disclosures- greg caldwell, od, disclosure€¦ · the interleukin-6 pathway is up-regulated in...
Post on 19-Oct-2020
14 Views
Preview:
TRANSCRIPT
-
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
-
7/30/2018
2
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
-
7/30/2018
3
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.
-
7/30/2018
4
- 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
-
7/30/2018
5
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
-
7/30/2018
6
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
-
7/30/2018
7
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?
-
7/30/2018
8
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
-
7/30/2018
9
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
-
7/30/2018
10
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
(
-
7/30/2018
11
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.
-
7/30/2018
12
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.
-
7/30/2018
13
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.
-
7/30/2018
14
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.
-
7/30/2018
15
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.
-
7/30/2018
16
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
-
7/30/2018
17
SAFETY
Safety and tolerability established in studies
with no serious adverse events reported.
Most common adverse event was transient
hyperemia.
Not recommended in patient
-
7/30/2018
18
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
-
7/30/2018
19
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
-
7/30/2018
20
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
-
7/30/2018
21
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
-
7/30/2018
22
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
top related