7/30/2018

1

CURRENT TRENDS IN

PHARMACOLOGY

Joseph Sowka, OD

Lori Vollmer, OD

Jessica Steen, OD

Greg Caldwell, OD

Joseph Sowka, OD is/ has been a Consultant/ Speaker Bureau/Advisory Board member for Novartis, Allergan, Glaukos, andB&L. Dr. Sowka has no direct financial interest in any of thediseases, products or instrumentation mentioned in thispresentation. He is a co-owner of Optometric EducationConsultants

The ideas, concepts, conclusions and perspectives presented

herein reflect the opinions of the speaker; he has not been

paid, coerced, extorted or otherwise influenced by any third

party individual or entity to present information that conflicts

with his professional viewpoints.

DISCLOSURE:

DISCLOSURES- GREG CALDWELL, OD,

FAAO

Will mention many products, instruments and companies during our

discussion

• I don’t have any financial interest in any of these products, instruments or companies

Pennsylvania Optometric Association –President 2010

• POA Board of Directors 2006-2011

American Optometric Association, Trustee 2013-2016

• Thank you to the members and those who join

I never used or will use my volunteer positions to further my lecturing career

Lectured for: Shire, BioTissue, Optovue

Advisory Board: Allergan

Envolve: PA Medical Director, Credential Committee

He is a co-owner of Optometric Education Consultants

Dr. Jessica Steen: None

Dr. Lori Vollmer: None

DISCLOSURE:

CASE

72 year old female. Presents with 6 week hx. of scalp pain, fatigue, weight loss, TVO OD.

Presents to optometrist with sudden vision loss OD

Findings: OD NLP; OS 20/20

Diagnosis: “papilledema” OD. Plan: refer to ophthalmologist next day

Presents to ophthalmologist: NLP OD; NLP OS

Diagnosis: bilateral AAION

CASE

74 year old male

Hx: 2 wks HA, 10 day jaw claudication, 5 days intermittent diplopia

FP referred to dentist: removed 2 decayed teeth

Days later went from 20/20 to NLP OD

Ophthalmology Dx: “blocked artery”; Referred to vascular surgeon-ordered carotid Doppler in 1 week

2nd eye 20/20 to NLP: AION. ESR 90

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CASE

78 year old female

Hx: 1 week occipital & jaw pain

FP tx: NSAIDS

2 days later: 1 hr TVL OU; OD recovered; OS not

FP tx: d/c NSAIDS: refer to ophthalmology

Ophthalmology: suspects NSAID ‘reaction’; Wait a week for NSAIDS to ‘wear off’ before coming in

Next day: OD NLP ESR 117

CASE

76 year old female

Muscle aches x 4 weeks; DX: viral

infection-abs

Worsens x 2 wks; Pain while chewing:

same dx/tx

Tabloid article: pain when chewing- see

eye doctor

General service eye hospital; Normal

exam

Sed rate 129 (+) TAB

(+) Prednisone: symptoms abate

GCA: PATHOPHYSIOLOGY

Idiopathic, multisystem inflammation

Internal elastic lamina: medium and large

The interleukin-6 pathway is up-regulated in GCA.

There is cellular infiltration of the muscular wall of

these vessels by T lymphocytes, macrophages,

histiocytes, plasma cells, and multinucleate giant

cells.

The resultant inflammation fragments the vascular

walls and leads to collapse of the vessel lumen with

resultant ischemia.

GCA: PATHOPHYSIOLOGY

Vessel occlusion: ischemia

Women:men 2:1 - 4:1

Caucasian > African American

Vascular distribution: GSTA 100%, vertebral 100%, ophth/post ciliary 75%

CF in 60%; 2nd eye involved in 65%: 1-10 days

Average age 75 yrs; 33/100,000 in 60-69y;

844/100,000 69+

GCA: MANAGEMENT

Treatment controversial

Rheumatologic: low dose oral (20 mg):good

Ophthalmologic: High dose: not so good

Depend upon severity of the disease

Pulse methylprednisolone 1-2gm IV (in patient)

- Very effective in prevention of second eye

- Occasionally restores vision

Tapered to 60-100 mg prednisone PO

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GCA: MANAGEMENT

Oral steroids only? - Curry et al: no good eyes lost on pulse;

Several good eyes lost on oral. Recovery of eyes on pulse, none

on oral

Taper dose to hold ESR down

Suppression of symptoms not adequate

Treat for up to 2-4 years

Alternatives: dapsone, methotrexate, dolobid, ASA

Poor prognosis

Systemic symptoms abate quickly with steroids

Visual loss often permanent; May progress despite aggressive

treatment

STEROID COMPLICATIONS

Suppression of the disease usually takes

months to years

Complications of long term steroid use

- Ulcers and gastrointestinal bleeding

- Osteoporosis

- Increased risk of heart disease

- Diabetes

- Decrease in bone density

- Increased risk of infections

- Thin skin, easier bruising, and slower healing of wounds.

