moderately severe AND§ Fairly good health= no further work-up required

¨ If the uveitis is:¡ Recurrent¡ Bilateral¡ Severe¡ Granulomatous OR¡ Resistant to standard treatment; ¡ AND History does NOT point to a specific condition= Non-specific baseline eval§ Work-up:

- CBC - Lyme titer (depending on what area of the U.S.)- ESR/CRP - PPD/anergy panel and Chest X-ray- ANA/RF - RPR or VDRL and FTA-ABS or MHA-TP- HLA-B27 - ACE

¨ CBC - $9 - 12¨ ESR - $5 - 7¨ CRP - $18 - 24¨ HLA-B27 - $36 - 49¨ ANA - $15 - 21¨ RF - $8 – 11¨ ACE - $20 - 28¨ VDRL/RPR - $6 -8

¨ FTA-ABS/MHA-TP -$18 - 25

¨ Lyme titer - $24 – 32¨ Chest X-ray - $75 –

250

¨ Total = $216 - 443

¨ If the history, symptoms, and/or signs point strongly to a certain etiology, then the work-up should be tailored accordingly¡ that is, the lab tests should be tailored for the

condition suspected ú Ex: Black female with a chronic, granulomatous uveitis

- likely chest x-ray, serum ACE and/or lysozyme, PPD, gallium scan of head and neck; consider biopsy of any skin or conjunctival nodule.

¨ Treat the disease properly¡ Minimize complications of the disease itself¡ Minimize complications of the treatment

¨ 2 main drugs/drops¡ Cycloplegics¡ Topical Corticosteroids

2/16/17

9

¨ Cycloplegia:¡ used for reduction of pain, ¡ break/prevent the formation of

posterior synechiae¡ also functions in the reduction of

inflammation

¨ Common cycloplegic agents include:¡ cyclopentolate 1-2% tid for mild-to-moderate,¡ homatropine 5% or ¡ scopolamine 0.25% or ¡ atropine 1% bid-tid for moderate-to-severe

inflammation¨ most common is the use of Homatropine 5% bid

¨ Steroids: necessary for the treatment of active inflammation

¨ Most commonly used:¡ Prednisolone acetate 1% (Pred Forte 1%) ¡ Prednisolone phosphate???¡ Loteprednol etabonate 0.5% (Lotemax)

ú Drop, gel, ung

¨ Durezol (difluprednate ophthalmic emulsion) 0.05%¡ Dosing QID¡ Thought to be as potent or even more potent when

compared to Pred Forte q2h¡ Minimal to no shaking of the bottle¡ No BAK

¨ Topical administration is most common though periocular injections and systemic meds are useful for posterior uveitis and difficult cases

¨ Dosing:¡ Pred Forte q1h or q2h¡ Durezol QID

¡ Lotemax ung qhs

¨ NOTE: it is crucial to taper your steroid treatment!¡ You will have a rebound inflammation if you simply

remove your patient from their steroids…

¡ How long???

¨ Treat beyond the cell & flare¡ 5-7 days

2/16/17

10

1. Remember the classifications.2. Determine if there is corneal involvement &

check IOP.3. Determine the severity.4. Is this a chronic problem?5. Treat strongly.

Return to Agenda

4/13/18

1

Nate Lighthizer, O.D., F.A.A.OAssociate Professor, NSUOCO

Assistant Dean for Clinical Care ServicesDirector of CE

Chief of Specialty Care Clinics

¨ What is electrodiagnostics testing?¨ Visual Pathway – Basic Understanding

¨ VEP¨ pERG¨ ffERG¨ mfERG

¨ Clinical Cases

¨ AKA Visually Evoked Response (VER)¡ Flash vs. Pattern

¨ Measures the entire visual pathway¡ From cornea to occipital lobe

¨ 3 electrodes¡ Ground¡ Reference¡ Measuring -> occipital lobe

ú 1” above inion

Reference Ground Active

VEP Electrodes

LATENCY (ms) AMPLITUDE (µv)

• Amplitude usually translates to the amount of axons conducting along the visual pathway

• Latency usually translates to the myelin status of the visual pathway

VEP

¨ Many optic nerve diseases are asymptomatic because central vision is not affected until late in the disease1

¨ Diagnosis and management of optic nerve disorders are often based on structural or subjective visual field tests2

1 Glaucoma. American Optometric Association. www.aoa.org2 Prata, Tiago MD, G. De Moraes MD, J. Liebmann MD, R. Ritch, C. Tello MD. (2009). Diagnostic Ability of Fast Transient Visual Evoked Potential

for Glaucoma Assessment [Poster & Abstract] American Academy of Ophthalmology. 128

VEP is an objective, functional test that can help discriminate between healthy and glaucomatous eyes2

http://www.aoa.org/

4/13/18

2

Structure FunctionFundus Photograph

(Subjective)Visual Field(Subjective)

Structure FunctionOptical Coherence Tomography

(Objective)ERG & VEP(Objective)






dead Suffering Alive

Glaucoma

VEP

OCTHRTGDX

Effect of epigallocatechin-gallate on inner retinal function in ocular hypertension and glaucoma: a short-term study by pattern electroretinogram. Graefes Arch Clin Exp Ophthalmol. 2009 Sep;247(9):1223-33. Epub 2009 Mar 17.

