saturday, july 7th

Program Location

The Westin Riverwalk Hotel 420 West Market Street, San Antonio, Texas 78205

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

Lectures presented by Alan Kabat, OD

8:00 am - 9:45 am OSD is NOT a 4 Letter Word COPE ID# 58280-AS

CEE Available 2 D/T Hours

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

10:15 am - 12:00 pm Dermatology 101 - Lessons for Eye Care Practitioners COPE ID# 58281-SD


12:00 pm - 1:00 pm Lunch & Visit Exhibits Lectures presented by Michael Chaglasian, OD

1:00 pm - 2:45 pm Glaucoma Update New Tools and Treatment Options COPE ID# 56782-GL


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

3:15 pm - 5:00 pm Ocular Emergencies for the Primary Care Optometrist COPE ID# 58307-AS


1

OSD IS NOT A FOUR-LETTER WORD!

Alan G. Kabat, OD, PA. 2018. All rights reserved.


Alan G. Kabat, OD, FAAO

Memphis, Tennessee

Promotional Speaker: OCuSOFT

Shire

Clinical Researcher: Bio-Tissue

Shire

Vmax Vision

Editorial Boards: Optometric Office (FVMG)

Optometric Physician (Jobson)

Review of Optometry (Jobson)

Advisory Boards: Avellino Labs

Bruder

EyeGate Pharma

OCuSOFT

Shire

Sun Ophthalmics

TearScience

Vmax Vision

Clinical Consultant: Bio-Tissue

Lacrivera

Vmax Vision

Per COPE stipulations, all disclosed financial relationships are current to within 12 months of this speaking engagement… July 7, 2018.

Complex disorder with numerous etiological factors

Confusing terminology

Numerous diagnostic strategies but no single confirmatory test

Numerous treatment options with variable / partial success

- Difficult to predict WHICH patients will be successful with WHICH therapy

Confusion leads to indecision… Indecision leads to fear…

OCULAR SURFACE DISEASE

2



STEP #1

LISTEN!!

Patients will give you clues to the diagnosis if you listen

closely and identify key complaints…

SYMPTOMS OF DED

Common complaints include:

• Burning

• Stinging

• Dryness

• Itching

• Grittiness

• Sandy

• Crusty

• Sore

• Tired

But also, listen for things like:

• Redness

• Blurry vision

• Fluctuating vision

• Difficulty with prolonged:

Reading

Computer work

Driving

Watching television

QUESTIONNAIRES

Permit quantification of symptoms in terms of severity and frequency

Many options

Validated by TFOS**

- Ocular Surface Disease Index (OSDI)

- Dry Eye Questionnaire (DEQ-5)

- Impact of Dry Eye on Everyday Living (IDEEL)

- National Eye Institute’s Visual Function

Questionnaire (NEI VFQ-25)

- Dry Eye-related Quality-of-Life Score (DEQS)

- Computer-vision Symptom Scale (CVSS-17)

3



TFOS DEWS IITHE OCULAR SURFACE (2017)

STEP #2

CONDUCT AN APPROPRIATE WORKUP

TFOS DEWS IITHE OCULAR SURFACE (2017)

4



THOUGHTS ON DIAGNOSTIC TESTING

TEARLAB

Measures tear osmolarity (osmolality)

- Normal: 280-295 mOsml/L

- >308 mOsm/L is considered hyperosmolar

- Inter-eye difference = hallmark of DED ( >8 mOsms/L between eyes)

Highly regarded by researchers; variable acceptance amongst clinicians

- Biggest issue is variability

CPT 83861-QW

INFLAMMADRY

Detects elevated MMP-9 in tears

- NON-SPECIFIC inflammatory biomarker

- QUALITATIVE, not quantitiative

May help to identify, classifying and monitor DED

May help determine best candidates for anti-inflammatory medications

CPT 83516-QW (Immunoassay for Analyte)

5



OCULUS KERATOGRAPH 5M

CPT 92285 (External Photography)

CPT 92025 (Corneal Topography)

Meibography

TF-Scan

NIKBUT

Meniscus Tear Height

Lipid Layer Assessment

TF-Dynamics

LIPIVIEW II

CPT 92285 (External Photography)

CPT 0330T (Digital Interferometry)

Meibography

- “Dynamic Meibomian Imaging”

Lipid Layer Thickness (LLT)

Blink performance

STEP #3

Determine the

MOST

LIKELY

CONTRIBUTORY

ELEMENT

6



OSD “BUCKETS”

Aqueous deficiency (Dry eye syndrome - H04.123)

Keratoconjunctivitis sicca (non-Sjögren’s - H16.223)

Sicca syndrome with keratoconjunctivitis(Sjögren’s syndrome - M35.01)

Filamentary keratitis (H16.123)

OSD “BUCKETS”

Anterior blepharitis (Unspecified blepharitis - H01.00-)

Meibomian gland dysfunction (Unspecified blepharitis - H01.00-)

Lagophthalmos (Unspecified lagophthalmos - H02.20-)

DON’T FORGET DEMODEX!!

ICD10 = B88.0

Demodex is an exoparasite of the skin, particularly common on the face

- Causes a form of blepharitis that can be challenging to differentiate from dry eye based on symptoms alone

- Potentially impacts the pilosebaceous glands (D. folliculorum) and Meibomian glands (D. brevis)

Requires not only basic lid hygiene but also acaricidal therapy

7



OSD “BUCKETS”

Anterior basement membrane disease (Other hereditary corneal dystrophies - H18.59)

Conjunctivochalasis (H11.823)

Pinguecula (H11.153)

Pterygium(Unspecified pterygium - H11.053)

OSD “BUCKETS”

Allergic conjunctivitis (Other chronic allergic conjunctivitis - H10.45)

Recurrent erosion of cornea (H18.83-)

Dermatochalasis (H02.83-)

Epiphora due to insufficient drainage (H04.223)

Stenosis of lacrimal punctum(H04.563)

STEP #4

IMPLEMENT APPROPRIATE THERAPY

FOR MLCE

8



Dry Eye Disease Diagnosis & Classification

TFOS DEWS II

TFOS DEWS II

STEP THERAPIES

Patient education

Environmental modification (humidifiers, etc.)

Dietary modifications (including EFA supplements)

Identification/elimination of contributory medications

Lid hygiene and warm compresses (home therapy)

Ocular lubricants

9



LID HYGIENE:MECHANICAL BLEPHAROEXFOLIATION

Induction therapy for blepharitis; removes margin debris & deposits

- Scurf & collarettes

- CD (Demodex)

- Meibomian gland caps

- Biofilm (?)

Performed q3-6 months for patients with chronic blepharitis

BlephEx

LidPro (Mibo Medical Group)

OCULAR LUBRICANTS

Proactive artificial tear recommendations based on prevailing etiology and individual need

- As noted in the report… “if MGD is present, then consider lipid-containing supplements”

- Other considerations should include:

Viscosity and/or gel-forming capability

Ophthalmic ointments

Osmolarity

Preservatives

WHEN SHOULD I USE A

PRESERVATIVE-FREE PRODUCT?

Even mild or transient preservatives can have a negative impact on the ocular surface when used excessively and/or long-term.

Patients using drops more than four times a day EVERY day should likely be on a PF formulation.

Also consider for:

- Patients with atopic disease

- Patients using concurrent chronic care drops (e.g. glaucoma)

- Patients with persistent epithelial disruption (i.e. staining)

10



WHEN SHOULD I USE A

GEL-DROP OR GEL PRODUCT?

Increasing viscosity helps to extend the residence time of a solution on the ocular surface.

Patients who report improved symptoms but limited duration of action with typical ATs may benefit from a gel or gel-drop.

The limiting factor of increased viscosity is diminished acuity, or increased BLUR.

ALWAYS sample a gel or gel-drop in-office to assess vision if it is to be used during waking hours.

Some also prefer to use a gel or gel-drop QHS.

- Questionable efficacy, as these will not last 6-8 hours.

WHEN SHOULD I USE A

LIPID-EMULSION PRODUCT?

Since the normal tear film contains a lipid component, it is rarely “wrong” to use a lipid-emulsion product.

Lipid-emulsions are specifically INDICATED for patients with evaporative dry eye due to MGD.

- Help to restore lipid component of tears.

- Increase lubricity of ocular surface; reduce “drag” of lid.

- May help to partially dissolve coalesced oils at MG orifices.

As with gels, the limiting factor when using a lipid-emulsion product is diminished acuity, or increased BLUR.

WHEN SHOULD I USE AN

OPHTHALMIC OINTMENT?

Ointments are most commonly used for patients with nocturnal lagophthalmos, QHS.

- Far greater retention time than gels.

- Far greater tendency for blur / reduced acuity.

Ointments may be necessary for patients with severe ocular surface disease (e.g. keratoconjunctivitis sicca) who have exhausted all other options for increased viscosity ATs.

Personal observation without a shred of scientific evidence… Older patients tend to tolerate ointments and gels

11



STEP THERAPIES

If above options are inadequate consider

Non-preserved ocular lubricants

Tea tree oil for Demodex

Tear conservation

- Punctal occlusion

- Moisture chamber goggles

Overnight treatments (ointments, etc.)

In-office, physical heating and expression of the meibomian glands

• Prescription drugs to manage DED

• Topical antibiotic or AB/steroid

• Topical corticosteroid (short-term)

• Topical secretagogues

• Topical cyclosporine

• Topical lifitegrast

• Oral macrolide or tetracycline ABs

TEA TREE OIL FOR DEMODEXIN-OFFICE TREATMENT

“One can prepare a mixture of 50% tea tree oil by diluting the tea tree oil in either macadamia or walnut oil…”

IN-OFFICE TEA TREE OIL TREATMENT

Oust Demodex Swabstix

- 50% Tea Tree Oil / 40% Sea Buckthorn Oil / 10% Caprylic Acid

12



TEA TREE OIL FOR DEMODEXCLIRADEX WITH T4O

T40 represents one of the 13 essential oils in TTO

- Found to be the most demodicidalof components

- MORE effective than TTO at equivalent percentages

No other commercially available source of T4O in the United States

Tighe S, Ying-Ying G, Tseng CG. Terpinen-4-ol is the most active ingredient of tea tree oil to kill Demodex mites. TranslVis SciTechnol. 2013 Nov;2(7):1-8.

ORAL IVERMECTIN FOR DEMODEX

STROMECTOL (Merck & Company)

- Antihelminthic agent; typically prescribed for parasitic disorders such as strongyloidiasis or onchocerciasis

- Demodex therapy = two 200-mcg/kg doses given 7 days apart

e.g. for a 165-pound adult, five 3-mg tablets at the time of diagnosis, and an identical dose to one week later.

- Most common side-effects include: nausea, diarrhea, dizziness and pruritus (all <3%)

Holzchuh FG, Hida RY, Moscovici BK, et al. Clinical treatment of ocular Demodex folliculorum by systemic ivermectin. Am J Ophthalmol. 2011

Jun;151(6):1030-1034.e1.

13



PUNCTAL OCCLUSION

Earliest “plugs” were developed in the 1970’s

Peak utilization through the late 1990’s- Declining 3rd party reimbursement in 2000’s saw a drop-off

- Original Delphi Panel (2006) and original DEWS report (2007) suggested that punctal occlusion was most appropriate for moderate-severe dry eye (Level 3)

TFOS DEWS II suggests EARLIER use of punctal occlusion (Step 2)

Newer materials may offer better, safer options

PUNCTAL OCCLUSION

Jehangir N, Bever G, Mahmood SM, Moshirfar M. Comprehensive Review of the Literature on Existing Punctal Plugs for the Management of Dry Eye

Disease. J Ophthalmol. 2016;2016:9312340.

PUNCTAL OCCLUSIONWHEN TO CONSIDER…

Dry eye associated with a rapid tear break-up time

Aqueous-deficient dry eye secondary to systemic disease (e.g. Sjögren syndrome)

Systemic medications that reduce tear production (e.g. antihistamines, antidepressants)

Symptomatic contact lens wear

Dry eye related to refractive surgery

Lid closure abnormalities

Corneal irregularities or scarring that affects tear stability

Toxic epitheliopathy

Superior limbic keratoconjunctivitis

Jones L, Downie LE, Korb D, et al. TFOS DEWS II Management and Therapy Report. Ocul Surf. 2017 Jul;15(3):575-628.

14



PRESCRIPTION DRUGSConsider in those patients who:- Fall primarily into the “aqueous deficient bucket”

- No longer have adequate control of symptoms with artificial tears alone

- Have positive evidence of inflammation (e.g. InflammaDry)

Demonstrate persistent ocular surface damage (NaFl or LG staining)

- Have concurrent systemic disorders that may be contributory (e.g. RA, SS)

Cyclosporin A 0.05% emulsion (Restasis & Restasis Multidose)- FDA-approved in 2003

- Indicated “to increase tear production in patients whose tear production is presumed to be suppressed due to ocular inflammation associated with keratoconjunctivitis sicca”

Lifitegrast 5% (Xiidra)- FDA-approved in 2016

- Indicated “for the treatment of the signs and symptoms of dry eye disease”

RESTASIS

Cyclosporine 0.05% emulsion

Allergan (Irvine, CA)

Approved for BID dosing

“… did not increase tear production in patients using anti-inflammatory eye drops or tear duct plugs.”