Let’s qualify this statement

Recently the Food and Drug Administration

(FDA) has granted a breakthrough therapy

designation to tocilizumab (Actemra,

Genetec) for the treatment of GCA. This is the

first innovative therapy for GCA in more than

50 years. The breakthrough therapy

designation is designed to speed the

development for treatments of serious

diseases such as GCA and certain cancers.

Unpublished results of the GiACTA trial, a

multicenter, randomized, double-blind, and

placebo-controlled study designed to test the

ability of tocilizumab, an interleukin (IL)-6

receptor antagonist, to maintain disease

remission in patients with GCA.

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- Patients were randomized to receive tocilizumab 162 mg

weekly injections plus a 6-month and 12-month

prednisone-taper compared to controls receiving

placebo plus similar steroid taper.

- The preliminary results indicate that patients receiving

high dose tocilizumab had superior disease remission at

1 year compared to the steroid-only taper.

- Further investigation from this study will attempt to

identify the lowest therapeutic dose of prednisone that

can be used in patients also using tocilizumab, the

amount of tocilizumab needed to induce remission, and

how long patients stay in remission on this therapy.

Tocilizumab does not directly treat GCA

- Reduces steroid load after disease has been adequately

treated by steroids and enhances disease remission

Steroids are main therapy

Studies are ongoing to see:

- What is the lowest steroid tapering dose that can be

used with tocilizumab

- Future studies may show tocilizumab as steroid

replacement

GiACTA trial-

- 1 patient with fatal MI and 1 with blinding AAION when

steroids stopped

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TOXIC AND NUTRITIONAL

NEUROPATHY

41 year old African American female presents for initial assessment

Sudden onset of glare and decreased vision in both eyes, starting 1 month ago. She reports previously having “perfect vision” all her life.

Numbness in her fingers

Denies taking any current medications or substances other than smoking cigarettes. Past history of smoking marijuana.

PERTINENT FINDINGS

Best corrected visual acuity:

- OD: 20/400

- OS: 20/200

Pupils:

- Equal, round, reactive however slow to release OD,OS, (-) RAPD

Confrontation Fields:

- Full to finger count OU

EOMs: full with no restrictions OD,OS

Color vision:

- Failed Ishihara OD,OS

POSTERIOR SEGMENT

Temporal disc pallor

OD, OS

Sectoral temporal RNFL

thinning of optic nerves

OU

REVISITING THE CASE HISTORY

When questioned more specifically in regards to

taking substances and her general health, she

reported having 3-5 “strong” drinks each day for at

least 5 years.

She reported a history of being hospitalized for a

vitamin deficiency one year ago, and the doctors had

told her it was likely related to alcohol abuse.

FOLLOW-UP EXAMINATION

MRI of brain, CT-scan, and EKG were all normal.

Blood work revealed high cholesterol, low

magnesium and iron levels. Patient was put on

Lipitor and mineral supplements.

Patient reports that vision has remained relatively

stable, with not much improvement.

TOXIC OPTIC

NEUROPATHY

Visual acuity: ranges from 20/40- 20/400

Presentation: painless, progressive,

bilateral, visual loss

Clinical signs: negative RAPD, temporal

optic nerve pallor, papillomacular

bundle damage seen on OCT, central or

cecocentral scotomas, and abnormal

color vision in both eyes

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TOXIC OPTIC NEUROPATHY

Causes: ethambutol, isoniazid, antimicrobials

(chloramphenicol, streptomycin, penicillamine),

halogenated hydroxyquinolones, vigabatrin,

disulfiram, tamoxifen, sildenafil, methanol, heavy

metals, fumes, solvents, alcohol and tobacco abuse.