Alive

Glaucoma

VEP

OCTHRTGDX

Alivedead







http://www.aoa.org/

http://www.aoa.org/

4/13/18

3

¨ Low contrast testing demonstrates degradation of magnocellular pathways¡ An early indication of glaucoma

¨ High contrast testing demonstrates degradation of parvocellular pathways ¡ An early indicator of central vision loss and issues

caused by problems before signal reaches optic nerve

**patient should be tested with best corrected vision**

ASSESSMENT OF NEURO-VISUAL FUNCTION ASSESSMENT OF NEURO-VISUAL FUNCTION


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¨ VEP is an objective, functional test that can help discriminate between healthy and diseased eyes

¨ Indications:¡ Glaucoma¡ MS/Optic neuritis¡ Optic neuropathies¡ Unexplained vision loss¡ Transient vision loss¡ Visual field defects¡ Amblyopia/Strabismus¡ Traumatic brain injury

¨ ERG’s are electrical signals that are a measure of the electrophysiological activity at the retina¡ ***Mid-retinal layers, ganglion cell layer, and nerve fiber

layer***

¨ Objectively measures retinal function**

¨ ERG’s can help improve sensitivity and specificity in diagnosing optic neuropathies and maculopathies like glaucoma and macular degeneration when used in conjunction with other tests

¨ Can also help the clinician differentiate between retinal and optic nerve disorders when used in conjunction with Visual Evoked Potential (VEP).

1. Concentric Stimulus Fields¡ Drug toxicity¡ Diabetic macular edema¡ AMD

2. Contrast Sensitivity¡ Glaucoma¡ Diabetic retinopathy

1. Concentric Stimulus Fields¡ Stimulus delivered at 15 flips/second¡ BCVA

ú Pt should be properly refracted for 24”¡ 24” testing distance¡ 100% contrast

¡ Right eye (OD) then Left Eye (OS)ú 25 seconds at 24 degreesú 25 seconds at 16 degrees

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2. Contrast Sensitivity¡ Stimulus delivered at 15 flips/second¡ BCVA

ú Pt should be properly refracted for 24”¡ 24” testing distance¡ 85% and 15%

¡ Right eye (OD) then Left Eye (OS)ú 25 seconds at High Contrast (Hc)ú 25 seconds at Low Contrast (Lc)

“In patients who are glaucoma suspects, pERG signal anticipates an equivalent loss of OCT signal by several years (as many as 8 years).Invest Ophthalmol Vis Sci. 2013;54:2346-2352) DOI:10.1167/iovs.12-11026

VEP ERG OCT VF

% of cell loss

0% 100%

• ERG shown to detect glaucoma while cells are alive, up to 8 years before OCT. (IOVS, 2013; Mar;54(3): 2346-52)• VEP may be able to detect glaucoma slightly earlier than ERG as the disease is shown to affect LGN before retina

(PNAS: 2010 Mar)• SAP requires approx 30% (6% to 57% range) cell death to register peripheral vision loss (Ophthalmology: 2013

Apr;120(4):736-44)• OCT detects glaucoma approximately 2 to 3 years before VF with about 15% RNFL loss (Est)

DiseaseCCTIOP

Healthy Cells

You Are Missing a Big Valuable Piece of the Puzzle!

Sick but Viable

dead Suffering Alive

Glaucoma

VEP

OCTHRTGDX


Alive

Glaucoma

VEP

OCTHRTGDX

Alivedead


“In patients who are glaucoma suspects, pERG signal anticipates an equivalent loss of OCT signal by several years (as many as 8 years).Invest Ophthalmol Vis Sci. 2013;54:2346-2352) DOI:10.1167/iovs.12-11026

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¨ Glaucoma¨ Optic Neuropathies ¨ Maculopathies

¡ AMD¡ Diabetic retinopathy¡ Diabetic macular edema¡ Macular toxicity

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Magnitude D

Value as a Prognostic Indication of Progression of OHT to Glaucoma

Visual Field and FDT: 25-50% sensitivity

OCT: approximately 70%

PERG: 77%

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Normal PERG Response

Magnitude, MagnitudeD and MagD/Mag Ratio are colorized.

Green indicates within normal limits Yellow indicates values are borderlineRed indicates outside normal limits

3 Quick Steps To Report InterpretationSignal Quality – Look for a green signal

Sinusoidal Peaks – Look for 3 humps

PERG Report – Data Table

Magnitude (uV) is defined as the strength of the patient’s response at a reversal rate of 15 reversals per second.

Larger magnitudes are typically generated from normal eyes. Smaller magnitudes typically indicate pathology.

As the contrast level drops or the stimulus size decreases, the magnitude will typically decrease.


MagnitudeD averages the signal within the 25 second test time and takes into account the magnitude strength and the phase variability throughout the test.

In a healthy patient, the phase response tends to be consistent throughout the test. In this case, MagD is close in value to Mag.

In a patient with disease, the phase response tends to be inconsistent throughout the test -MagD will be significantly reduced in comparison with Mag.


MagD/Mag Ratio is the most repeatable measurement test-over-test. The closer the ratio is to 1.0, the lower the phase variability throughout the test, and the healthier the patient’s response. Variability in phase may indicate pathology.

MagD/Mag ratio can used to monitor patients over time.

Data Table

SNR - Signal to Noise Ratio shows how strong the signal is at 15Hz compared to noise at 15Hz. Larger numbers indicate stronger PERG signals compared to the noise.

SNR values like 5, 15, >20 show strong PERG response. Numbers less than 2 are typical of a weak response.