10-28-2016: FDA approval for RESTASIS® Multi-Dose Preservative-Free (MDPF).

CYCLOSPORINE A - MOA

Calcineurin inhibitor

Blocks transcription of cytokine genes in activated T-cells

Ultimately blocks production of IL-2

- Diminishes subsequent T-cell proliferation and activation

“… its precise mechanism of action in dry eye is unknown.”

15



CYCLOSPORINE A - MOA

Actions in OSD:

Reduction of activated T-lymphocytes

Reduced markers of conjunctival apoptosis (CD40, CD40L and Fas)

Reduction of pro-inflammatory cytokines (IL-6)

Beneficial effect on conjunctival epithelium

- Normalization of conjunctival squamous metaplasia

- Increase in goblet cell density (191%)

Increased tear production (Schirmer)

* 0.005% ophthalmic emulsion

* In HUMAN (in vivo) clinical trials

* After 6 months of treatment

• Donnenfeld E, Pflugfelder SC. Topical ophthalmic cyclosporine: pharmacology and clinical uses. Surv Ophthalmol. 2009;54(3):321-38.

• Kunert KS, Tisdale AS, Gipson IK. Goblet cell numbers and epithelial proliferation in the conjunctiva of patients with dry eye syndrome treated with cyclosporine. Arch Ophthalmol. 2002;120(3):330-7.

• Brignole F, Pisella PJ, De Saint Jean M, et al. Flow cytometric analysis of inflammatory markers in KCS: 6-month treatment with topical cyclosporin A. Invest OphthalmolVis Sci. 2001;42(1):90-5.

• Sall K, Stevenson OD, Mundorf TK, et al. CsA Phase 3 Study Group. Two multicenter, randomized studies of the efficacy and safety of cyclosporine ophthalmic emulsion in moderate to severe dry eye disease. Ophthalmology. 2000;107(4):631-9.

XIIDRA

Lifitegrast 5% solution

Shire (Waltham, MA)

Approved for BID dosing

LIFITEGRAST - MOAActivation and migration of free lymphocytes to the ocular surface are key steps in the inflammatory process associated with dry eye disease

This process is initiated and influenced by the binding of the T-cell integrin lymphocyte function antigen-1 (LFA-1) to intercellular adhesion molecule-1 (ICAM-1).

Lifitegrast acts as an ICAM-1 decoy; it prevents the binding of LFA-1 with ICAM-1 on the inflamed epithelial cell surface.

Activation and homing of T-cells is prevented.

The cycle of T-cell mediated inflammation on the ocular surface is broken.

1. Expression2. Recruitment

3. Activation4. Release

16



LIFITEGRAST CLINICAL TRIALS

Four 12-week clinical trials

- Total of 2,133 patients

12-month safety study

- 331 patients

Co-primary endpoints

- Eye dryness score (symptom)

- Inferior NaFl corneal staining (sign)

CLINICAL RESULTS – SYMPTOMS & SIGNS

O

P

U

S

-

1

O

P

U

S

-

2

O

P

U

S

-

3

SAFETY / ADVERSE EVENTSRESTASIS

• One of the safest chronic-use ophthalmic drugs available

• Notable AEs

• Stinging upon instillation: 17% (10%)

• Delayed onset of action

XIIDRA

• Good safety in Phase 2 & Phase 3 clinical studies (OPUS / SONATA)

• Notable AEs (5-25%):• Instillation site irritation (burning)

• Blurred vision (on instillation)

• Dysgeusia (taste alteration)

17



OTX-101 A/K/A SECIERA (SUN PHARMA)

Described as a “nanomicellar cyclosporine solution for topical ophthalmic administration”

- Nanomicelles - self-assembling, nano-sized (particle size ≤500 nm) colloidal dispersions with a hydrophobic core and hydrophilic shell... used as carriers for solubilizing hydrophobic drugs.

- Helps to improve tissue penetration of drugs, enhance and sustain drug levels, and reduce systemic side effects

Completed Phase 3 clinical trials; filed NDA in late 2017

STEP THERAPIES


Oral secretagogues

Autologous/allogenic serum eye drops

Therapeutic contact lens options- Soft bandage lenses

- Rigid scleral lenses

ORAL SECRETAGOGUES

Options:- Pilocarpine (Salagen)

- Cevimeline (Evoxac)

Action: - Cholinergic parasympatheticomimetic agonists

- Bind to muscarinic (M1 and/or M3) receptors causing pharmacological stimulation of exocrine glands

- Primarily affect the salivary and lacrimal glands; also causes smooth muscle contraction

Specifically indicated for the treatment of xerostomia (dry mouth) in patients with Sjögren syndrome- Technically off-label for dry eye

- Ideally used only under a rheumatologist or internist’s supervision

18



ORAL SECRETAGOGUES

Common side-effects include:

- Excessive sweating

- GI irritation, nausea, vomiting, diarrhea

- Rhinitis

- Excessive salivation, salivary gland enlargement

- Miosis, headache

- Bradycardia, tremor

Severe reactions can include:

- Arrhythmias, AV block

- Severe hypotension

- Bronchospasm

INCREASED TEAR SECRETION VIA ELECTRICAL IMPULSE

TrueTear (Allergan)

- Formerly Oculeve

- Described as a “non-surgical, non-pharmaceutical, externally applied device” that employs “neurostimulation of the trigeminal nerve” to increase tear volume

- Rechargeable, hand-held unit

- Disposable hydrogel tip

FDA-cleared in April 2017

Good candidates are “at least 22 years old and have dry eye from inadequate tear production”.

Robinson M, Lewis RA, Sierra P. Intranasal lacrimal neurostimulation versus two control applications for acute tear production inmoderate to severe dry eye. American Academy of Optometry 2016. Anaheim, CA.

19






20



Prospective, 6-month, open-label, single-arm, non-randomized study

40 subjects with mild-severe DED

4 subjects were concurrently using topical cyclosporine (Restasis) BID

Provided intranasal stimulation device to be used at home QID (or more as needed)

Follow-up assessments at Days 7, 14, 30, 60, 90 and 180.

Outcome measures – EFFICACY:

1° - mean Schirmer score (under topical anesthesia), unstimulated vs. stimulated (with CTA)

2° - ocular surface staining, TBUT, and subject-assessment of DED symptoms and severity

Outcome measures – SAFETY:

1° - AEs

2° - CDVA, IOP, SLE, DFE

Friedman NJ, Butron K, Robledo N, Loudin J, Baba SN, Chayet A. A nonrandomized, open-label study to evaluate the effect of nasal stimulation on tear

production in subjects with dry eye disease. Clin Ophthalmol. 2016 May 4;10:795-804.





21







AUTOLOGOUS SERUM EYE DROPS

Autologous: - (cells or tissues) obtained from the host

individual

Serum:- protein-rich liquid that remains when

cellular blood components are removed

Features:- patient-specific

- hypoallergenic

- non-preserved

- 20% - 50% concentration

- frozen / ~1 wk after opening

- typically dosed q2hKabat AG. Customized Solutions for the Dry Eye Patient.

Review of Optometry. 2015 Oct. 152(10):100-8.

22



AUTOLOGOUS SERUM EYE DROPS

Mangan R, Lehman S. How (and Why) to Make Autologous Serum. Review of Optometry. 2012 Mar. 40(3):42-54.

23



ALLOGENIC SERUM EYE DROPS

Elate-Ocular™

Cambium Medical Technologies; Atlanta, GA- “… a pro-regenerative allogeneic (not autologous) human platelet-derived

topical ophthalmic product intended for use in treating the symptoms of chronic dry eye…”

- “… formulated from the novel processing of base human platelets sourced from healthy and generally younger eligible donors (versus patients) from U.S. blood collection centers.”

IND (investigational new drug application) filed in August 2017

Currently proceeding with Phase 1 / Phase 2 clinical trial

STEP THERAPIES


Topical corticosteroid for longer duration

Amniotic membrane grafts

Surgical punctal occlusion

Other surgical approaches (e.g. tarsorrhaphy, salivary gland transplantation)

24



AMNIOTIC MEMBRANE THERAPY

May be indicated for corneal complications associated with severe dry eye disease, i.e.- Filamentary keratitis

- Persistent epithelial defects

Mechanism(s) of action:- Biological bandage

- Carrier for ex vivo expansion of corneal epithelial cells

- Substrate (basement membrane) transplant

- Promoter of epithelialization

- Suppressor of inflammation*

- Inhibitor of scarring*

- Inhibitor of angiogenesis*

- Anti-microbial agent*

Dua HS, Gomes JA, King AJ, Maharajan VS. The amniotic membrane in ophthalmology. Surv Ophthalmol. 2004 Jan-Feb;49(1):51-77.


CORNEA• Persistent epithelial defects

and perforations

• Neurotrophic keratitis

• Limbal stem cell deficiency

• Pseudophakic bullous keratopathy

• Infectious keratitis

• Chemical burns

CONJUNCTIVA• Pterygium surgery

• Conjunctivochalasis surgery

• Tumor excision and reconstruction

• Symblepharon prevention

• Chemical burns

• Stevens-Johnson syndrome

• Glaucoma filtering surgery

25




Cryopreserved:- PROKERA® (BioTissue)

PROKERA® Slim, PROKERA® PLUS, PROKERA® CLEAR

Dried / dehydrated: - AmbioDisk (Katena/IOP Ophthalmics) –

9, 12, 15 mm

- AmnioTek-C (ISP Surgical) –

12 mm

- aril (Blythe Medical) –

5, 8, 10.5, 15 mm

- BioDOptix® (BioD) –

9, 12, 15 mm

- Eclipse (Ophthalogix) –

10, 12, 14, 16 mm

- ReNovo Oculus (RegenMed Group) –

12 mm

- VisiDisc (Skye Biologics) –

10, 12, 15 mm

- Others… ?

AMT: CLINICAL SCIENCE

AMT: CRYOPRESERVED OR DEHYDRATEDIs one really BETTER than the other?

Other considerations:

- Ease of use

- Patient comfort

Courtesy: YouTube & Dr. Derek Cunningham, Austin, TX Courtesy: YouTube & Dr. Peter J. Cass, Beaumont, TX

26



AMT: SOONER OR LATER?

~1.5M on Rx

Past or Present

Mild

Dry EyeSevere

Dry Eye

Moderate

Dry EyeCurrent AMT UseIdeal AMT Use

• Complete diffuse staining

• Severe inflammation

• Severe symptoms or is neurotrophic

• Severe fluctuating vision

• Every other therapy has failed

• “Trainwreck”

• Some staining (25%)

• Some inflammation

• Some fluctuating vision

• May have pain & symptoms

• 1-2 top-line therapies have failed

• Is already on Restasis/Xiidra

Questions? Email me at: [email protected]

DERMATOLOGY 101: LESSONS FOR EYE CARE PRACTITIONERS

1 Alan G. Kabat, OD, PA. 2017. All rights reserved.

Memphis, Tennessee

Promotional Speaker: OCuSOFT

Shire

Clinical Researcher: Bio-Tissue

Shire

Vmax Vision

Editorial Boards: Optometric Office (FVMG)

Optometric Physician (Jobson)

Review of Optometry (Jobson)

Advisory Boards: Avellino Labs

Bruder

EyeGate Pharma

OCuSOFT

Shire

Sun Ophthalmics

TearScience

Vmax Vision

Clinical Consultant: Bio-Tissue

Lacrivera

Vmax Vision

Per COPE stipulations, all disclosed financial relationships are current to within 12 months of this speaking engagement… July 7, 2018.