Clinical Pearl: When you encounter a pt with TB,

consider/ inquire ethambutol use and evaluate to TON

NUTRITIONAL OPTIC

NEUROPATHY

Due to similarities in appearance and

pathophysiologic responses, toxic optic

neuropathy and nutritional optic neuropathy

cannot be distinguished clinically from one

another and consequently both are typically

discussed together.

NUTRITIONAL OPTIC

NEUROPATHY

Causes: B-complex vitamin deficiencies including

thiamine (B1), riboflavin (B2), niacin (B3), pyridoxine

(B6), cobalamin (B12), and folic acid.

Associations: malnutrition and less economically

established living environments, poor nutrition

associated with alcoholism/drug use, poor nutrient

absorption with bariatric surgery

TOXIC AND NUTRITIONAL OPTIC

NEUROPATHIES

Dyschromatopsia begins early on and can be the initial sign

Patients may notice certain colors to be more dull compared to before

Patients may experience neurologic symptoms of “stocking and glove” peripheral neuropathy, especially in B12 vitamin deficiencies

TOXIC OPTIC NEUROPATHY

Not all cases of toxic optic neuropathies are isolated to the optic nerve. Other structures that may be involved include the retina, chiasm and optic tracts.

The etiology for toxic optic neuropathy is unclear. It is thought that the toxin(s) cause disruption to free radicals leading to mitochondrial damage of the nerve tissue.

This may be for their similar presentation to Leber’sand Dominant optic atrophy as they all share a common pathogenesis of mitochondrial injury.

Ethambutol used in treating tuberculosis is the most common offending agent.

TOXINS: VIGABATRIN

Vigabatrin (Sabril) is a selective, irreversible, inhibitor of GABA

transaminase for refractory complex partial seizures and

infantile spasms.

Vigabatrin has clearly been shown to cause a dose-dependent,

permanent peripheral field constriction.

The earliest reports of toxicity were after 11 months of

exposure. The vision loss is usually asymptomatic and spares

the macula, but sub-clinical depression of macular function and

color vision deficits have been reported.

The mechanism has not yet been fully demonstrated, but most

likely involves toxicity to both retinal photoreceptors and

ganglion cells.

Possibly induces a taurine deficiency that leads to toxicity

- Taurine supplementation may prevent toxicity

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ORDERING THE APPROPRIATE

TESTS

Ordering the MRI:

- Specify orbits and chiasm

- With and without gadolinium enhancement (contrast)

- High resolution

- Fat suppression

ORDERING THE APPROPRIATE

TESTS

Ordering systemic tests

- CBC with differential

- Metabolic panel

- Urine analysis for bicarbonate

- Serum levels of complex vitamin B and red blood cell

folate

• Serum B12 for pernicious anemia

• Red blood cell folate levels for general idea of

nutritional status

- Heavy metal screening (lead, thallium, and mercury)

Variable, as it depends on the nature of the substance or

nutritional deficiency.

Often dependent on the dosage and duration of exposure to the

toxic substance. Following discontinuation of the substance, it

is possible for some visual improvement over several days or

weeks.

In some early cases, vision has found to return to normal. The

difficulty remains being that the diagnosis is often made once

the damage is irreversible, resulting in permanent vision loss.

Once the nerve tissue has atrophied, it does not regrow or

regain function.

PROGNOSIS PROGNOSIS

Stop offending agent immediately, this may allow for some reversal of the process

If there is some recovery, visual acuity recovers before color vision

In acute cases, vitamin supplementation of 100 mg/d thiamine, 1 mg/d folic acid, 1000 mg/d vitamin B12 for at least 6 months

CASE

• 65 year old white male presents for evaluation of “anterior uveitis” of the right eye which began 4 days ago

• Has been self-medicating with Lotemax every 2 hours for 4 days without improvement

• Medical History

• Right knee replacement 2010

• Right (1990) and left (1991) hip replacement

• Psoriasis

• Ocular history

• Scleritis (OD 2006)

• “Multiple episodes of uveitis affecting both eyes for the last 20 years”

• Medications

• Aleve (as needed for joint pain)

• Omega 3, multivitamin

• Humira (40mg once per month)-last injection 1 month ago

CASE

• BCVA 20/25 OD and OS

• Trace cells, 1+ flare OD

• Area of focal posterior synechia OS

• IOP 14mmHg OD and OS

• 1+ NS OD and OS

• Unremarkable DFE

• Anything else you may want to know about?