Data Table

Artifacts are caused by blinking or patient movement. They are detected and counted. A high number of artifacts will effect the amount of data that can be analyzed.

The goal is to have a low number of artifacts. We want the patient to be comfortable and blink when necessary, but not excessively. The goal is less than 10. If tests results show Artifacts greater than 10, the test should be repeated.

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Abnormal PERG

Missing 3 humps

Yellow indicates values compared to normal are borderline

Red indicates values are outside normal limits

Stimulus Mini-ganzfeld Photoreceptors & Bipolar

Flicker Electroretinogram(Flicker ERG)

Retinal signal recorded at the

lower lid in response to flash

stimuli of high frequency

¨ Tests the outer retina ¡ Photoreceptors (rod & cones)¡ Bipolar cells

¨ Test of overall retinal functioning¡ May not pick up small retinal issues

¨ Flash flicker stimulus

BCVA

2-3°

OCT 12° mfERG21°

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Flicker ERG

Full Field

¨ Tests the outer retina ¡ Photoreceptors (rod & cones)¡ Bipolar cells

¨ Test of overall retinal functioning¡ May not pick up small retinal issues

¨ Flash flicker stimulus

¨ ffERG indications:¡ DM & diabetic retinopathy

ú Monitoring progressionú Monitoring improvement with treatment

¡ Retinal dystrophies/diseaseú Rod/cone problems ú RP

¡ Pt symptoms:ú Color vision issuesú VF defectsú Decreased visionú Unexplained decreased vision

¡ Testing retinal function with significant media opacities¡ Indicator for prognosis following cataract surgery

ú Is the retina functioning well or not?

ERG for Early Detection

ERG for Evaluating Retinal Dysfunction Flicker ERG for Treatment Evaluation

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Flicker ERG ReproducibilityICC in Healthy eyes

Protocol Parameter ICC

Flicker ERG Magnitude 0.93Phase 0.98

Wills Eye Hospital, ARVO 2016

Retinal Evaluation in Eyes with CRVO

ERG vs FA : Predictive value of Vascularization

FA:52%ERG:94% Flicker ERG is a good predictor of ischemia

Flicker ERG can be used to evaluate DR

Flicker ERG can be used to monitor patients and evaluate referals

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Healthy Dysfunction

Flicker ERG Report

Magnitude is the cone/bipolar signal strength

Phase is the timing of the cone/bipolar response

Magnitude and Phase Variancerepresent the consistency of the strength and speed of the signal

respectively

Healthy Dysfunction

Flicker ERG Report

Magnitude area is the cone/bipolar combined signal strength of the 6

luminance levels

Phase area is the cone/bipolar combined

signal timing of the 6 luminance levels

Macular Function Evaluation in Eyes Without Cataracts

Ganzfeld

1. Ratanapakorn T, Patarakittam T, Sinawat S, Sanguansak T, Bhoomibunchoo C, Kaewpanna S, Yospaiboon Y. Effect of cataract on electroretinographic response. J Med Assoc Thai. 2010;93:1196-9.

2. Pérez-Salvador García E, Pérez Salvador JL. Variability of electrophysiological readings in mature cataracts. Arch Soc Esp Oftalmol. 2002;77:543-51.

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Macular Function Evaluation in Eyes With Cataracts

Ganzfeld

Cataract

1. Ratanapakorn T, Patarakittam T, Sinawat S, Sanguansak T, Bhoomibunchoo C, Kaewpanna S, Yospaiboon Y. Effect of cataract on electroretinographic response. J Med Assoc Thai. 2010;93:1196-9.

2. Pérez-Salvador García E, Pérez Salvador JL. Variability of electrophysiological readings in mature cataracts. Arch Soc Esp Oftalmol. 2002;77:543-51.

Macular Function Evaluation in Eyes With Cataracts

Cataract

ISCEV* Recommend using ERG for the evaluation of retinal function in patients with media opacities.

*(International Society of Clinical Electrophysiology of Vision)

iscev.org/standards/proceduresguide.html

VEP FFERG1. Glaucoma & glaucoma

suspects2. Unexplained vision

loss3. Transient vision loss4. Unexplained VF

defects 5. Unreliable VF6. Optic neuropathies7. Optic neuritis/MS8. Amblyopia9. TBI

1. DM & retinopathy2. RP & its variants3. Cone dystrophies

& Rodmonochromat

4. Symptoms:¡ “Night blindness”¡ Restricted

peripheral fields¡ Color vision

deficits¡ Unexplained

decreased vision5. To get an idea of

retinal functioningin a pt with mediaopacity

PERG1. Glaucoma &

glaucoma suspects2. Unexplained VF

defects 3. Unreliable VF4. Optic neuropathies5. Maculopathies

1. AMD2. Diabetic macular

edema3. High risk med use

(Plaquenil)4. Generalized DR

Nate Lighthizer, O.D., F.A.A.OAssociate Professor, NSUOCO

Assistant Dean for Clinical Care ServicesDirector of CE

Chief of Specialty Care Clinics

Return to Agenda

http://iscev.org/standards/proceduresguide.html

Clear as Mud: Managing Glaucoma Suspects in Modern OptometryANDREW KEMP, OD FAAOCLINICAL ASSISTANT PROFESSORCOMMUNITY EYE CLINIC/CEDAR SPRINGS EYE CLINICUNIVERSITY OF HOUSTON COLLEGE OF OPTOMETRY

Disclaimers

Financial disclaimersNone…..