Allergic

Infectious viral

bacterial

parasitic

Inflammatory

Papulosquamous

DERMATOLOGY:

CATEGORIES & ETIOLOGIES

Hyperplastic

Neoplastic benign

pre-malignant

malignant

A = Asymmetry

B = Bordersb = bleeding

C = Colorc = circulation

D = Diameter

E = Evolving…



AKA: acrochordon, “skin tag” or skin polyp

A small, benign, usually pedunculated (stalked) tissue growth, varying in size from ~2-5 mm may be skin colored or hyperpigmented

round to oval; may be multilobular

non-infectious (unlike viral papillomas)

More commonly noted in obese individuals; may be associated with pregnancy, diabetes

Most frequently noted in skin folds – neck, axillae, eyelid canthi or adnexa

Usually asymptomatic; painful only if inflamed or irritated



Lesions are treated only if they display bleeding or irritation, pose a significant cosmetic concern or interfere with function (e.g. lid ptosis)

Treatment options include: Cryotherapy with liquid nitrogen

Surgical removal: may be removed via ◦ Surgical scissors or shavebox

◦ Electrodessication and curettage

Chemical cautery (trichloroacetic acid)



Most common benign tumor of the elderly

Proliferation of epidermal cells

Frequently occur in sunlight-exposed areas

Presentation: Well-circumscribed, rough-surfaced round or oval

lesions with uneven pigmentation

Flat or slightly elevated in early stages

Later becomes dome shaped and more wart-like with a “stuck-on” quality

◦ “barnacles of aging”

Ocular: typically affect the upper lids & adnexa



Medical therapy: Superficial lesions can be treated with

trichloracetic acid

Cryotherapy carries risk of pigmentary changes & scarring

Surgical removal is the treatment of choice; options include: Shave biopsy (smaller lesions)

Light curettage, electrodesiccation, or a combination of the two (larger lesions)

Laser & dermabrasion surgery have also be used with some success

AKA: solar keratosis

Most common sun-related growth

Usually occur in fair-skinned individuals (who burn easily and tan poorly) with occupations or hobbies that expose them to excessive UV exposure

May be a precursor of squamous cell carcinoma

Presentation:

chiefly found on the sun-exposed areas of the face, ears, forearms, hands, back, chest, or shoulders

multiple discrete, slightly elevated, scaly reddish-brown lesions; may present with central ulceration

usually 3-10 mm in diameter and gradually enlarge



Patient education regarding sun exposure

Medical therapy (FDA approved):

Fluorouracil 5% (Efudex®)

Imiquimod 5% (Aldara®)

Diclofenac 1% gel (Voltaren®)

PDT with δ-aminolevulinic acid(Levulan®)

Other options include chemical peels or dermabrasion

Residual lesions treated surgically

BEFORE DAY 14 DAY 30

• Facial lesions: BID for 3-4 weeks

• For other body sites: BID for 6-8 weeks



Most common malignant skin tumor

Predominant in elderly, fair-skinned individuals

Chronic sun exposure = significant risk factor

Slowly progressive & rarely metastatic

Presentation:

translucent, raised nodule with "pearly" margins; over time, telangiectatic vessels may develop

ulceration may occur at the lesion's center

Morpheaform variety lies under surface – very difficult to assess

Photo courtesy of Dr. Mike Dufek (Miami, FL)



PREVALENCE OF ANATOMIC LOCATION:

OCULAR BCC

Accounts for <10% of all basal cell carcinomas

Presents as a firm, pale, waxy yellow plaque with indistinct borders

More aggressive and invasive despite being less obvious

More likely to show recurrence



Biopsy is CRITICAL!

Treatment of choice is surgical:

Wide margin excision with frozen border section

◦ 3 mm for clearly defined lesions (Nemet et al, AJO 8/06)

Mohs micrographic surgery

Exenteration only in extreme cases

Cryotherapy, radiation, or chemotherapy for those unable or unwilling to undergo surgery

much lower rates of success

Aldara (imiquimod) has shown promise with smaller, non-aggressive BCC

Less common than basal cell carcinoma (5-10%)

Predominant in elderly, fair-skinned, sun-exposed individuals

May convert from benign lesions (e.g., actinic keratosis)

Slightly more aggressive than BCC

low rate of metastasis

Characteristic appearance:

a roughened, scaly patch, mildly elevated and red

may have crusted and/or bloody margins

patients describe the lesion as “a scab that won’t heal”



Management for squamous cell carcinoma is identical to that for BCC. Excisional biopsy

Mohs surgical technique

Realize that SCC is somewhat more aggressive than BCC, with greater propensity for: Perineural invasion

Metastasis

Recurrence



7th most common cancer in the U.S.

Significant tendency toward growth & metastasis… Melanoma is responsible for 75% of skin cancer deaths in

the United States.

Primary risk factors:

1. Changing nevus

2. Increased age (> 60 years)

3. Large numbers of moles (common acquired and atypical) or history of multiple, atypical moles

4. Fair complexion

5. Family history of melanoma

6. Geographic location in sunny climates



Any suspected melanomas should be IMMEDIATELY referred for biopsy… Exceedingly high incidence of metastasis and rapid

rate of growth

Most potentially life-threatening of all skin cancers

Management for melanoma is identical to that for BCC. Excisional biopsy

Mohs surgical technique

papulo- :

Papule – a small solid elevation of skin, generally < 5 mm in diameter

-squamous : Denoting a tendency to scale or exfoliate; a

condition that results in “flaking”



Idiopathic disorder of the sebaceous glands affects forehead, cheeks, chin, nose, and eyelids

more common in older patients, women, those with fair skin (i.e. Northern European descent)

Presentation: General: erythema (“skin flushing”),

telangiectasia, coarseness of skin (may result in rhinophyma or “WC Fields nose”), and inflammatory papulopustular eruptions resembling acne

Ocular: chronic, unrelenting blepharitis, thickened lid margins and meibomian stasis; may see secondary conjunctivitis, hordeola/chalazia, canalicultis

1. ERYTHEMATOTELANGIECTATIC

2. PAPULOPUSTULAR ROSACEA

3. PHYMATOUS (RHINOPHYMA)

4. OCULAR ROSACEA

.



Recognize and avoid triggers!

Dietary:

Hot drinks (coffee, tea, soup)

Alcohol

Spicy foods

Environmental:

Excessive UV or heat

Smoking

Stress

Medical therapy: Tetracycline (250-500 mg daily-tid), doxycycline (50-100

mg daily-bid) or minocycline (100 mg daily) X 2-4 mos. ◦ Remember drug interactions and side-effects

Topical metronidazole as adjuvant to systemic therapy Topical and systemic corticosteroids are contraindicated Courses of isotretinoin (Accutane™) 0.5-1 mg/kg/d for 4

months may be helpful for recalcitrant disease

Soolantra

Mirvaso

Rhofade

Surgical Care: permanent telangiectasias and rhinophyma may be treated by electrosurgery, laser, or dermabrasion



Lid hygiene – ??

CONSIDER DEMODEX!!

Copious lubrication (lipid-restorative products)

Topical medications: Corticosteroids – ??

Restasis® (cyclosporine 0.05%) – ??

Remember – topical therapy is palliative; systemic treatment is warranted



A papulosquamous disorder of the sebum-rich areas of the scalp, face, and trunk may be linked to Pityrosporum ovale (a yeast)

induced/aggravated by humidity, trauma, seasonal changes, emotional stress

Intermittent, active phases with burning, scaling & itching, alternating with inactive periods increased activity in winter and early spring

Manifestations range from mild dandruff to exfoliative erythroderma; occurs as “cradle cap” in infants

seborrheic dermatitis



Dandruff often responds to frequent shampooing Keratolytics - salicylic acid, tar, selenium sulfide & zinc

Antifungals - ketoconazole (helps reduce P. ovale reservoirs)

Medicated shampoos may be used on scalp, body lesions and in beards, but not other facial skin or eyelids

Medical therapy: Topical antifungals - 2% ketoconazole cream

Topical steroids are discouraged except for short-term use, as they may hasten recurrences & foster dependence

Topical immunosuppressants - tacrolimus or pimecrolimus(OFF-LABEL) in recalcitrant cases

Systemic, low-dose isotretinoin in the most severe cases

◦ 10 mg po qod◦ de Souza Leão Kamamoto et al. Low-dose oral isotretinoin for moderate to severe seborrhea and seborrheic

dermatitis: a randomized comparative trial. Int J Dermatol. 2017 Jan;56(1):80-85.

Lid hygiene is paramount!

Lid scrubs are appropriate

Warm compresses and lubrication therapy may help further alleviate symptoms

Other agents:

Dandruff shampoos, etc. for scalp and body should NOT be used in the eyes, but should be advised for concurrent areas of seborrhea

Ketoconazole for blepharitis is controversial…



Hyperproliferation of epidermal keratinocytes

Unknown etiology; activated T-cells identified

Exacerbations triggered by trauma, stress, alcohol, medications, and infection

Presentation:

Scaly, “silvery” plaques with underlying erythema

Obvious on scalp, joints (elbows, wrists), extremities

Psoriatic arthritis: stiffness & pain in the distal joints

Ocular findings can include blepharitis, conjunctivitis, nodular episcleritis and even uveitis

Symptoms: itching, generalized discomfort; painful ulcerations can result from scratching



Non-invasive therapy includes daily sun exposure, sea bathing, topical moisturizers, and relaxation.

Medical therapy: Topical coal tar or salicylic acid compounds Topical anthralin (Anthralin®, Psoriatec®)

Topical calcipotriene (Dovonex®, a vitamin D analog)

Topical corticosteroids (e.g. Aristocort®, Diprolene®)

◦ Systemic corticosteroids are generally ineffective and may exacerbate the disease

Ultraviolet light treatment (PUVA) In severe cases retinoids (e.g. Tazorac®), methotrexate,

cyclosporine, and hydroxyurea may be used

IV/IM biologics: Infliximab (Remicade)

◦ physician administered (infusion)

Adalimumab (Humira)

Etanercept (Enbrel)

Ustekinumab (Stelara)

Secukinumab (Cosentyx)

Ixekizumab (Taltz)

Oral medications:

Apremilast (Otezla)



AKA: “wart”

Benign proliferations of skin and mucosa caused by human papilloma virus (HPV) transmitted by direct or indirect contact

can affect any area on the skin and mucous membranes; often seen on hands, feet

may be variably pigmented or flesh-colored with keratinized surface; “black dots” are pathognomonic

Presentation: two main types Verruca plana – round, flat-topped and slightly elevated with

a granular surface appearance

Verruca digitata – “cauliflower” surface appearance on stalk of varying length; may have numerous finger-like projections

http://www.dermnet.com/virusinfectionsclinic/warts4/webpics/pictures/warts47.html

http://www.dermnet.com/virusinfectionsclinic/warts4/webpics/pictures/warts47.html

http://www.dermnet.com/virusinfectionsclinic/digitatewarts1/webpics/pictures/digitatewart10.html

http://www.dermnet.com/virusinfectionsclinic/digitatewarts1/webpics/pictures/digitatewart10.html



Treatment is difficult, though verruca often resolve spontaneously (~65% over 2 years)

Options include: Benign neglect

Topical salicylic acid preparations (Compound-W®)

Vesicants (cantharidin*, podophyllin)

Other agents include imiquimod (Aldara®), cidofovir, tretinoin, and 5-fluorouracil.

Surgical removal:

◦ Chemocautery with trichloroacetic acid

◦ Cryoablation (liquid nitrogen) or photoablation

◦ Electrodesiccation and curettage

◦ Surgical paring / excision

* Moed L, Shwayder TA, Chang MW. Cantharidin revisited: a blistering defense of an ancient medicine. Arch Dermatol 2001;137(10):1357-60.



Associated with a large DNA poxvirus

More commonly seen in children

In adults, disease may be sexually transmitted

Presentation:

multiple raised papules or pustules with umbilicated centers; filled with a cheese-like material

typically affects the trunk, hands, face, & lid margins

when sexually transmitted, affects genitalia, thighs, buttocks and peri-anal regions

Usually asymptomatic; may cause itching or tenderness in some individuals

follicular response seen in extreme cases



Self-limited, typically resolving spontaneously over 3-12 months; however, to prevent autoinoculation or transmission to close contacts, therapy may be beneficial.

Medical therapy (all are off-label): Topical vesicants (e.g. cantharidin, podophyllin)

Topical retinoids (e.g. tretinoin [Retin-A])

Topical imiquimod

Surgical management: Chemical cautery via trichloracetic acid, tincture of iodine, or

silver nitrate

Cryotherapy with liquid nitrogen

Laser photoablation



Definition: a hereditary predisposition to allergy or hypersensitivity

Affects ~3-12% of the population

Manifestations:

dermatitis, urticaria

asthma, rhinoconjunctivitis, etc.

Caused by inappropriate cellular immune response; Type I (a.k.a. IMMEDIATE) hypersensitivity reaction

AKA: atopic eczema

Focal manifestation of a systemic condition

Presentation: Erythema, scaling, lichenification, pigmentary changes

Typically affects the “skin crease areas” – antecubital & popliteal areas, corners of the mouth, neck, behind the ears, outer canthi, or eyelids

Ocular: blepharitis, atopic keratoconjunctivitis (AKC), papillary conjunctival reaction, Trantas dots (limbal deposits of eosinophils), atopic cataracts, and keratoconus.

Symptoms: pruritis (itching) & discomfort AKC often presents with ocular pain and lacrimation



Stress control!