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CASE

• “Oh yeah, typically I know when a uveitis

episode is coming…I get a psoriasis patch a

couple of days before…”

UVEITIS MANAGEMENT

• Manifestation of approximately 30 disease

• All share features of intraocular inflammation

UVEITIS

• May be a result of:

• Infection

• Tuberculosis, Lyme disease, cytomegalovirus, syphilis,

herpes virus

• Systemic disease

• Sarcoidosis, Behcet’s disease, Vogt-Koyanagi-Harada

syndrome, ankylosing spondylitis, juvenile idiopathic

arthritis

• “Undifferentiated” non-infectious cause

• Inappropriate immune system response to inflammatory

trigger

ANTERIOR UVEITIS

• Most common presentation

• Typically well-managed with topical steroids

• And adjunctive agents (cycloplegics)

INTERMEDIATE, POSTERIOR,

AND PANUVEITIS

• First rule out infection, or treatable underlying systemic

disease (and masquerade syndromes)

• Chronic inflammatory states require long term treatment

• Periocular and systemic steroids often required

PERIOCULAR AND

INTRAVITREAL STEROIDS

• Triamcinolone acetonide

• Kenalog (off-label for intraocular injection)

• Commonly used for periocular injections

• Triescence (preservative free)

• On-label for intraocular injection

• Abbreviated “IVTA”

• Ozurdex (0.7mg dexamethasone implant)

• Lasts 3-6 months

• Retisert (fluocinolone acetonide 0.59mg)

• Iluvien (fluocinolone acetonide 0.19mg)

• May last up to 36 months

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THE TROUBLE WITH LONG TERM

STEROIDS

• Periocular and intravitreal (Kenalog, Triescence, Ozurdex,

Retisert, Iluvien)

• Elevated IOP, cataract

• Systemic (prednisone)

• Elevated blood pressure

• Blood glucose dysfunction

• Weight gain

• Osteoporosis

• GI ulceration

• Fluid retention

• Neuropsychiatric effects

WHAT ELSE HAVE WE GOT?

• Non corticosteroid options:

• 1) Disease modifying antirheumatic drugs (DMARDs)

• Methotrexate, azathioprine, mycophenolate mofetil

• Hydroxychloroquine

• Suppress the entire immune system

• 2) Biologic agents

• Bioengineered complexes which target specific

immunologic modulators

• Suppress downstream inflammation

• TNF-alpha inhibitors, interleukin-blockers

BIOLOGIC AGENTS IN UVEITIS

• Humira (adalimumab subcutaneous injection 40mg/0.8mL)

• TNF alpha inhibitor

• TNF alpha is a proinflammatory signaling protein

upregulated in many forms of uveitis

• Indicated for the treatment of non-infectious intermediate,

posterior, and panuveitis in adults

• June 2016

• 80mg initial dose; followed by 40mg every two weeks-

starting one week after initial dosage

ADVERSE EFFECTS OF TNF

ALPHA INHIBITORS

• Demyelinating disease

• Induction, or unmasking of

• “Lupus-like syndrome”

• Autoantibody formation

• Hepatitis B activation

• Reactivation of latent tuberculosis

• Possible increased risk of lymphoma

• Medical vs. systemic disease?

DRIVE TOWARDS PRECISION

MEDICINE

• Other biologic agents used in rheumatologic disease are

being explored In uveitis treatment

• Underlying pathogenesis of uveitis varies

• Specific immune system targets may be central in one

disease state—and not another

• Goal will be to identify a particular pathway target in an

individual to effectively suppress inflammation

• Individualized approach

RHOPRESSA

• Netarsudil (0.02%)

• Rho-kinase and norepinephrine transport inhibitor

• Dosed once daily in the evening (QHS)

• Preserved with BAK 0.015%

• FDA approved December 18, 2017

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RHO-KINASE INHIBITORS

• Rho family includes 3 guanosine triphosphate (GTP)-

binding proteins which regulate cell shape, motility,

proliferation and apoptosis

• RhoA, RhoB, RhoC

• Regulate smooth muscle contraction in the TM and ciliary

body

• Rho kinase inhibition relaxes trabecular meshwork cells

• Increase trabecular outflow

• May also affect ocular blood blow and retinal ganglion cell

survival

• Role in development of fibrosis?