Outline

What are the risk factors for glaucomaHow are these risk factors determined

What new technology can we utilize to evaluate those risk factors

Making the Diagnosis

Must combine many different risk factors, patient information and test results

How risky are each risk factor?

No one data point can make the diagnosis

Prevalence of Glaucoma

Over 3 million people in the US have glaucoma

Over 50% of glaucoma cases are undiagnosed

Access to care concerns

Prevalence of Glaucoma

Ref. nei.nih.gov/eyedata/glaucoma#1

Suspicious Optic Nerve Head

What to look for?Rim Tissue

Thickest to thinnest? Focal notching?

Asymmetry in cup size/rimOverall optic nerve head size/depthCorresponding nerve fiber layer defects?Alterations to the vasculature that imply loss of rim tissue

Ok So the Nerve Looks Suspicious….How Concerned Are You?

Look at the patient as a wholeExam findings Risk factors Life expectancyQuality of Life

Decide on additional testing as necessary and appropriate follow-up

But First…Remember…

“There is very little truth in our knowledge of glaucoma, or medicine in general for that matter. Even the accepted evidence of fact is highly suspect.”

Harold Quigley, MD

How is someone at risk for glaucoma?

Ocular hypertensionAgeThin superior or inferior neuroretinal rim

Especially temporally

Follows or does not follow ISNT rule

Increased vertical C/D ratioDefects in the retinal nerve fiber layerFamily history Race (Hispanic, African descent, Asian) Vascular diseaseTrauma

Smoking/AlcoholDiabetesCorneal thicknessCorneal hysteresisMedicationsDisc hemorrhageVisual field defectsSleep apneaMigraines

How Do We Know These Are Risks For Glaucoma?

Randomized Clinical TrialsThese are the basis for all we know and is our attempt to find the “truth”

Must understand limitations and know that the “truth” is very hard to find. It is very hard to limit human bias and to establish proper controls

Glaucoma Truths?

Ocular Hypertension Treatment Study (OHTS)Early Manifest Glaucoma Trial (EMGT)Advanced Glaucoma Intervention Study (AGIS) Collaborative Initial Glaucoma Treatment Study (CIGTS)Rotterdam Study (RS)Diagnostic Innovations in Glaucoma Study (DIGS)

Baltimore Eye Study (BES)Los Angeles Latino Eye Study (LALES)European Glaucoma Prevention Study (EGPS)Collaborative Normal Tension Glaucoma Study (CNTGS)Barbados Eye Study (BBES)

ALL of these studies were finished at least 20 years ago….

Glaucoma Risk FactorsSTUDY AGE African

DescentHISPANIC ASIAN FAMILY

HXDISC HEME

MYOPIA HYPEROPIA HIGH IOP

SMOKING

OHTS

EMGT

AGIS

CIGTS

RS

DIGS

BES

LALES

EGPS

CNTGS

Glaucoma Risk Factor - Age

Yes! It is a risk factorThe age at which you are at risk depends on race

Age 60 AA 4% prevalenceAge 80 AA 12% prevalence

Either more common with age or more commonly diagnosed

Study of 5000 Greeks over age of 59, 57.1% were undiagnosed

Risk Factor - Age

Frailty increases riskAssessment of patients overall health profile

Besides IOP, age is the most significant risk factor

Life ExpectancyGoal of therapy is to hopefully prevent any visual disability due to glaucoma

May be affected by age of the patient

Per CDCMale approx. 76Female approx. 811 in 4 patients are expected to reach 90 yrsIn 2014, over 72,000 in the US were 100 or more (up 44% since 2000)

Glaucoma Risk Factors

STUDY AGE African Descent

HISPANIC ASIAN FAMILY HX

DISC HEME


SMOKING

OHTS

EMGT

AGIS

CIGTS

RS

DIGS

BES

LALES

EGPS

CNTGS

Risk Factor – African Descent

At least 4-6x greater riskYounger than average at diagnosis (49)

African Americans > 80yrs are at 5x higher risk that AA 50-60

Tend to also have faster progressing glaucomaMore resistant to treatment

Greater in males than femalesMales tend to be more undiagnosed

Risk Factor – African Descent

Larger discs and larger cups

Thinner CCT and lower CH

Native Africans and African Caribbean are at a significantly higher risk

Glaucoma Risk Factors

STUDY AGE African Descent

HISPANIC ASIAN FAMILY HX

DISC HEME


SMOKING

OHTS

EMGT

AGIS

CIGTS

RS

DIGS

BES

LALES

EGPS

CNTGS

Risk Factor - Hispanic

Similar/slightly less risk than African American

LALES confirmed 3-4X risk

Higher risk for both OAG and OHT

High prevalence of cardiovascular disease



HXDISC HEME


SMOKING

OHTS

EMGT

AGIS

CIGTS

RS

DIGS

BES

LALES

EGPS

CNTGS

?