Avoidance of allergens (dust mites, peanuts, egg, milk, fish,

soy), and irritants (chemicals, harsh soaps, high humidity, wool, and acrylic)

Medical therapy: Topical steroids are the mainstay of treatment

◦ Typically used QID to start

◦ Kenalog® (triamcinolone acetonide 0.1%)

◦ Elocon® (mometasone furoate 0.1%)

Oral antihistamines may provide symptomatic relief

Elidel® (pimecrolimus) & Protopic® (tacrolimus)

◦ Typically used BID to start

◦ Topical immunomodulatory agents

◦ Both carry FDA “black box” warning (mid-2005)…



Results from direct skin exposure to allergens or other irritants, e.g.

acids, alkalis, resins, or other chemicals; dyes, plants, preservatives, cosmetics, metals; excessive moisture

Type IV (a.k.a. DELAYED) hypersensitivity

Presentation:

Erythema, edema, exudative vesicles; may result in crusting, eczema, or lichenification if not treated

Ocular: eyelid edema & induration, conjunctival edema & hyperemia, papillary response

Symptoms: profound itching, lacrimation



Remove the offending agent!

Avoid harsh soaps and detergents, irritating fabrics and chronic scratching

Medical treatment:

conservative use of topical steroids

wet saline compresses to exudative lesions

oral antihistamines for control of itching

oral steroids only if control of symptoms with topical treatment is not sufficient

Glaucoma Update: New Tools 2018

Michael Chaglasian, OD 1

Michael Chaglasian, OD, FAAOChief of Staff, Illinois Eye Institute

Associate Professor, Illinois College of Optometry

[email protected]

Consultant: Reichert, Carl Zeiss Meditec,

Advisory Boards:Aerie, Allergan, Alcon/Novartis, Bausch+Lomb

Research Grants:Topcon

New IOP Monitoring and Measuring:Senimed TriggerFishiCare HomeOcular Response AnalayzerCorneal Hysteresis

New Medications:VyzultaRhopressaRoclatan

Drug Delivery:Bitmatoprost Ring

Travoprost

Progression AnalysisPerimetry

OCT



2 minutes from 6 IOP measures in one yr

Out of 525,600 min in one year

IOVS 2003

Arsani S, Zeimer R, Wilensky J, et al. Large diurnal fluctuations in intraocular pressure are an independent risk factor in patients with glaucoma. J Glaucoma. 2000;9:134‐142.

1

5.76

0

1

2

3

4

5

6

7

Diurnal IOP Range 3.11 mm Hg Diurnal IOP Range 5.4 mm HG

Relative Risk of Disease

Progression

5-6x GreaterRisk



“Glaucoma is a 24‐h disease and the absence of individual patient data on circadian IOP dynamics constitutes a gaping deficit in our knowledge.Recent studies have demonstrated the feasibility of A‐IOP‐M. It can be expected that it will become part of the routine diagnostic evaluation of glaucoma patients by 2020.”

Curr Opin Ophthalmol 2015, 26:214–220

A new measurement principle – Ocular Volume Change

IOP exerts force on the eye shell, leading to ocular volume changes. Sensing through the ocular shell is influenced by ocular biomechanics; Tissue elasticity an individual variable.

pressure

strain gauge

contact lens

tissue biomechanics

The first ever FDA approved Contact Lens Sensor system, March 2016

Automated recording of Ocular Volume Changes (OVC) over 24 hours

Proven safe system

Repeatable 24 hour profiles

Individual signature‐like profiles

Highly sensitive

Patient‐ & practitioner‐independent

Promising clinical benefits

SENSIMED Triggerfish®



Potential Roles: (need further investigation)

OVC as a new biomarker to PREDICT the course of the disease vs. just monitoring the progression

OVC as a CLASSIFIER for Glaucoma patients having normal pressure (NTG)

OVC as a new and additional endpoint to assess the EFFECTIVENESS OF INTERVENTION

HOWEVER, THERE ARE LIMITED DIRECT COMPARISONS BETWEEN VOLUME CHANGE AND IOP

Predicting those who are at highest risk for progression is important

Being able to predict the risk of progression in advance of that progression having occurred (above a particular threshold) for each patient would help us move away from the current “wait and see routines”

Being able to predict in advance future progression rate would help drive earlier and more objective decisions around performing surgical intervention on higher risk patients.

De Moraes et al., 2016

Parameters associated with faster MD change at P < 0.25 were the:• number of large peaks while awake, • mean peak ratio while asleep, • mean peak ratio while awake, • wake‐to‐sleep slope and,• variability from the mean while awake.



Interpretation of CLS results remains a challenge. At present, the main value of CLS measurements seems to be in documenting relative changes of IOP‐related events and their timing.

Medication effects on IOP may not be as observable due to less effect on the 24 hour rhythm

Currently Sensimed is still investigating and exploring the appropriate business model and clinical utilization for the US

FDA Approved , but not currently available

Mansouri, Weinreb. Curr Opin Ophthalmol 2015, 26:214–220

Potential Roles:

Early Detection

Individualized Therapy

Alternative Interventions

Improved Adherence

Mansouri, Weinreb. Swiss Med Wkly. 2012;142:w13545

http://icare‐usa.com/

March 2017



The Icare® HOME tonometer is a handheld, battery operated device that measures intraocular pressure (IOP) without the need for topical anesthetic.

The device is intended as an adjunct for monitoring IOP of adult patients (self‐use). The HOME tonometer is designed for use at home or on the go.

IOP, date, time, eye recognition (right/left) and measurement quality are all stored in the internal memory.

Patient cannot view IOP readings

Data is transferred to a PC for further analysis by the prescribing physician.

New features: positioning light, automatic eye recognition system, series or single measurements, new user interface panel.



1. Asrani S, Chaterjee A, Wallace DK, et al. Evaluation of the ICare rebound tonometer as a home intraocular pressure monitoring device. J Glaucoma. 2011

2. Halkiadakis I, Stratos A, Stergiopoulos G, et al. Evaluation of iCare‐ONE rebound tonometer as a self‐measuring intraocular pressure device in normal subjects. Graefes Arch Clin ExpOphthalmol. 2012

3. Rosentreter A, Jablonski KS, Mellein AC, et al. A new rebound tonometer for home monitoring of intraocular pressure. Graefes Arch Clin Exp Ophthalmol. 2011

4. Sakamoto M, Kanamori A, Fujihara M, et al. Assessment of iCare ONE rebound tonometer for self‐measuring intraocular pressure. Acta Ophthalmol. 2014

Potential Areas of Error:1. Rebound tonometry may be less accurate in the higher

IOP range (>23mm Hg)

2. Overestimation with increasing CCT

Munkwitz S, Elkarmouty A, Hoffman EM, et al. Comparison of the ICare rebound tonometer and the Goldmann applanationtonometer over a wide IOP range. Graefes Arch Clin ExpOphthalmol. 2008Rosentreter A, Jablonski KS, Mellein AC, et al. A new rebound tonometer for home monitoring of intraocular pressure. Graefes Arch Clin Exp Ophthalmol. 2011

No significant safety issues reported for the Icare® TA01i or ic100 tonometers with a large number sold worldwide (40,000+) and in the United States (11,000+)

In use by health care personnel with varying degrees of tonometer experience and some of which have little or no ophthalmic training.

No significant safety issues reported for the Icare® HOME tonometer or its predecessor, Icare ONE; over 2,000 tonometers in use worldwide

Majority in Europe after Icare ONE received CE mark in late 2009 and was introduced in 2010.

171 patients 10 (6%) stopped b/c of difficulty in using the device27 (16%) unable to achieve certification

HOME and GAT were within 5 mmHg

116 of 127 patients (92%)MD of ‐0.33 mmHg (SD 3 mmHg)

No corneal abrasions or adverse events

Ophthalmology 2016;123:1675‐1684



Glaucoma suspects and ocular hypertensives prior to initiating treatmentGlaucoma patients disease progression and in office IOP that is at or near target IOP goalsStable glaucoma patients with high risk factors for progressionPatients with poor compliance where additional IOP information may demonstrate critical need for laser or surgical procedurePatients who would benefit from having additional IOP information

iCare Home is available for purchase nowThere is no CPT code (not reimbursable)

Fee is charged to patient for use of device over a three to five (5) day period

Practitioner and Staff are trained and “Certified”

Patient is selected and is trained in office.Approximately 10‐20 minutes

Patient uses device at home for 3 Days5‐6 readings per day

Patient returns device to office. Linkage to software to download the data.

Reviewed with patient.

Adjustment to treatment plan if warranted.



Data Interpretation:Highest Peak IOP out of office?Higher Mean IOP?Highest Fluctuation of IOP?

Are there good clinical indicators for this test?What about “environmental” factors?Will it improve medication compliance?

Taking Glaucoma risk assessment to the next level:

THE ROLE OF CORNEAL HYSTERESIS

Ocular Response Analyzer

(Reichert)

Michael Chaglasian, ODIllinois Eye Institute Illinois College of [email protected]

1. Glass DH et al. Invest Ophthalmol Vis Sci. 2008;49:3919‐3926.2. Wells AP et al. Invest Ophthalmol Vis Sci. 2008;49:3262‐32683. Taylor DA et al. Corneal Biomechanics. In: Copeland RA Jr., Afshari NA, eds.: Copeland and Afshari’s Principles and Practice of

Cornea. Two Volume Cornea Textbook. Jaypee Brothers. 2012:148‐157.

Section 1: Introduction to Corneal HysteresisBioengineering of the Eye: Emerging Concepts

Viscoelastic tissue with complex, interconnected microstructure1

Geometrical attributes are not a surrogate for biomechanical properties1

• eg: CCT does not describe viscoelasticity

The eye appears to be a mechanical structural continuum2

• Tissue properties may provide additional diagnostic information3

27

©2002 Park et al. Invest Ophthalmol Vis Sci.



1. Vincent J. Basic elasticity and viscoelasticity. In: Vincent J, ed. Structural Biomaterials. 3rd ed. Princeton, NJ: Princeton University Press; 2012:1‐28.

2. PubMed Search for “hysteresis” on October 3, 2014 returned 7696 results. 3. Hjortdal JO1. On the biomechanical properties of the cornea with particular reference to refractive surgery. Acta Ophthalmol Scand Suppl.

1998;(225):1‐23.

Section 1: Introduction to Corneal HysteresisHysteresis: Not a New Concept

A measurement that characterizes response to application and removal of force (load/unload)1

• Found in materials or systems that do not instantly follow forces applied to them but react slowly, or

dissipate a portion of the applied energy 1

More than 7500 papers published on hysteresis in a variety of medical fields2

• Various tissues and structures (tendon, lung, arteries, etc)

• The importance of Corneal visco‐elasticity had been discussed and explored (EX‐VIVO)prior to the ORA3

28

Classic “Hysteresis Loop”Sir James Alfred Ewing Identified the phenomenonof hysteresis and coined theterm in 1890

Hysteresis Property:“More like a Shock Absorberand NOT just a Coil Spring”

1. Luce DA. J Cataract Refract Surg. 2005;31:156‐162.2. Dupps WJ Jr. J Cataract Refract Surg. 2007;33:1499‐1501.3. Glass DH et al. Invest Ophthalmol Vis Sci. 2008;49:3919‐3926.

Section 1: Introduction to Corneal Hysteresis What is Corneal Hysteresis (CH)

The only in‐vivo measurement of corneal/ocular biomechanics• CH specifically refers to the output

of the measurement process performed by the Ocular Response Analyzer (ORA)1,2

Corneal Hysteresis reflects the ability of the corneal tissue to dissipate energy 1

• Function of viscoelastic damping2

• Not a characterization of stiffness3

Provides insight into ocular properties that were not previously understood or conceived of

29

Ocular Response Analyzer measurement signal

David Luce, PhDInvented the concept of Corneal Hysteresis

Section 1: Introduction to Corneal Hysteresis CH: Average Values in Normal Subjects

1. Fontes BM J Refract Surg. 2008 Nov;24(9):941-5. 2. Carbonaro. The Heritability of Corneal Hysteresis and Ocular Pulse Amplitude A Twin Study doi:10.1016/j.ophtha.2008.02.0113. Lam A. Et Al. Optom Vis Sci. 2007 Sep;84(9):909-144. Kamiya Et Al. J Refract Surg. 2009 Oct;25(10):888-935. Ortiz Et Al. J Cataract Refract Surg. 2007 Aug;33(8):1371-56. John Et. Al. 2007 Spring;39(1):9-14

CH Values in Normals around the worldN CH*

Brazil1105 10.1 ± 1.8

UK2272 pairs 10.2 ± 1.2

China3125 10.9 ± 1.5

Japan4204 10.2 ± 1.3

Spain588 10.8 ± 1.5

USA6 44 10.5 ± 1.2

*CH units are mmHg



CH: Risk Factor for Glaucoma

Low CH (<9 mmHg) = Higher Risk

High CH (>12 mmHg) = Lower Risk

Less significant RF contribution:

• CH 9‐12 mmHg

As with any RF, CH alone cannot be considered a definitive indicator of glaucoma, though it may be an indicator for further evaluation particularly in presence of other glaucoma risk factors

Other Related Findings

Corneal hysteresis has been shown to be lower in various types of glaucomatous eyes in comparison to normal eyes; these include POAG, PACG, NTG, and pseudoexfoliative glaucoma.