MECHANISM OF ACTION

• “Triple action response”

• 1) Increases trabecular outflow (RKI)

• 2) Reduction of aqueous fluid production (NET)

• 3) Episcleral venous pressure reduction (RKI)

RHOPRESSA ADVERSE

EVENTS

• #1: Hyperemia

• Rho-kinase inhibition causes vasodilation

• Corneal verticillata

• AKA “whorl keratopathy” found in patients taking

amiodarone

• Subepithelial corneal deposits

• Most resolved after drug discontinuation

• No effect on vision

• Subconjunctival hemorrhage

EFFICACY

• Initial concerns with efficacy

WHERE DOES RHOPRESSA

FIT IN?

• Efficacy is similar to timolol 0.5% (BID)

• Likely a second line treatment

• Seems to work better with low/moderate IOP

(

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LUCENTIS FOR NPDR

WHAT ELSE?

Search for other therapeutic modalities

- Potentially less destructive tissue effects PRP

- Reduce risk of progression to PDR and severe visual

acuity loss.

Anti-VEGF agents show promise in

treatment of NPDR and already shown to

been effective in treating DME.

VEGF IN NPDR

Intraocular levels of VEGF correlate with

severity of DR.

As VEGF levels increase, feedback loop

created, further enhancing intraocular

ischemia and promoting further VEGF

release.

Theory: Halt the feedback loop and block

VEGF release or VEGF receptor binding.

PARADIGM SHIFT

Several studies demonstrated superiority of

anti-VEGF agents over macular laser for

treatment of DME.

Number of trials show when DME is treated

with anti-VEGF therapy many patients exhibit

a reduction in DR as a positive byproduct.

RISE AND RIDE

The phase III study

Established the safety and efficacy of

ranibizumab (Lucentis, Genentech) for DME

Demonstrated that anti-VEGF therapy yielded

improvement in DR severity score (DRSS)

- 37.2% 2-step improvement

- 13.2% 3-step improvement

RISE AND RIDE

Subgroup analysis focused on individuals

with DRSS scores between 47 and 53 (high

risk for progression to PDR)

Ranibizumab yielded stabilization or

improvement in severity in 75% of these

patients.

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DRCR.NET

Protocol S trial conducted by the Diabetic

Retinopathy Clinical Research Network

(DRCR.net

Lucentis 0.3 mg dose initially approved for

DME. (approved dose for DME)

Protocol S trial only included Lucentis 0.5

mg dose approved for all other indications.

LUCENTIS FOR NPDR

Lucentis’s approval includes ALL patients

with DR (though the population in Protocol S

trial was largely patients with PDR).

Just over one-quarter of DR patients without

DME experienced at least a 3-step

improvement in the (ETDRS-DRSS).

Approximately 38% had at least a two-step

improvement.

LUCENTIS VS PRP

Recommended dosing of one injection per

month for DR vs. PRP treatments.

Two year results from Protocol S

demonstrated that Lucentis 0.5 mg was

noninferior to PRP on mean change in

visual acuity at two years.

LUCENTIS VS PRP

Lucentis demonstrated some significant

advantages in the Protocol S trial compared

with PRP.

- Reduced peripheral visual field sensitivity loss

- Reduced need for vitrectomy

- Reduced possibility of developing DME and vision

impairment.

LUCENTIS FOR NPDR

April 2017 Lucentis (ranibizumab) approved

in US for treatment of all types of NPDR

Even in absence of DME

AFILBERCEPT

Phase 2b study, aflibercept (Eylea,

Regeneron) shown to be noninferior and

superior to PRP for treatment of PDR.

Patients gaining 3.9 more letters of BCVA at

52 weeks compared with PRP in an intention-

to-treat population and +4.0 letters in a per-

protocol population.

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AFILBERCEPT

Regeneron currently conducting Phase III

PANORAMA trial for evaluating efficacy of

Eylea on improving moderately severe to

severe NPDR among patients WITHOUT DME

using two undisclosed dosing regimens.

AFILBERCEPT

58% patients in the anti-VEGF group

experienced a 2-step or greater

improvement from baseline in DRSS at 24

weeks compared to 6% in the sham group.

WHO TO TREAT?

PDR

- Active and symptomatic

- High-risk asymptomatic NPDR

DME

- Prior treatment with laser laser

- DME and/or prognosis for the fellow eye

Uncontrolled A1C levels or advanced

systemic disease

Compliant with follow up

WHO TO TREAT?