Risk Factor – Asian

Eastern Asians have known anatomical risk for chronic narrow angle glaucoma due to flatter corneas and shallow anterior chambers

50% of ALL glaucoma blindness is from Chinese ethnicity H A, Quigley, Broman AT The Number of

People Glaucoma World Wide in 2010 and 2020



HXDISC HEME


SMOKING

OHTS

EMGT

AGIS

CIGTS

RS

DIGS

BES

LALES

EGPS

CNTGS

Risk Factor – Family History

Limit familial tendency to close blood relatives (parents and siblings)

2x to 10x higher risk with + family history

60% of diagnosed glaucoma cases have a family history of the disease

Genetic Testing in Glaucoma

Genetic testing is becoming more prevalentMyocilin – JOAG and POAGTBK1 – Normal tension glaucomaLOXL1 - Pseudoexfoliation (however not linked to PEX glaucoma…)CYP1B1 – Primary congenital glaucomaPITX2/FOXC1 – Axenfeld-Reiger SyndromeOptineurin and TBK1 – normal tension glaucoma

HOLD UP….these only account for 5% of all glaucoma….



HXDISC HEME


SMOKING

OHTS

EMGT

AGIS

CIGTS

RS

DIGS

BES

LALES

EGPS

CNTGS

Risk Factors – Disc Hemorrhage

World Glaucoma Association states that a disc hemorrhage is one of the most important findings in the diagnosis of glaucoma

NOT diagnostic

More common in NTG

DH presents 2x risk for developing POAG in ocular hypertensives


Typically cross the disc marginPeripapillary portion resolves first

Most commonly inferior/temporal

95% of hemorrhages are within 2 clock hours of an existing retinal nerve fiber layer defect

Can be a sign of progressing glaucoma


Recent study evaluating OHTS data showed a significant portion of disc hemorrhages were missed

84% missed

% of patient in OHTS to develop glaucoma5.2% without DH13.6% with DH – but think of all who didn’t….

The Fast Progressor

Need to monitor for the “yellow liners”

Disc hemorrhages can help



HXDISC HEME


SMOKING

OHTS

EMGT

AGIS

CIGTS

RS

DIGS

BES

LALES

EGPS

CNTGS

Risk Factor - Myopia

Blue Mountain Eye Study: Any amount of myopia increases risk of glaucoma 2-3 times

> 3D of myopia associated with even greater riskBeijing Eye Study - > 6D of MyopiaMyopic anatomy tends to have larger discs and thus larger C/D ratios

Careful with testing reliability of extremely high myopesAlso higher incidence of altered disc appearance

Risk Factor - Myopia

Could be more about axial length and not the degree of myopia

Pigmentary glaucoma higher prevalence in high myopes

Overall – Myopes at 2x higher risk



HXDISC HEME


SMOKING

OHTS

EMGT

AGIS

CIGTS

RS

DIGS

BES

LALES

EGPS

CNTGS

No one cares about hyperopes…. but watch out!

Risk Factor - Hyperopia

Higher Incidence of flatter corneas and more narrow angles

Especially with thick lenses!Use your A-scan if you got it!

Hyperopes tend to have smaller discs and smaller C/Ds so….

Presence of a larger C/D (a +4.00 with a 0.7/0.7) is highly suspicious of glaucoma



HXDISC HEME


SMOKING

OHTS

EMGT

AGIS

CIGTS

RS

DIGS

BES

LALES

EGPS

CNTGS

Glaucoma Risk - IOP

Related to the development and progression of glaucoma but it does not make the diagnosis

Not necessary or sufficient for the development of glaucoma

IOP is not longer under the definition of glaucoma

Only modifiable risk factor

Glaucoma Risk IOP

Risk actually increases at 16 mmHg not 21mmHg

Long term variation is NOT an established riskCircadian variation is NOT an established risk

MAIN risk associated with HIGHER MEAN IOP

Glaucoma risk - IOP

Standard measuring technique – Goldmanntonometry – per the WGA

2.5 mmHg variable intra and 4 interobserverIOP asymmetry is a SIGNIFICANT risk factor

IOP asymmetry of 3 mmHg 6% probability to develop glaucoma>6 mmHg 57% probability Time for gonioscopy!

Glaucoma Risk - IOP

Lui 2012IOP highest at night (however 30% of POAG and normal do not go up at night)

Over 70% of African Americans and 90% of Caucasians presenting with IOP > 25mmHg will NOT have glaucoma – at least initially

Glaucoma Risk - IOP

What is your “Pucker Factor”?

00.10.20.30.40.50.60.70.80.9

1

18 20 22 24 26 28 30 32 34 36

IOPDavanger, Ringwold , etal. The probability of having glaucoma at different IOP levels. ActaOphthal 1991.

What Are You Really Measuring?

???

What Are You Really Measuring?

Goldmann applanation measures the pressure it takes to applanate the cornea

Generally it measures how much pressure it takes to make the internal pressure equal the external pressure (not taking into account corneal hysteresis – more on this later….)

y

1 atm = 760mmHg 20 mmHg

780 mmHg

Where Does Glaucoma Occur?