Low Hysteresis Associated with OAG and Visual Field Asymmetry

• More sensitive than CCT or IOP

Low‐baseline corneal hysteresis is associated with a greatermagnitude of IOP reduction following various glaucoma therapies including topical prostaglandin therapy and SLT.

Prakavan M. J Ophthalmic Vis Res 2014Anand A, et al. Invest Ophthalmol Vis Sci 2010Heirnisis C. Graefes Arch Clin Exp Ophthalmol 2013

Corneal Hysteresis Studies:

CH is repeatable, typically with good correlation R / L

No diurnal variation in normal eyes

Small decrease with age (as with CCT)

• Appears to be valuable to repeat procedure

CH is low with high (>30) IOP

• And may rise after hypotensive therapy

CH is low following LASIK (use IOP cc measure)

CH is low in corneal pathology (Keratconus)

• Neither of these suggest increased risk of glaucoma



Why is CH relevant in Glaucoma?

34

(Low) CH has been consistently shown to be independently and strongly associated with or

predictive of glaucoma progression

Corneal Hysteresis as a Risk Factor forGlaucoma Progression:

Conclusions:

The CH measurements were significantly associated with risk of glaucoma progression. Eyes with lower CH had faster rates of visual field loss than those with higher CH.

The prospective longitudinal design of this study supports the role of CH as an important factor to be considered in the assessment of the risk of progression in patients with glaucoma.

Ophthalmology 2013;120:1533‐1540

Corneal Hysteresis and Progressive Retinal Nerve Fiber Layer Loss in Glaucoma

CONCLUSIONS:

Lower CH was significantly associated with faster rates of RNFL loss over time.

The prospective longitudinal design of this study provides further evidence that CH is an important factor to be considered in the assessment of the risk of progression in patients with glaucoma.

Am J Ophthalmol 2016



CH Predicts the Development of Glaucoma

200 Glaucoma Suspects followed for 4 years

2002: Clinical research with ORA commences

2005: The 1st generation ORA was made commercially available

2012: Generation II ORA was launched

3rd Generation “ORA G3” introduced September 2015

Measures:

• Corneal Hysteresis (CH)

• Goldmann‐correlated IOP (IOPg)

• Corneal compensated IOP (IOPCC)

Ocular Response Analyzer Technology

• Becomes a second tonometer for the office.

• Can be used on all patients.

Corneal Compensated IOP: An IOP measurement that is less influenced by corneal properties than Goldmann or other tonometers. This value is closer to the “true pressure” and has been shown to be a better indicator of glaucoma than Goldmann. Matches GAT on average, so numerical “Scale” is the same

Corneal Hysteresis: An indication of corneal biomechanical properties that has been show to be independently predictive of future glaucoma progression. Reimbursable under CPT 92145.Typical average value is 10.5. Typical Range is 8‐14. Low is bad

IOPg: A Goldmann‐correlated IOP measurement for reference purposes so that clinicians can appreciate what a Goldmann would read simultaneously with the IOPcc value above.

Waveform Score: A signal analysis algorithm that rates the “quality” of the measurement signal on a scale of 0‐10. The higher the value, the more reliable the IOP and CH values are. 6‐10 is excellent. 4‐5 is not so good. 3 or below is poor.

Section 4: Ocular Response Analyzer TechnologyInterpretation of measurement values



IOPcc = Corneal Compensated IOP

40

An IOP measurement that is less influenced by corneal properties than Goldmann or other tonometers.

This value is closer to the “true pressure” and has been shown to be a better indicator of glaucoma than Goldmann.

Matches GAT on average, so numerical “Scale” is the same

In post‐LASIK/refractive surgery and in Corneal Pathology (KC, Fuchs’)

CH is NOT a reliable indicator of glaucoma risk due to modified biomechanics• In these situations there is increased importance of IOPcc

There a need to educate ORA users for correct interpretation of CH values:

Children have significantly higher CH values than adults, which should be taken into consideration when determining glaucoma risk

CH values are artificially low with very high IOP (30+)

41

Special considerations:

Implementing ORA in Clinical Practice:

ORA will NOT replace Goldmann tonometry• Advantageous to have different tonometric devices

Evidenced based guidelines needed for low/medium/high CH values

QUESTIONS:

How often to repeat?

How does the ORA best fit into practice workflow?• Screening room (eg, like an auto‐refractor)

• Or only on select patients?

Where does ORA fit into the measurement process?• Prior to the patient getting into the chair

• Prior to anesthesia (before measurement of CCT)



How am I using ORA and Corneal Hysteresis?

Obtaining CH on new glaucoma and glaucoma suspects

Using IOPcc on LASIK patients

Obtaining on progressing patients and other potentially high risk patients

Adjusting therapy and management for patients with low CH

Last “new” class of medication to be FDA approved

Timoptic

Betagan

Trusopt (1995)

Alphagan 0.2%

Pilocarpine

Argon Laser

No OCT

Fundus CamerasPolaroid or 35mm slide

Encouraged “drawing” ONH

Humphrey PerimeterSTATPAC but No True Progression Analysis

No Randomized Clinical Trial data had been published

OHTS, EMGT, AGIS, CNTGSG



Cosopt

Lumigan 0.03%; 0.01%

Travatan; Travatan Z

Alphagan P 0.1%

Azopt

Combigan

Simbrinza

Zioptan(preservative free PGA)

Cosopt PF

No new mechanism of action (MOA)*

*Rescula (unoprostone) 2000 and 2012. Likely activity on BK channels in TM

VyzultaTM

Latanoprostene bunod

FDA Approved, Available NOW

RhopressaTM

Netarusdil

Approved, available now

RoclatanTM

Netarusdil + latanoprostPossibly in 2019

Latanoprostene bunod is a dual mechanism, dual pathway molecule, consisting of latanoprost acid, linked to an Nitric Oxide‐donating moiety, which enhances trabecular meshwork/Schlemm’s canal (conventional) outflow by inducing cytoskeletal relaxation.

Latanoprost plus nitric oxide (NO)

Kaufman, P. EXPERT OPINION ON PHARMACOTHERAPY, 2017



Latanoprostenelatanoprost

Increases uveoscleraloutflow

Bunod donates Nitric Oxide (NO)Exerts its effect in trabecular smooth muscle

Resulting in trabecular relaxationand increased conventional outflow

Cavet ME, et al. Invest Ophthalmol Vis Sci. 2014;55(8):5005-5015. Ellis DZ, et al. Invest Ophthalmol Vis Sci. 2009;50(4):1808-1813.

Nitric Oxide may have other therapeutic roles in the eye and optic nerve

Latanoprostene = latanoprostIncreases uveoscleral outflow

Bunod donates Nitric Oxide (NO)Exerts its effect in trabecular smooth muscle

Resulting in trabecular relaxation and increased conventional outflow

NO may have other therapeutic roles in the eye and optic nerve

Cavet ME, et al. Invest Ophthalmol Vis Sci. 2014;55(8):5005-5015. Ellis DZ, et al. Invest Ophthalmol Vis Sci. 2009;50(4):1808-1813.

Kang JH, et al. JAMA Ophthalmol. 2016;134(3):294-303.

Diet

Nitrate (NO3- ) Nitric oxide (NO )Nitrite (NO2- )

Bacterial enzymesin mouth

Enzymatic and nonenzymatic reactions in our blood and tissues

Study Design: Assess the relation between dietary nitrate and new glaucoma cases (63,893 females and 41,094 males)

Lowest quintile of nitrate intake (~80 mg/d) compared with the highest quintile (~240 mg/d)

Result:Participants consuming the highest amounts of nitrates from green leafy vegetables had a 44% reduced relative risk of POAG with early paracentral vision loss and a 21% lower relative risk of all POAG



Study designRandomized (2:1 [LBN:timolol]) phase 3, multicenter, double‐masked, parallel‐group studies

2 treatment groupsLBN, 0.024%, qhs for 3 months

Timolol, 0.5%, bid for 3 months

Weinreb RN, et al. Ophthalmology. 2016;123(5):965-973.

APOLLO LUNAR

Number of subjects* 420 387

Mean baseline IOPLBN Timolol

26.7 mm Hg26.5 mm Hg

26.6 mm Hg26.4 mm Hg

Weinreb RN, et al. Br J Ophthalmol. 2015;99(6):738-745.



Nocturnal IOP with latanoprostenebunod treatment was 2.5 mmHg lower than baseline

Liu J et al Am J Ophthalmol 2016;

Liu J et al Am J Ophthalmol 2016;

LBN had higher OPP

Not included on FDA labeling

Latanoprost with New MOA with Nitric Oxide of improving TM outflow

More effective (~1.23 mmHg) than latanoprost

7.5‐9.1 mmHg lower IOP

Side EffectsConj. Hyperemia= 6%



First Line TherapyAlternate/Replacement for latanoprost/PGA

Good for all? Better for those with more advanced disease? Better for those with lower IOP?

Switch/Adjunctive TherapyWhen small additional IOP is needed, advantage of maintaining single bottle therapy

PGA w/ adjunctive med and not @ targetSwitch to LBN w/ adjunctive

No data on adjunctive therapy role

Rhopressa.com



Netarsudil ‐ MOA:1. ROCK causes alteration of cellular components of

the trabecular meshwork and Schlemm’s canal;rho kinase inhibitors decrease resistance in the trabecular meshwork outflow pathway and promote reduction of IOP.

2. ROCK inhibition lowers EVP

3. NET inhibition lowers AH production

Lin, et al Discovery and Preclinical Development of Netarsudil, a Novel Ocular Hypotensive Agent for the Treatment of Glaucoma. J Ocul Pharmacol Ther. 2017

Ciliary Processes

CORNEA

Uveoscleral Outflow

NET

RKI

Trabecular Meshwork

Episcleral Veins

Schlemm’s Canal

NET

RKI

Rhopressa (Netarsudil): An Investigational Drug Candidate for Glaucoma

THREE IOP LOWERING MECHANISMS:

1. ROCK inhibition relaxes TM1, increases outflow1,2

2. ROCK inhibition lowers Episcleral Venous Pressure (EVP)3

3. NET inhibition reduces AH production2

1. Wang SK, Chang RT. Clin Ophthal 2014;8:883-890.2. Wang RF, Williamson JE, Kopczynski C, Serle JB. J Glaucoma 2015. 24(1):51-54. 3. Kiel JW, Kopczynski C. J Ocul Pharmacol Ther 2015; 31:146–151.

Rhopressa™ QD met the criteria for non‐inferiority to timolol BID for the primary efficacy analysis(forbaselineIOP<25, <27 and<28mmHg

Mean IOP Reduction ~ 3.9 ‐ 4.1 mmHg



The three studies demonstrated up to 5 mmHg reductions in IOP for subjects treated with RHOPRESSA 0.02% once daily in the evening.

For patients with baseline IOP < 25 mmHg, the IOP reductions with RHOPRESSA 0.02% dosed once daily were similar to those with timolol 0.5% dosed twice daily.

For patients with baseline IOP equal to or above 25 mmHg, however, RHOPRESSA 0.02% resulted in smaller mean IOP reductions at the morning time points than timolol 0.5% for study visits on Days 43 and 90;

the difference in mean IOP reduction between the two treatment groups was as high as 3 mmHg, favoring timolol.

Conjunctival Hemorrhagesporadic sub‐conjunctival petechiae

Cornea Verticillataasymptomatic non‐toxic lipid deposits

only visible via biomicroscopy evaluation

Instillation Site Painsame incidence as timolol

transient

Corneal Verticillatafrom amiodarone



Potential drug of choice as adjunctive therapy to PGAswhen additional IOP lowering is desiredAdjunctive studies have NOT been completed

Rhopressa™ Advantages

Efficacy vs. other adjunctive therapies

QD PM dose

Lack of serious and systemic drug‐related AE’s

• Long duration of medication delivery• 3 to 6 months or more

• Obviously compliance benefits

• Good safety profiles thus far

• Good efficacy compared to drop therapy

• Retention for some devices may be a challenge

• Injection delivery for other devices is a hurdle



Large silicon ring that sits in the fornix

Visible @ medial canthus

Helps identify ring

Sustained drug delivery for 6 months

20% IOP reduction at all time points in clinical trials

Slightly less than timololBID

PGA continuous dose effect

High Retention Rate93% @ 3 months

88% @ 6 monthsMinimal Discomfort

Side Effects:Ring:

Increased mucous in AM

Medication:Hyperemia, etc.

Phase 3 Trials continue

Unclear how it will be marketed, Rx’d

http://www.sec.gov/Archives/edgar/data/850693/000119312514254394/d750005dex992.htm

• No Topical SEs• 7‐9 mmHg IOP

reduction• Phase 3 Trials now



Visual Field Testing

Remains an essential exam component.In fact, indications for more frequent testing on patients.