Anti-VEGF treatment initiated due to a

particular presenting feature

- Progression of retinal hemorrhages

- Edema

- Neovascularization

- Vitreous hemorrhage

HOW TO TREAT?

Mild NPDR with no DME can likely be

followed off therapy.

Treatment of moderate to severe NPDR is

discretionary but could potentially halt or

regress DR severity.

HOW TO TREAT?

Loading phase (three to six anti-VEGF

injections at a 4- to 6-week interval) to gain

control of DR and establishing a biologic

effect.

Interval for retreatment extended after the

loading phase through the first year of

therapy.

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HOW TO TREAT?

Patients with PDR demonstrate an exquisitely

high response rate to anti-VEGF therapy.

Patients with DME often require more

frequent treatment and a more gradual

extension after the loading phase than those

being treated for PDR.

LATANOPROSTENE BUNOD

0.024% FOR GLAUCOMA

VYZULTA

Latanoprost bunod (LBN) 0.024%

Nitric oxide (NO) donating prostaglandin

analog

Both uveoscleral aqueous outflow (through

the prostaglandin action) AND trabecular

outflow channels (through the nitric oxide

actions).

LBN (VYZULTA)

Enhancing outflow through TM has been

limited to effects of trabeculoplasty and

miotics.

LBN metabolized by corneal esterases:

- latanoprost acid

- butanediol mononitrate (BM)

NO is subsequently released by BM in human

TM cells after application of LBN.

NO IN THE BODY

NO synthesized from L-arginine by enzyme

nitric oxide synthases (NOS)

- NOS1 (neuronal)

- NOS2 (inducible)

• Expressed in pathological conditions (infection, inflammation)

- NOS3 (endothelial)

Ubiquitous with many physiological roles in

the body

All three expressed in the eye.

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NO IN THE BODY

NO is endogenous signaling molecule

Activates soluble guanylate cyclase (GC)

NO-GC-cyclic guanosine monophosphate

(NO-GC-1-cGMP) pathway implicated in IOP

reduction and retinal pathology in GLC

NO-GC-1-cGMP) Pathway

LBN

Directly improves outflow through TM,

Schlemm's canal and distal scleral vessels

by inducing cytoskeletal relaxation via the

soluble guanylyl cyclase-cyclic guanosine

monophosphate (sGC-cGMP) signaling

pathway.

NO IN THE EYE

Other possible mechanism regulation of

Schlemm’s canal and TM cell volume.

As aqueous flows deeper into the

juxtacanalicular TM towards Schlemm’s

canal, the open spaces available for fluid to

flow through decrease.

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VOYAGER STUDY

Concluded that once-daily dosing of LBN had

IOP reductions greater than those from

latanoprost. (9 mm Hg vs. 7.77 mm Hg

p

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SAFETY

Safety and tolerability established in studies

with no serious adverse events reported.

Most common adverse event was transient

hyperemia.

Not recommended in patient

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ANTIBIOTICS (ANTI-INFLAMMATORY)

Tetracycline analogs

• Doxycycline

• Minocycline

Enhances the effects of

• Coumadin

• Digoxin

Idiopathic intracranial hypertension

• Pseudotumor cerebri

Hyperpigmentation

105

BENIGN INTRACRANIAL HYPERTENSION

“IT’S NOT RARE IF IT’S IN YOUR CHAIR”

8-19-2010

8-31-2010

(12 days)

9-13-2010

10-6-2010

8-19-2010

OMG

6 MONTHS LATER 1 YEAR LATER

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ALPHA 1 BLOCKERSFloppy iris syndrome!

Treatment of enlarged prostate:

• Uroxatrol (Alfuzosin)

• Flomax (Tamsulosin)

• These two agents LIKELY have the highest incidence of causing floppy iris syndrome, as they are selective for alpha 1a receptors, which also predominate in the eye

Treatment of CHF and/or hypertension

• Coreg (Carvedilol)

• Alpha1/beta 2 blocker

Treatment of refractory hypertension:

• Hytrin (Terazosin)

• Alpha 1 blocker

111

ALPHA 1 BLOCKERS

Floppy iris syndrome and miosis!

After 4 rounds of phenylephrine, tropicamide, and

cyclopentolate, if poor dilation

• Iris hooks

What happens at the time of making the incision?

• Tricks with different viscoelastic agents

Post op day 1, IOP 43

• What’s the caution?