Comparison of Ocular Ultrasonography and Magnetic Resonance Imaging for Detection of Increased Intracranial Pressure. Patterson D, et.al. Frontiers in Neurology. 2018

Glaucoma RisksSTUDY AGE African


HXDISC HEME


SMOKING

OHTS

EMGT

AGIS

CIGTS

RS

DIGS

BES

LALES

EGPS

CNTGS

Glaucoma Risks - Smoking

How? Nicotine binds hemoglobin reduces oxygen perfusion

No true established risk for POAG

BEWARE!! Sleep apnea + smoking + obesity –DEADLY trio

Glaucoma Risks

STUDY HIGH BP LOW BP DIABETES SLEEP APNEA

ALCOHOL

VISUAL FIELD

C/D MIGRAINE TRAUMA

OHTS

EMGT

AGIS

CIGTS

RSDIGS

BES

LALES

EGPS

CNTGS

Glaucoma Risks – High BP

LALES study showed risk if systolic BP was greater than 160Other studies have actually stated high BP was protective

Think ocular perfusion pressure (related to translaminar pressure theory we just talk about)Ocular perfusion =

2/3(DBP+1/3(SBP-DBP)) – IOP

Glaucoma Risks


ALCOHOL VISUAL FIELD

C/D MIGRAINE TRAUMA

OHTS

EMGT

AGIS

CIGTS

RSDIGS

BES

LALES

EGPS

CNTGS

Glaucoma Risks – Low BP

Yes! Diastolic < 60 and systolic < 90All about optic nerve perfusionHighest risk with the “nocturnal dippers”

Careful with B-blockers!Other things can affect glaucoma in a similar way

Reynaud’sCarotid deficiency/blockage

Consider communicating with PCP/Cardiologist

Glaucoma Risks



C/D MIGRAINE TRAUMA

OHTS

EMGT

AGIS

CIGTS

RSDIGS

BES

LALES

EGPS

CNTGS

Glaucoma Risks - Diabetes

TheoriesDiabetes alters vascular autoregulation – decreasing ocular perfusionHyperglycemia can increase the risk of neuronal injuryHyperglycemia can increase fibronectin in the TM thus increasing impairment to outflow

Overall – Yes it increases glaucoma riskDiabetic complications can make diagnosis of glaucoma very difficult

Glaucoma Risks



C/D MIGRAINE TRAUMA

OHTS

EMGT

AGIS

CIGTS

RSDIGS

BES

LALES

EGPS

CNTGS

?

Glaucoma Risk – Sleep Apnea

20-40% of obstructive sleep apnea (OSA) patients have glaucoma

Many are LTG or NTG

Combined with low BP – DANGEROUS!

Bioavailability of nitric oxide is reduced in patients with sleep apnea

Glaucoma Risks



C/D MIGRAINE TRAUMA

OHTS

EMGT

AGIS

CIGTS

RSDIGS

BES

LALES

EGPS

CNTGS

Glaucoma Risk - Alcohol

Not much of an independent risk

Frequent smoking is associated with frequent alcohol intake

Glaucoma Risks



C/D MIGRAINE TRAUMA

OHTS

EMGT

AGIS

CIGTS

RSDIGS

BES

LALES

EGPS

CNTGS

Glaucoma Risk – Visual Field Defects

Depends – are you pre or post-perimetric in your decision making?

40-50% loss of ganglion cells before first defect in VF

Each study considers different aspects of VF (MD, PSD, VFI**, GHT)

Risk – Visual field

Some studies have some that SWAP perimetry can detect earlier visual field lossFrequency doubling technology has also shown benefits for early detection

Central VF defects in Early Glaucoma

De Moraes CG, et. Al 39.5% of glaucoma suspects had abnormal visual field defects when their 24-2 was normal

Early glaucoma 61.5%

10-2 defects have greater correlation with QoL

SITA Faster adds 10 central points to 24-2 SITA Fast and eliminates false negative testing

Glaucoma Risks



C/D MIGRAINE TRAUMA

OHTS

EMGT

AGIS

CIGTS

RSDIGS

BES

LALES

EGPS

CNTGS

Glaucoma Risk – C/D

World Glaucoma Congress“The main thing ophthalmologists have mastered in documenting optic nerves is the ability to draw concentric circles”

Your patients deserve better!You must be evaluating the neuroretinal rim

Rim ratiosFollows ISNT or notOptic nerve head sizeFocal changes to the nerve

Rim Config Affects C/D Estimation

The ISNT Rule

Only valid in 37% of normal nerves per disc photo assessmentOnly 44% in RNFL measurementsNasal rim was the most variable

Consider the IST rule

Glaucoma Risks - Migraines



C/D MIGRAINE TRAUMA

OHTS

EMGT

AGIS

CIGTS

RSDIGS

BES

LALES

EGPS

CNTGS

Glaucoma Risk - Migraines

Derived from theory that migraines are primarily a vascular disease

Sign of vascular dysregulationVasospasm – inappropriate dilation or constriction may be associated with POAG

Recently review revealed a 1.6x higher risk (especially in younger individuals)

True risk is still unclear

Glaucoma Risks

STUDYc HIGH BP LOW BP DIABETES SLEEP APNEA


C/D MIGRAINE TRAUMA

OHTS

EMGT

AGIS

CIGTS

RSDIGS

BES

LALES

EGPS

CNTGS

Glaucoma Risks - Trauma

ABSOLUTELY!!

Blunt trauma, penetrating trauma****, chronic inflammation, acute blood loss

Signs of trauma – pupil defects, irregular dilation, synechia, iris atrophy, excessive pigment dispersion (grade 3 or greater), lens displacement, hyphema***

Scheie Pigment Grading System

+ 4 pigmentPictures By: Sihota R, Kumar S, Gupta V, et al. Early Predictors of Traumatic Glaucoma After Closed Globe Injury: Trabecular Pigmentation, Widened Angle Recess, and Higher Baseline Intraocular Pressure. Arch Ophthalmol.2008;126(7):921–926.

doi:10.1001/archopht.126.7.92

Cyclodialysis

Glaucoma Risks - Trauma

Need SIGNIFICANT amounts of angle recession to cause IOP issues

> 180 degrees of angle recession

Blunt trauma – higher incidence in the first year or at year 10

Glaucoma Risk - Trauma

Cyclodialysis was only seen in 18% of patients who developed glaucoma after blunt trauma

Was present in 35% of patient of whom did NOT develop glaucomaProtective?