Recent papers have suggested that the 24‐2 test pattern has limited ability to detect central field defects

50% of retinal ganglion cells are found within 4.5mm of fovea

Macula region comprises only 10% of overall visual field area though it is responsible for 60% of area of visual cortex

Damage to central 100 associated with diminished contrast sensitivity, reduced reading ability

24‐2 Pattern on Retinal SurfaceVF testing under samples the macula. Possibility of small defects going undetected



12 testLocations6 deg sep

64 testLocations2 deg sep

24‐2 10‐2



Good Test Takers, Younger patients

Minimal to no defects on 24‐2

OCT Macula/Ganglion Cell scan is abnormal

High Risk Patients

Perhaps good idea as part of baseline for many suspects and ocular hypertensives

Alternate with 24‐2More frequent VFs when possible



Is disease present ?

How bad is it ?

Is it getting worse?

Case example of “early”,normal‐tension glaucoma.

The optic nerve photograph shows thinning of the inferior optic nerve neuroretinal rim (A) with a superior paracentral visual field defect (B).

SD‐OCT imaging confirms corresponding inferior RNFL thinning seen both on the thickness map and quadrant thickness (C) and inferotemporal macular thinning of the ganglion cell and inner plexiform layers (D).RNFL

RNFLGCA

Is my patient getting worse?

How can I tell for certain?Variability in perimetric testing

Challenges of structural assessment

Newer Question:What is the rate of progression?

Can we quantify this?



Baseline exams.Establishes initial visual field status.

VFI Rate of Progression Analysis.

• Trend Analysis of patients

overall visual field history

Today’s Visual Field. • Complete report of

current visual field exam

including PD, VFI,

progression analysis and

GPA Alert.

Detecting progression remains one of the most difficult tasks in glaucoma Mx

One Example:It can be hard to distinguish disease progression from exam variability and/or aging changes

There is no consensus on the best technique or criteria to detect progression, or what amount would be clinically significant.

Research and Literature does not easily translate into daily clinical care.

Progression may be measured by:

Functional change in visual field; structural change in the optic disc or retinal nerve fiber layer; or combined functional and structural change.

Accomplished through clinical examination, ophthalmoscopy, threshold perimetry, and imaging.



Most patients with glaucoma do progress if monitored for a long enough time

Even with IOP in the “normal range”59% of treated patients in EMGT (Leske et al 2007)

Treatment regimens should parallel the rate of patient’s progression

Slow progressors (majority) may need minimal intervention to maintain a high QoL

Rapid progressors (minority, ~20%) often require substantially more aggressive IOP reduction

Caprioli J. AJO 2008

Avg. rate = ‐1.0 dB/yr~30 yrs to perimetric blindness

HighTG = ‐1.31 dB/yr

NormalTG = ‐0.36

ExfoliativeG = ‐3.13~10 yrs to p. blindness

Heijl Ophthalmology 2009;116:2271–2276



MD = ‐4 dB MD = ‐13 dB MD = ‐29 dB

Mean Deviation

HAP Staging Scale: 0 to ‐6 dB = Early‐6 to ‐12dB = Moderate

> ‐12 = Severe

‐1 dB ‐5 dB ‐25 dB5 Years IOP = 44 mmHg

~ ‐5 dB/yr

Some rates of progression put patient at risk of visual disability

Most do not follow this path

Estimated ~ 17% of patient (even under care)

Fast Rates of Progression =

‐> 0.5 ‐ 1.0 dB per year or higher (varies w/age)However, slower rates in younger patients are still at risk due to longer life with disease

Luke J. Saunders, Felipe A. Medeiros, Robert N. Weinreb & Linda M. Zangwill (2016) What rates of glaucoma progression are clinically significant?, Expert Review of Ophthalmology, 11:3, 227-234, DOI: 10.1080/17469899.2016.1180246



Average 50 yo pt. @ ‐0.6 dB/year

20 years to ‐12dBdefined as severe VF

17 more yrs to ‐22dBdefined as “statutory blindness”

70 yrs

87 yrs*assumes a linear rate of progression

60 yo @ ‐1dB/yrStarting at ‐10dB

At 80 yrs =

90 yo @ ‐1 dB/yrStarting @ ‐2 dB

At 100 yrs+



Ophthalmology 2013;120:512–519

Ophthalmology 2013;120:512–519

Detecting Visual Field Progression in Glaucoma

Factors Impacting Progression Measure• Long Term Fluctuation• Reliability• Confirmatory Testing

• Ability to Efficiently Review the Data



Baseline Exams

Visual Field Index

Most Recent Test

The VFI Bar• historical and

projected VFI loss

Loss to date

Projected future loss100%

Arch Ophthalmol. 2009;127(12):1610‐1615

Event analysis‐ compares baseline to most recent data; change as dictated by criteria has occurred or not.

Trend analysis‐ looks at the significance of rate of change over time.

Identifies progression by looking at patient behavior over time. Uses all data points and a linear regression formula

Weakness‐ progression is not necessarily linear

Event analysis and trend analysis are complementary.Without event analysis, we have no early detection of glaucoma or early detection of progression in patients having glaucoma diagnoses. Without rate analysis, we have no ability to decide if detected changes are clinically significant.



Trend Analysis“Measures the rate of change”

A regression line is drawn to determine rate of change for all the data that has been collected over time.

Using VFImeasures a % rate of change

Most valuable when multiple VF tests have been completed

Good for identifying fast progressors

Baseline

Most Recent Exam

‐1.1%

EventAnalysis

What Rate of Loss is Significant?Greater than: ~1‐1.5%/yr (vary w/age, loss at Dx, etc.)

‐0.1% ‐1.4%



Stable cases = <0.3 dB/year

Progressive cases= >0.9 dB/year (“catastrophic”)

Consider doing 3 fields in first year and one every 6 months the next year

At a total of 5 in 2 years, good identification of the catastrophically worsening patient

Then scale back to 1 per year

Many already known to be generally stable don’t need this intensity

Important: Change Baseline Exams



Event AnalysisAsks “Has this changed”, compared to baseline an appearance on consectutive tests

Point by Point basis

Mostly used in early follow up time period

But also helpful in middle and late stages

Good for slow progressors

Look for shaded triangles indicating a single point that is worsening over consecutive tests

Point By Point Progression Analysis• Shows which point have progressed from baseline

Event Progression Analysis

GPA Summary Report:

Trend Line looks okay,Event Analysisis NOT!

‐1.0%



Michael Chaglasian, [email protected]

Ocular Emergencies

M. Chaglasian, OD 1

Ocular Emergencies for the Primary Care Optometrist

Michael Chaglasian, OD, FAAOAssociate ProfessorIllinois Eye Institute

Illinois College of [email protected]

Disclosure

No relevent disclosures for this presentation.

What is a “True” Emergency?

Pain (vs. discomfort)

Current or potential for:

Vision loss

Structural damage

Needs immediate (same day) attention

Ocular Emergencies

M. Chaglasian, OD 2

“True” Emergency

History is key to differentiating emergency versus urgency Phone or in person

Proper triage is essential

After hours protocol

Your office and your specialists

Medico-legal implications

History

Vision

One or both eyes?

Visual field

Sudden or gradual

Blurred or lost?

Diplopia?

Mono or Bino

Pain

Redness

Onset

Trauma

Contact lenses

Recent ocular disease or surgery

Other diseases

cardiac, vascular, or autoimmune

viruses

Medications or recent changes to medications

Nausea/vomiting

Emergency Exam

Acuity

Visual fields

Pupils

Ocular Motility

External examination

SLE

IOP

Fundus exam

Ocular Emergencies

M. Chaglasian, OD 3

Emergency Kit

Eye shield

Pressure patch

Sterile eye wash

Alger brush

Forceps

Golf spud

pH paper

Bandage CL’s

Diamox

Topical drops

Antibiotics

NSAID’s

Steroids

Cycloplegics

“True” Emergency

Chemical Burns

Alkaline

Central Retinal Artery Occlusion

Both have extremely high risk of severe and permanent vision loss which can be prevented via immediate intervention and treatment

Chemical Trauma

Acid exposure Only penetrate through epithelium car battery, vinegar, and

some refrigerants

Alkaline exposure Penetrates tissues more easily and

have a prolonged effect lime, (plaster, cement) lye,

ammonia found in household cleaners, fertilizers, and pesticides

Have patient bring agent if possible

Ocular Emergencies

M. Chaglasian, OD 4

Chemical Burns Copious irrigation

anesthetic

speculum

sterile saline v tap water

Contacts can be removed after irrigation

Sweep fornices – repeatedly

Examination after irrigation and neutralization of pH

Debride necrotic tissue

Want neutral pH of 7.0 –check q15min with pH paper

Chemical Burns

Determine area of involvement

Assessed by extent of FL staining

Assess depth of conjunctival penetration

Vascular ischemia, necrosis of limbal and bulbar conjunctiva

Loss of limbal vascular plexus is key indicator to severity of permanent vision loss

Check IOP

Tonopen

IOP meds

Roper Hall Classification of Ocular Burns

Grade Prognosis Limbal Ischemia Corneal Damage

1 Good None Epithelial Damage

2 Good Less than 1/3 Haze but iris detail visible

3 Guarded 1/3‐1/2 Total haze that obscures iris

4 Poor >1/2 Opaque cornea

Ocular Emergencies

M. Chaglasian, OD 5

Alkali Chemical Burn

50 yo CM bricklayer

Mortar splashed in eyes 1 day prior

Went to ER, eyes rinsed, given drops and Augmentin

c/o FBS, OD; OS feels fine

VA: OD HM; OS 20/20-2

pH: 10 OD, 7.4 OS

Alkali Chemical Burn

Needs more irrigation and debridement

Emergency amniotic membrane transplant (AMT)

Chemical Burn Management

Cycloplegic

AB or AB/steroid combo ung

Pain control Cyclo, steroids, NSAIDs

Artificial tears

Pressure patch BCL not tolerated

Oral narcotics/NSAID

Topical sodium ascorbate 10% and Citrate Oral

Doxycycline

Diamox

Tarsorraphy

Glue/permanent

AMT

Limbal stem cell transplant

Uninjured eye - autograft

Close relative – allograft

Corneal transplant

Artificial corneas

Ocular Emergencies

M. Chaglasian, OD 6

Chemical Burn - Ocular Sequelae

Advanced glaucoma

Eyelid destruction

Symblepharon

Cicatricial Entropion - months

Trichiasis

Ectropion

Ankyloblepharon

Descemet membrane detachment

Retinal detachments

Chronic Dry Eye

Persistent epithelial defects/ RCE

Infectious keratitis

Stromalysis

Perforation

Irreversible intraocular damage

Phthisis bulbi

Hypopyon

Amniotic Membrane Transplant (not Bandage)

Used as a surgical graft, where the tissue is integrated into the host. Amniotic membrane provides the scaffold for re-epithelialization.

Amniotic membrane is the innermost layer of the placenta, with 3 layers: Epithelium

thick basement membrane: supports epi call migration and inhibits apoptosis

Avascular stromal matrix: rich in growth factors & protease inhibitors

16. Sippel KC, et al. Amniotic membrane surgery. Curr Opin Ophthalmol 2001;12:269-281

AM applied with epithelial-basement side facing UP, stroma DOWNActs as basement membrane for corneal epithelium to grow over

AMT

When used as a graft, AM is typically glued or sutured in place, and epithelium is expected to grow over it.

AMT has an low immune response, so few rejections

Shown to: 1. epithelialization

2. fibrosis, inflammation, scarring

3. provides an anti-inflammatory and anti-scarring effect that minimizes the buildup of scar tissue

Other uses: Stevens-Johnson syndrome

Bullous /band keratopathy, pterygia

Prevent post-op adhesion of conj/sclera in trabeculectomy

Ocular Emergencies

M. Chaglasian, OD 7

CRAO

Sudden, painless, unilateral loss of vision

(+) APD

Swollen, pale posterior pole

“Cherry red” spot

• Vascular attenuation &/or boxcarring of flow in arteries & veins

• May see an embolus in vessel on optic nerve

CRAO

47yoCF with 3 day h/o blur, OS, with severe loss yesterday

Had been seen twice in previous week

1 MD, 1 OD

Dx: Dry eyes

Tx: Artificial tears

Spoke to tech yesterday

Casual about coming in

OD OS

20/20 Distance Acuity CF 1’

(+) APD

12 TA 12

BP 128/79

WNL SLE WNL

Patient findings

Ocular Emergencies

M. Chaglasian, OD 8

CRAO

In office AC paracentesis & digital massage

ASA

To Cardiologist

Echocardiogram

To ER

Blood work

ESR: rule out Temporal Arteritis

To PCP

Hematology workup

To Retina

Brimonidine Vision Never Improved

CRAO

Echocardiogram

Dilated aortic root

associated with connective tissue dx

Blood work:

ESR: minimally elevated

Elevated homocysteine level

amino acid in blood derived from the digestion of protein-rich foods

Elevated PTT (Partial thromboplastin test)

Other hypercoagulability factors negative

Negative CT, MRI, MRA

CRAO Causes

Emboli

74% cholesterol

10.5% calcific

15.5% platelet-fibrin

Thrombosis

Vasculitis

GCA

Post-trauma

In patients of 70 years of age and older, giant cell arteritis is more likely to be the cause than in younger patients.