112

ANTI-ARRHYTHMICS

Treatment of cardiac arrhythmia

• Cordarone (amiodarone)

• Corneal deposits

• Optic neuritis

113

65 YEAR OLD WOMAN

Patient reports decreasing vision over past 6-9 months.

Especially at near

Vision 20/50 OU

TOPOGRAPHY TOPOGRAPHY

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6 MONTHS LATER

20/25 BVA

OD

6 MONTHS

LATER

20/25 BVA

OS

67 YEAR OLD MAN COMPLAINS OF

VISION SLOWLY DETERIORATING OVER

THE PAST 8 MONTHS

History of NA-ION 10 months ago OD

Patient sees family physician for physical due to recent NA-ION

Patient has not been to PCP for 35 years

Patient started Cardarone

VA 20/80 OD 20/25 OS (9 months ago)

VA 20/400 OD 20/200 OS (today)

CF: severe constriction OU

SLE: vortex corneal whorls OU

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AMIODARONE OPTIC NEUROPATHYOSTEOPOROSIS MEDICATIONS

Bisphosphonates:

• Fosamax (Alendronate)

• Actonel (Risedronate)

• Episcleritis

• Uveitis

• Iritis

Typically, the benefit of using these agents outweigh the risks for

ocular side effects

Encourage patients to get regular ophthalmic exams and to report

any acute changes!

124

COX-2 SPECIFIC INHIBITORS

Celebrex (celecoxib)

• Cataracts

• Glaucoma

• Conjunctival hemorrhage

• Vitreous floaters

Hey Celebrex, where did your brothers Vioxx and Bextra go?!?!

Oh how we miss them…

125

AUTOIMMUNE AGENTSTreatment of Multiple Sclerosis

• Gilenya (fingolimod)

• FDA-approved oral agent for the treatment of

relapsing forms of multiple sclerosis (MS) in

September 2010.

• Macular edema

• FAME - Fingolimod-Associated Macular Edema

126

52 YEAR OLD WOMAN

History of MS was switched from Tysabri (natalizumab) to Gilenya

(fingolimod)

Blurred vision in her left eye, BVA 20/40

• Noticed blurred vision 7-8 weeks after starting Gilenya

127

GILENYA

(FINGOLIMOD) & FAMEPrior to starting medication

• Follow up in 3-6 months after medication started

Be aware of FAME

If FAME occurs

• Stopping Gilenya typically will reverse edema

• May need topical NSAID and/or steroid

128

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ANOTHER GILENYA (FINGOLIMOD)

AND FAME

129

AUTOIMMUNE AGENTS

Treatment of rheumatologic conditions

• Rheumatoid arthritis, systemic lupus erythmatosis

Plaquenil (hydroxychloroquine)

• Bull’s eye maculopathy

PLAQUENIL

Hydroxychloroquine (Plaquenil) - Anti-malarial

Ophthalmic side effects (infrequent with current dosing ranges):

• Irreversible retinal damage has been observed (“chloroquine

retinopathy”).

• If there are any indications of abnormality in the color vision, visual

acuity, visual field, or retinal macular areas, or any visual symptoms

(eg, light flashes or streaks), d/c drug stat

REVISED RECOMMENDATIONS ON SCREENING FOR

CHLOROQUINE AND HYDROXYCHLOROQUINE

RETINOPATHY

Recommendations were 2002 by the American Academy of Ophthalmology

Improved screening tools and new knowledge about prevalence of toxicity have prompt the change

1% after 5-7 years of use or a cumulative dose of 1000 grams (Plaquenil)

There is no treatment for this condition

Therefore must be caught early

Screening for the earliest hints of functional or anatomic change

Plaquenil toxicity is not well understood

REVISED

AGAIN

7/30/2018

23

PLAQUENIL ZONE

AUGUST 2014

BILATERAL COMPROMISE OF THE PIL (WHITE ARROWS) AFTER COLLAPSE OF PERIFOVEAL RETINA (RED DASHED ARROWS) WITH FLYING SAUCER ATTACK (BLUE ARROWS)

71 YO WOMAN

With Lupus and hypertension

Medications:

Clonazepam

Plaquenil 200 mg BID, 15 years

81 mg ASA

Prednisone

Losartan

VA 20/25 OD/OS (mild cataracts)

Patient was told to see an ophthalmologist in 2013

2016

7/30/2018

24

2016