Glaucoma RisksSTUDY MEDICATIONS RNFL CORNEAL THICKNESS

OHTS

EMGT

AGIS

CIGTS

RS

DIGS

BES

LALES

EGPS

CNTGS

?

Glaucoma Risks - Medications

Steroids! – Yes but incidence of steroid response is generally unknown

Estimate – 5% of general population significant% of POAG population (however may only 4-5mmHg increase)Opinion: higher risk with Durezol

Biggest issue is with narrow anglesantihistamines, antidepressants, birth controlMany more


OHTS

EMGT

AGIS

CIGTS

RS

DIGS

BES

LALES

EGPS

CNTGS

Glaucoma Risk – RNFL Defects

Newest and greatest – but be careful! Can add confusionEarly indicator – confirmed by hundreds of studiesHowever, no real consensus on what is clinically significant RNFL lossREMEMBER! Other diseases can cause RNFL defects….

Glaucoma Risks - RNFL Defects

55 yo HMBlur at near and diabetic eye examPMH: Diabetes, HTNMeds: UnknownPOH: NoneBCVA: 20/20 OU IOP: OU 21 mmHgSLE: Unremarkable DFE: ….

Glaucoma Suspect?

Macular Ganglion Cell Complex

In same cases, GCC may precede RNFL loss in glaucomaDiagnostic ability of GCC was comparable to RNFL in NTG and POAGGCC has been shown to be useful in tracking advanced glaucoma with minimal RNFLDifferent OCTs measure this differently


OHTS

EMGT

AGIS

CIGTS

RS

DIGS

BES

LALES

EGPS

CNTGS

But…

But…

Glaucoma Risk - CCT

First established as risk factor in OHTSIncluded patients IOP > 25Avg corneal thickness per OHTS patients

555-588 um535-545 um avg per total population

OHTS stated if you had a thickness < 555um you had an increased risk for developing glaucoma

Glaucoma Risk - CCT

…. But….Hommer etal, Wang etal, Asoaka etal, Mitza etal(all reporting at ARVO 2008) – CCT is NOT related to risk for glaucoma. Ocular rigidity IS which is NOT correlated to CCTMee etal – NO correlation between CCT and VF loss or progression of VF lossMedeiros 2011 – CCT had NO correlation with deforming effects at the level of the optic nerve

“OHTS analysis was flawed and CCT is not a risk of anything. The only thing it does is make our applanation pressure even more flawed – in a way we CANNOT predict

Glaucoma Risk - CCT

Medeiros F, Weinreb, R. Is Corneal Thickness an Independent Risk Factor for Glaucoma? Ophthalmology 2012.

“In conclusion, the results of Brandt et al suggest that the use of CCT correction forumulas for GAT measurements is probably of little values in clinical practice.Instead of attempting to use these formulas, clinicians are probably better off incorporating risk information as provided by validated predictive models for glaucoma development. However, the conclusion that CCT is a true independent risk factor for glaucoma is not validated at this time and requires further investigations.

AT MOST, CCT is related to increased risk in the development of glaucoma in ocular hypertensives

Here is where Corneal Hysteresis Comes in….

What Is Corneal Hysteresis?

Describes how the cornea responds to loading and unloading of an applied force

Not a fixed property

This response is based on the viscoelastic properties of the cornea

What Does Viscoelastic Mean?

Exhibits both elastic and viscous propertiesElastic

The tendency of a material to return to its normal shape after a force is appliedSteel is a very elastic material

Viscosity The measurement of a fluids resistance to flow due to internal friction

What Makes The Cornea Viscoelastic?

Elastic propertiesMostly provided by the collagen fibrils within the corneal stroma and Bowman’s membrane1

Viscous propertiesMostly provided by the extracellular matrix (glycosaminoglycans (GAGs) and proteoglycans (PGs))1

Important in regulating spacing of collagen fibrils and maintaining transparency

What Can Affect Corneal Hysteresis?

Increases corneal hysteresis Decreases corneal hysteresisDiabetes Hypoxia

Aging Corneal hydration

Smoking Corneal ectasia (keratoconus, pelucid, etc.)**

Increased estrogen

Decreased thyroid hormone - maybe

Eye rubbing - maybe

How Is Corneal Hysteresis Measured?

ExtensometryTissue sample of set length is fixed within brackets and a load is applied. The resulting extension of the tissue is a measurement of hysteresis

Corneal tissue

How Is Corneal Hysteresis REALISTICALLY Measured?

Air puff tonometry (Indirect measure)Ocular Response Analyzer – Reichart

Measures peak reflectance of a collated beam aimed at the cornea

Will occur at applanation (x2)

Each peak represents the pressure to applanate the cornea (x2)Difference between these measurements is the implied corneal hysteresisNot a direct measurement

Ocular Response Analyzer

Ocular Response Analyzer

The instrument will provide 3 different measurements

IOPg – the average of the two applanationpressuresIOPcc – IOP calculated based on ???CH – the difference between the first applanationpressure and the second

How Does This Relate To Glaucoma?