Ocular Emergencies

M. Chaglasian, OD 9

CRAO

Incidence

3.5/10,000 in general population

92% of patients have </= CF acuity

Only ~ 8% will experience VA improvement

Two thirds of patients experience 20/400 vision while only one in six will experience 20/40 vision or better.

Risk Factors

Age >40

Systemic conditions

HTN, DM, CV dx, prior MI, stroke, hypercholesterol, hypercoagulable state

Social/Medication history

Smoking

CRAO Testing

ESR & CRP

r/o GCA

CBC/lipid profile

Cardiology referral

risk of MI

Carotid Doppler –r/o emboli from carotid

Auto-immune

Inflammatory

Hematology workup

Coagulopathies

Younger pts

CRAO

Retina suffers no detectable damage up to 97 minutes

BUT sustains massive, irreversible damage after 4 hours

Hayreh SS, Zimmerman MB, Kimura A, et al. Central retinal artery occlusion. Retinal survival time. Exp Eye Res 2004;78:723‐36.

Ocular Emergencies

M. Chaglasian, OD 10

CRAO & Mortality

Patients with emboli have a 56% mortality rate over 9 years, compared to 27% for an age-matched population without emboli

Life expectancy of patients with CRAO is 5.5 years compared to 15.4 years for an age-matched population without CRAO

CRAO – Acute treatment

• Lower IOP• Anterior chamber paracentesis

• remove 0.1 to 0.4 ml of aqueous fluid within the first 24 hours.

• Digital ocular massage• Some use 3‐Mirror Lens

• IOP lowering agents

CRAO – Acute treatment

Move occlusion

Carbon/carbogen inhalation

CO2 dilates arterioles & increases O2 delivery to ischemic tissues

Paper bag – dilate retinal vessel Remove embolus

Local intraarterial fibrinolysis (LIF) was associated with similar visual outcomes but increased rate of adverse reactions when compared to observation in the EAGLE study.

The study did not recommend LIF for acute CRAO.

Ocular Emergencies


CRAO

Risk of neovascularization NVD, NVI, NVG

Reports from 2.5-35%

18.2% @ an average of 8.5 weeks post CRAO

Ocular neovascularization following central retinal artery occlusion: prevalence and timing of onset. Eur J Ophthalmol. 2010 Nov‐Dec;20(6):1042‐6.

Urgencies

Giant Cell Arteritis

Endophthalmitis

CRVO

Papilledema

Optic neuritis

Corneal abrasion

Iritis

Corneal ulcer

Penetrating injury

Ruptured globe

Lacerations

Corneal foreign body

Retinal detachment

Orbital cellulitis

Giant Cell Arteritis / Temporal Arteritis

Ocular Emergencies


Background on GCA

Giant cell arteritis (GCA) is the most common primary vasculitis in adults.

Histopathologically, GCA is marked by generalized granulomatous inflammation of medium- to large-sized vessels that occurs in the elderly.

Patients commonly note associated symptoms such as headache, jaw claudication, diplopia, myalgias, and constitutional symptoms.

The most commonly feared sequela of GCA is permanent visual loss secondary to arteritic anterior ischemic optic neuropathy (AAION).

Since the vision loss from AAION can progress rapidly, and can involve the fellow eye within a matter of days, GCA is considered an ophthalmologic emergency.

Giant Cell Arteritis / Temporal Arteritis

Inflammation of medium & large sized arteries of the body, restricting blood flow & causing pain

VA loss usually unilateral, but risk of loss in other eye if not treated within 1 week

Elderly (>60), white, female

Scalp tenderness, jaw claudication, HA, loss of appetite, weight loss, fatigue

Need stat ESR & temporal artery biopsy Normal Sed Rate: F= (age+10)/2 M= age/2

GCA Exam Findings

CRAO

AION

Flame hemes, cotton wool spots

Pale, swollen disc

6th nerve palsy

Ocular Emergencies


Treatment

High dose systemic steroids

60-100mg qd

IV methylprednisone

250 mg q6h x 3 days

Aspirin

Referrals: Neurology, Rheumatology, Ophthalmology

Temporal Artery Biospy

Color duplex ultrasonography

Ocular Urgencies

Trauma

Penetrating/non-penetrating

Hyphema

Blowout fractures

Ruptured Globe

Lacerations

Corneal Abrasions

Foreign Bodies

Retinal detachment

Orbital Cellulitis

Iritis

Corneal ulcer

Optic neuritis

Acute exophthalmus

Trauma

2,500,000 traumatic eye injuries /yr in US

40,000-60,000 lead to visual loss

40% of all new cases of monocular blindness

80% occur in men

75% are work related

Average age 30

Ocular Emergencies


Ocular Trauma

Closed Globe Open Globe

Burn

Contusion

Laceration Laceration

Penetrating Perforating

Rupture

Hyphema Grading

Grade 1 - Layered blood occupying <1/3 of the anterior chamber

>50%

Grade 2 - 1/3-1/2 of the anterior chamber

Grade 3 - Layered blood filling 1/2 to less than total of the anterior chamber

Grade 4 - Total (100%) clotted blood, aka 8-ball hyphema

<10%

Traumatic hyphema

r/o rupture

Fox shield

Restrict activity/head elevation

Hospitalization?

D/C blood thinners

ASA, NSAID’s

Atropine

Pred Forte qid

~30% have elevated IOP

Beta blocker

Gonio ~ 1 month later

r/o sickle/sickle trait

10-20% re-bleed rate

More common w/Gr. 3-4

corneal staining, glaucoma, optic atrophy

Systemic aminocaproic acid (ACA)

Ocular Emergencies


Angle Recession

Blunt trauma which causes a hyphema is more likely to also cause an angle recession

Between 2 and 20% of patients with angle recession will go on to develop glaucoma

Traumatic Glaucoma

patients with damage to greater than two-thirds of angle are also more likely to develop glaucoma

glaucoma associated with angle recession may develop months to years following the injury

Glaucoma is related to magnitude of hyphema,

Only 13% get when hyphema is less than half of AC

Bed rest (head elevated) or very limited activity along with patching are usually recommended.

Management

Early Phase Glaucoma and Acute Trauma

Acute Inflammation / Iritis

Hyphema

red blood cells in the anterior chamber

results from a tear in the angle that breaks a blood vessel

rebleeds occur up to 7 days after trauma

Ocular Emergencies


Hyphema

Measure the percent of hyphema in AC

Measure the IOP

may have very high IOP

NO gonioscopy,

must wait 7 days to prevent causing a rebleed

Check sickle cell status

Those with SC may need AC wash out

Medications: Early Phase

For Inflammation:

Cycloplegia:

w/ atropine 1% BID, Homatropine 5%

Topical steriods:

prednisolone acetate 1% QID

NO aspirin products: rebleed

Elevated IOP from Hyphema

PGAs:

Not an option for early phase

Good option b/c uveoscleral outflow

Beta Blockers

Timoptic XE, Betagan, etc.

Alphagan

Topical or Oral CAI’s

Cosopt or Combigan= good option

The usual duration of an uncomplicated hyphema is 6 days

Anterior Chamber “Wash Out”

Ocular Emergencies


Trauma - Penetrating Injury

If rupture- STOP exam

Fox shield and to hospital for exam under anesthesia

CT if foreign body can’t be seen

Systemic antibiotics

Compromise protective outer layers, increasing the risk of infection

Risk of endophthalmitis

Intraocular contents may be outside the globe

Trauma - Laceration

Corneal

Conjunctival

Lid

Be alert with high velocity injuries for intraocular foreign bodies

Seidel’s sign: (+) full thickness laceration

Corneal Lacerations

Full thickness

protect w/ shield & immediate referral

Partial thickness

treat as abrasion

Ocular Emergencies


Corneal Laceration

41yoCM- construction foreman

Nail ricocheted off a wall and hit his OD 1 day prior – felt OK

Today, 5/10 pain, photophobia, FBS

h/o metallic FB 10 ya

Recent tetatnus shot

Corneal Laceration

Va OD: 20/20; OS: 20/25

(+) epi defect

(+) AC rxn

(-) Seidel’s sign

TA 9 mmHg, OU

Lid eversion negative

Fundus exam WNL

+ Ocuflox

+ Cyclogyl

Get CT to r/o intraocular foreign body

Corneal Laceration

1 day follow up, feels 50% better

Va 20/30

No epithelial defect

+ stromal haze

Decrease Ocuflox

Start Pred-Forte

Ocular Emergencies


Conjunctival Lacerations

SLE

Subconj heme

(+) Fl stain

DFE

Mild Majority are self-limiting Antibiotic, patch, follow up 1 day

Severe

Antibiotic, patch & refer

Blow Out Fracture

Direct trauma to the globe causes an increase in intra-orbital pressure & decompression via orbital floor fracture

Maxillary bone & posterior medial wall

Periorbital swelling, ecchymosis & restricted eye movement

Diplopia, hypesthesia of cheek & teeth, orbital pain

Most common sign is limited upward or downward gaze due to entrapment of IR or IO

Crepitus

palpate the bony rim of the orbit or lid

small bubbles of air "pop" when compressed.

Management

When should surgical repair of blowout fractures be considered? Fractures with persistent symptoms (typically double vision or pain) are

usually candidates for surgical repair. Timing of the repair varies, but most often is within two weeks of the injury. Initial repair may consist of any of the following:

• exploration of fracture site and repositioning of bone• release of trapped tissue from fracture site• covering of fracture site with synthetic material

What long-term problems may develop following blowout fractures? Most fractures heal without long-term effects. However, strabismus

surgery (eye muscle surgery) is sometimes necessary for persistent double vision. Occasionally, persistent double vision can be treated with non-surgical methods (prism glasses or botulinum toxin injections)

Ocular Emergencies


Blow Out Fracture

Ice packs 24-48 hours, no nose blowing

Recovery can be spontaneous - 2-3 days

Systemic antibiotics

Can trigger orbital cellulitis, angle recession glaucoma, & RD.

Prompt surgery if poor cosmesis, persistent diplopia, enophthalmus, pediatric patient with entrapment

Corneal Abrasion

Acute pain & photophobia

May need anesthetic to perform exam

Debride loose epi if necessary

Antibiotic/cycloplegic/NSAID

Pressure patch v. Bandage CL

RCE issues

Corneal Abrasion

44yoCM

CC: Pocked in OS with belt buckle 1 day prior

: S/P PRK OU

(+) FBS, photophobia, redness

Antibiotics Cycloplegic Treat any associated anterior

chamber reaction BCL? Debridement of loose tissue RCE issues Fingernail, paper, fingernail, pre‐existing EBMD

Ocular Emergencies


Corneal/Conjunctival Foreign Body

• History important

• ? object

• High speed?

• DFE

• SLE

• Lid eversion

1) Removal:irrigation, moistened cotton swab, spud, needle, forceps, Alger brush

2) Antibiotic/cyclo/patch/BCL

3) Steroids for scar modulation after defect healed

Rhegamatogenous Retinal Detachment

Symptoms: Flashes Vitreous separates from

the retinal pigment epithelium

Floaters Separation at retinal

vessel may leak blood into the vitreous

Decreased VA from macular involvement can lead to severe, permanent vision loss

Separation of neurosensory retina from the underlying RPE, by fluid from the vitreous cavity and into the sub-retinal space.

Time course of retinal break or defect to time of detachment is highly variable and unpredictable

Rhegamatogenous RD

Develop from Retinal Defect:

Hole or Break in sensory retina

Frequently from Posterior Vitreous Detachment (PVD)

Other Forms of Retinal Detachments:

Exudative

Tractional

Ocular Emergencies


Retinal Detachment

• 51yo AAM presents to Urgent Care @ IEI• CC: Sudden blurry vision superiorly OS

• x1 week, painless & progressive(-) trauma(-) flashes

• POH: Cataract extraction, OU • LEE: 2 years ago at IEI, no SRx

• PMH: HTN, NIDDM (controlled)

Entrance Examination

• VA sc: OD 20/60+1 PH: 20/60+2• OS 20/50-1 PH: 20/40+2

• Pupils: PERRL 1+APD(OS)

• EOMs: FROM OU

• CVF: FTFC OD• Constricted superiorly OS

Slit-Lamp Examination

OD OS

Adnexa/Lids: 1+ MGD 1+ MGD

Conjunctiva/Sclera: W&Q W&Q

Cornea: Unremarkable Unremarkable

Angles: 4+T/4+N 4+N/4+T

Anterior Chamber: D&Q D&Q

Iris: Unremarkable, (‐)NVI Unremarkable, (‐)NVI

Lens:PCIOL in place, intact,

clearPCIOL in place, intact,

clear

IOP (Goldmann): 14 12

Anterior Vitreous: Unremarkable (+)Shafer’s sign

Ocular Emergencies


Rhegmatogenous Retinal Detachment

Patient education:

risk of permanent vision, need for IMMEDIATE retinal referral.