Mechanical Theory of GlaucomaThe IOP differential at the lamina cribosa will cause the cribosa to bend backwards

This can cause direct damage to the RGC axons by interrupting axonal flowMechanical damage leads to apoptosis

So The Cornea Predicts The Sclera?

That’s the idea….Similar ECM of the corneal stroma and the sclera

Thought to predict the stiffness of the lamina cribosa, scleral canal and the peripapillary sclera

Corneal biomechanics could predict optic nerve head morphology and risk for glaucomaCorneal hysteresis may indicate how well the eye/optic nerve head are compensating for the internal pressure

What Is A “Normal” Hysteresis

Average corneal hysteresis – 10.2Can range 9.6 to 10.7

No diurnal variationNo really strong normative data between racesNo strong normative data for ageNo difference between male and female

Corneal Hysteresis in Glaucoma

Average hysteresis for patients with glaucoma

8.0

Hysteresis in an IOP independent risk factor for glaucoma – all types

Associated with faster progressing glaucoma

Corneal Hysteresis in Glaucoma

Hysteresis has been shown to improve after therapy initiationGreater IOP lower response with prostaglandin and SLT is associated with an initial lower CHAfrican – Americans have a lower CHAssociated with larger mean cup depth/larger C/D ratioAssociated with ONH deformation after short term IOP increase

What Do We Have To Monitor Glaucoma Suspects

OCTVisual fieldsIOPDirect observation/fundus photographyGonioscopyCorneal hysteresis

OCT – AngiographyVEP/ERG

OCT – Angiography – What Is It?

New software upgrade on many OCTsDetects blood flow through sequential b-scans and recreates the vascular tree in different retinal layersDetect the scattered light off of moving particles Can only see FLOW and cannot detect leakage

OCT - Angiograpghy How Does This Apply To Glaucoma

Vascular (hemodynamic) theory of glaucomaHayreh, 1970 “glaucoma is a disease wherein the normal balance between the IOP and blood pressure in the choroidal, supplying the optic disc and retrolaminar part of the nerve is disturbed. This results in vascular insufficiency…”Decreased perfusion could lead to ischemia and ultimately apoptosisAssociated with disautoregulation

What Does Normal Look Like? Where To Look in Glaucoma?

OCT-A will divide the scan (Choroid/Peripapillary capillaries/Vitreous)In glaucoma, we care about peripapillary capillaries

Inner RNFL, run parallel to axons, few anastomoses

Like OCT/RNFL – asymmetry is important

OCT-A Glaucoma Suspect

67 AAFPOH: paternal grandfather had glaucomaPMH: diabetes, high cholesterol, hypertensionBCVA: 20/20 OU mild myopeIOP: 19 mmHg and 20 mmHgSLE: unremarkable, angles open

How Does This Change My Management?

As of now…not much

There is good correlation between findings of OCT-A and the extent of loss on OCT and visual fields

Vessel density is less in patient with glaucoma (macular and optic nerve)

Limitations

Data is still variable/no established normatives

Scan reliability is questionable

Which came first? Loss of VD or RNFL?

Liu L, Jia Y, Takusagawa HL, et al. Optical Coherence Tomography Angiography of the Peripapillary Retina in Glaucoma. JAMA Ophthalmol. 2015;133(9):1045–1052. doi:10.1001/jamaophthalmol.2015.2225

Electro Diagnostics In Glaucoma

Visual Evoke Potential (VEP)Thought to fill in a gap of diagnosing glaucoma suspects pre-perimetrically

Multiple types of VEPPromising when targeting magnocellular pathway in multifocal modality

Transient VEP measures latency of the signal to the visual cortex

Limited use

VEPs In Glaucoma

UPDATE****Medicare in Texas will NOT pay for VEP when used for glaucoma

Electroretinagram (ERG) In Glaucoma – The Good

More promising than VEP because it can measure RGC functionLongstanding proven history in glaucomaThere are multiple types of ERGs with varying stimulus size, freq, etc. that allow for isolation of different responsesMore significant correlation with suspected central involvement

ERGs – The Good

Reduced ERG has been linked to a more likely conversion from normal to glaucomatous field defects

Reduced ERG has been linked to faster RNFL loss

ERGs in Glaucoma – The Bad

Does not isolate the RGCs

Affected by concomitant macular disease

Susceptible to environmental interference, media opacity, visual correction

ERGs In Glaucoma – The Ugly

UPDATE****Medicare in Texas will NOT pay for ERG when used for glaucoma

Glaucoma Suspect Monitoring Schedules

No set monitoring schedules for glaucoma suspects – watch out

The tests required to assess must be tailored to the patient – NO standard protocols

The Low Risk Suspect (Opinion)

Typically following every 6 – 12 monthsTesting recommended

Dilated fundus exam/Disc photo (1/year)IOP measurement (every visit)

Goldmann is still the gold standardCorneal Hysteresis (Initial/expected change)OCT ONH with ganglion cell analysis (1/year)Visual field if needed (1/year)Gonioscopy if needed (Initial/expected change)

The High Risk Suspect (Opinion)Typically following every 1 month– 6 monthsTesting Recommended

Dilated fundus exam/Disc photo(1-2/year)IOP measurement (every visit)Corneal hysteresis (Initial/expected change)OCT ONH with ganglion cell analysis (1-2/year)Visual fields (2-4/year)Gonioscopy (initial visit/with expected change)

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