Patient Treatment and Outcome:

RRD Statistics

Prevalence: RRD 10-15/100,000• 70%: Non-Traumatic

• 50% myopic• 1-3D: 4x risk, >3D: 10x risk

• 10% increased risk in fellow eye• 10%: Trauma• 20%: Post-Cataract Surgery

• S/P Cataract Extraction• 10 year risk: 6x risk

• S/P Refractive lens exchange • 2-8% RRD within 1 month

• 20 - 30% have lattice degeneration

SYMPTOMATOLOGY

Often asymptomatic and thus detected on routine examination

Inferior and temporal location from atrophic holes Patients less aware of these slowly progressive RDs as superior and nasal

fields of view are less sensitive

Flashes/Floaters. Yes or No? Not noticed while sleeping Unilateral symptoms often masked Not affecting central vision Slow progression/change Frequent “Red Herring” TIA, acephalgic migraine, PVD w/o detachment PVD Follow Up: 6-8 weeks of exam detection or with increased

symptoms

Ocular Emergencies


Key Findings for Referral

Finding a retinal break

Finding subretinal fluid

May not find break, but it’s likely there as that’s how the fluid got in

Other Signs:

Acute PVD

Pigment cells in vitreous or vitreal heme

Techniques to help:

Scleral depression and 3-Mirror retinal exam

OCT

OCT for RD

Use Wide-field Mode

Helpful in Differential diagnosis

Helpful in determining macular status

“on or off”

Treatment

Laser Slit lamp or Laser Indirect Ophthalmoscopy

LIO for more peripheral breaks

For subclinical holes and breaks with limited SRF and areas of contact between the retina and RPE remain

Laser is applied at the border of the attached and detached retina, the photocoagulation creates “seal” that prevent further progression of the break/detachment

Monitor Asymptomatic Breaks?

Low (~5%) risk for progression

Ocular Emergencies


Treatment

Pneumatic Retinopexy (62-78%) Oil/Gas bubble with laser

Pars Plana Vitrectomy: small incision Fluid-Air, air-gas exchange, silicone oil injection with

laser

Scleral Buckle: for larger RDs

Thin scleral band placed under conjunctiva to indent sclera towards retina followed by laser or cryotherapy

Decreased in utilization in favor of PPV due to numerous SEs

Clinical Pearls - Urgency

Macula Off Duration Mean Postoperative VA†

≤10 days 20/41

11 days to 6 weeks 20/121

>6 weeks 20/178

Macula On Status Timeframe

Progressive/large Immediate/next day

Stable/small/inferior <5 days

†Scleral buckle repairs

Endophthalmitis

Incidence 0.13%

( review of 215 articles from 1963-2003)

Symptoms:

Pain, decreased vision, photophobia, redness

Signs:

Corneal edema, hypopyon, vitritis,

Ocular Emergencies


Endophthalmitis Vitrectomy Study (1995)

420 patients < 6 weeks post CE or 2o IOL c s/s of endophthalmitis

Randomized to +/- systemic antibiotics

Randomized to ParsPlanaVitrectomy (PPV) v AC tap & vitreous injection with antibiotics

Results:

Patients with > LP: Tap and inject (no need for immediate PPV)

Patients with < LP: Immediate PPV, and inject

3 fold increase in the frequency of achieving 20/40 or better acuity

Acute Angle Closure Glaucoma

Classic Symptoms:

Unilateral, painful eye

Blurred vision, halos

Nausea, vomiting

Characteristics:

Older, white, hyperopic females age > 30 yrs

Peak age 55-70

First-degree relative with ACG

History - previous episodes, medications, surgeries, etc.

When can the angle close?

Ocular Emergencies


Acute Angle Closure Glaucoma

Symptoms: Pain, halos around lights, redness, nausea, vomiting

Signs: Corneal edema, fixed,oval mid-dilated pupil, ciliaryflush, AC inflammation, glaukomflecken

Extremely elevated IOP

Gonioscopy

Indentation

Both eyes

CLINICAL FEATURES:

Acute Angle Closure Attack:

diffuse conjunctival hyperemia

cloudy, edematous cornea

fixed, oval, mid‐dilated pupil

VA often significantly reduced

IOP ranges 40‐70+ mm Hg

inflammation / aqueous cell/flare

“CLASSIC” PATIENT SYMPTOMS:

These symptoms are associated with “Acute” Angle Closure deep, aching pain (high IOP)

redness, tearing, photophobia

blurred vision, halos (edema)

nausea, vomiting (pain)

Headache

Note:

Many patients do NOT have these symptoms

Ocular Emergencies


GONIOSCOPY

Look for PAS (peripheral anterior synechia) as evidence of angle closure

Gonioscopy of both eyes to confirm a narrow angle approach (symmetry)

Only Indentation gonioscopy shows this, not three mirror.

Gonioscopy Lenses Posner 4 mirror

» Handle

Sussman 4 mirror» No handle

» www.ocular-instruments.com

Indentation Gonioscopy

A. = Appositional angle closure

B. = Synechial angle closure

Ocular Emergencies


Gonioscopy on the Web!

www.gonioscopy.org

When can the angle close?

Management - Acute Angle Closure Glaucoma

Oral CAI’s (250 - 500 mg Diamox) Tablet form only, not Sequel form Sequel takes too long to act

Topical fixed combination: Combigan / Cosopt Iopidine (if available)

Topical steroids

When IOP < 45, add 1-2% pilocarpine

Definitive Treatment: Laser Peripheral Iridotomy (LPI) Eliminates pupillary block

Prophylactic LPI of fellow eye

Ocular Emergencies


Corneal Ulcer

Peripheral vs Central

Infection

Staph, strep, moraxella, pseudomonas

Pain, redness, photophobia

CL wear

Chronic eyelid disease

SLE: focal accummulation of inflammatory cells in excavation with overlying epi defect

Corneal Ulcer

15yoCF

Being treated elsewhere for Corneal ulcer, OS

> 1 week with fortified antibiotics, oral AB’s

SCL wearer

Fell asleep on a road trip

VA sc: OD 20/20, OS 20/400 PH NI

Differential Dx

Infiltrate

Ulcer

Pseudomonas

Fungal

Acanthamoeba

Ocular Emergencies


Corneal Ulcer Treatment

Discontinue CL wear

Antibiotic

BESIVANCE (besifloxacin) 0.6%

1 gtt q15minX 2 hrs, then hourly while awake

Cycloplegic

Culture if available, if central, if >3mm

Corneal Ulcer Treatment

Fortified agents?

subconjunctival loading dose injection of 0.3 cc gentamicin mixed with 0.3 cc lidocaine at the time of presentation

Steroids when defect is closed to modulate scarring The SCUT study (Steroids for Corneal Ulcers Trial), a large series

involving 500 patients that was published in the Archives of Ophthalmology, found no overall difference in three-month BSCVA and no safety concerns with adjunctive corticosteroid therapy for bacterial corneal ulcers

If NI, consider fungal or acanthamoeba….

Optic Neuritis

Unilateral, acute loss of vision Women, 20-45yo, AA Strong association with MS The patient’s history may reveal the following signs and symptoms of optic

neuritis: Preceding viral illness Rapidly developing impairment of vision in 1 eye or, less commonly, both

eyes: During an acute attack Dyschromatopsia in the affected eye: Occasionally may be more

prominent than the decreased vision [4]

Retro-orbital or ocular pain: In association with the vision changes and usually exacerbated by eye

movement; the pain may precede vision loss Uhthoff phenomenon, in which vision loss is exacerbated by heat or

exercise

Ocular Emergencies


Optic Neuritis: Signs and Symptoms

Varying degrees of vision reduction:

Ranging from a mild decrease in visual acuity to complete vision loss, which is often monocular but can be binocular

scotomas, ocular or orbital pain, worse on EOM’s

(+) APD, color vision & VF loss

Abnormal contrast sensitivity and color vision:

In almost all patients with adult optic neuritis who have decreased visual acuity

Optic Neuritis: Signs and Symptoms

Field defects: May include altitudinal, arcuate, nasal step, central

scotoma, cecocentral scotoma

Initially, the optic nerve head may appear normal.

Papillitis (swollen disc) may be seen in one third of patients with optic neuritis

Evaluation and Workup

Magnetic resonance imaging (MRI) is highly sensitive for and specific in the assessment of inflammatory changes in the optic nerves, and for central nervous system white matter lesions.

MRI also helps to rule out structural lesions.

Labs. Only if other forms of neuritis are possible

Erythrocyte sedimentation rate

Thyroid function tests

Antinuclear antibodies

Angiotensin-converting enzyme

Rapid plasma reagin

Mitochondrial deoxyribonucleic acid (DNA) mutation studies

Ocular Emergencies


Management

Visual function begins to improve 1 week to several weeks after onset, even without any treatment

Permanent residual deficits in color vision and contrast and brightness sensitivity are common

Pharmacologic therapy in optic neuritis (ON) is directed at ameliorating the acute symptoms of pain and decreased vision caused by demyelinating inflammation of the nerve; varying regimens of corticosteroids have been used for this purpose.

IV steroids do little to affect the ultimate visual acuity in patients with optic neuritis, but they do speed the rate of recovery;

Some clinicians advocate IV steroids in patients with either severe or bilateral vision loss

Optic Neuritis Treatment Trial

448 pts

Oral placebo, IV steroids with placebo orals, or oral steroids

The primary goal was to determine whether oral or IV steroids altered the visual outcome in patients with acute optic neuritis.

IV steroids accelerated recovery of VA initially, but provides no longterm benefit.

Oral steroids provided no visual benefit and was associated with a higher rate of recurrence.

Initial MRI result, if abnormal with white matter abnormalities, was the single most important predictor of the future risk of MS Routine blood tests of no value

If Possible MS

For patients with optic neuritis whose brain lesions on MRI indicate a high risk of developing clinically definite MS, treatment with immunomodulators:

interferon [INF] beta-1a,

INF beta-1b,

glatiramer acetate

(may be considered)

Ocular Emergencies


Papilledema

Bilateral optic nerve head edema, secondary to increased ICP

Decreased acuity may not be presenting symptom

Headache

Need imaging to rule out space occupying lesion

Lumbar tap/CSF studies

Pseudotumor Cerebri - Dx. of exclusion

Central Retinal Vein Occlusion

Non-ischemic v. Ischemic

Ischemic – less common, more severe with poorer prognosis

NVG/NVI

q1month x 6months, q2-3 months x 6 months, q4-6 months x 3 years

Men > 50

<40: Needs systemic workup

antiphospholipid antibody syndrome

Poor acuity, possible APD

Hemes, dilated vessels, CWS, retinal & macula edema

Lower IOP

Neovasculogenesis:

Chronic retinal hypoxia is theorized to initiate the production of an angiogenic substance / vasoproliferative substance which elicits new blood vessel growth.

Vascular Endothelial Growth Factor (VEGF)

Iris tissue is the primary site for developing neovascularization.

Progresses through several stages:

Ocular Emergencies


Angle Closure Stage

Time frame for development to this stage:

can be variable, from days to months

NVG is known as the:

"Ninety day glaucoma“, because of its rapid onset

Features:

pain, photophobia

decreased Va

increased IOP, high

conj. congestion

iritis

corneal edema

rubeosis iridis

ectropian uvea

synechial angle closure

First Step= Medical treatment.

Medical therapy is directed at lowering the IOP, reducing the anterior segment inflammation and making the patient more comfortable.

Note the similarities and differences to the management of primary acute angle closure

Rapid IOP Reduction:

Acetazolamide: 250 mg x 2

Beta blocker and Alphagan

Anti-inflammatory:

prednisolone acetate 1%

Atropine 1%

For pain and inflammation

Referral for Avastin and PRP

Ocular Emergencies


Central Retinal Vein Occlusion

Prompt referral to PCP

FBS, ESR, CBC, lipid profile, FTA-ABS

Strong association with HTN, DM, POAG

Check BP and IOP in office

Hyperlipidemia, hyperviscosity

Macula edema treatment:

Avastin

Ozurdex

Kenalog

PRP

Orbital Cellulitis

Usually results from spread of infection from paranasal sinuses

CT

ENT consult

Tx with IV antibiotics

Must distinguish from Preseptal

Both present with lid edema, pain, redness

FEVER

PROPTOSIS

PRECIPITATING EVENT

ANY AGE, SEX, RACE

Patient “Emergencies”

Ocular Migraine

Redness/itching/burning/discharge

Subconjunctival hemorrhage

Gradual change in visual acuity

Lid bumps (non- painful)

Refractive changes

Ocular Emergencies


Take Home Message

Be prepared

Have appropriate equipment/ referrals in place

Take the time to train your staff

You are ultimately responsible

Be methodical in your thinking & your examination

Know when it’s OK to treat, and when you must refer

Thank you!

saturday, july 7th

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