EVERYTHING THERAPEUTIC: SAN ANTONIO

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Printable Course Notes
November 21-22, 2015
Westin Riverwalk Hotel
420 West Market Street l
San Antonio, TX 78205
presents:
Saturday, November 21st
Morning Lectures
7:30 am
-
8:00 am
Registration, Continental Breakfast, & Visit Exhibits
8:00 am
9:45 am
-
9:45 am
10:15 am
Lectures presented by Sherry Bass, OD, FAAO:
Essentials Of Fundus Autofluoresence in Retinal Disease
Break & Visit Exhibits
10:15 am
-
12:00 pm
Retinal and Optic Nerve Grand Rounds Challenging Cases You Don’t See Every Day
12:00 pm
-
1:00 pm
Lunch & Visit Exhibits
Options 2 & 3 Require Pre-Registration
Afternoon Lectures Option 1
Lecture presented by Leonid Skorin,
OD, DO, FAAO
OD, DO, FAAO
OD, DO, FAAO
1:00 pm - 1:50 pm
A Practical
Approach to
Headache
Management
1:00 pm - 1:50 pm
A Practical
Approach to
Headache
Management
1:00 pm - 1:50 pm
A Practical
Approach to
Headache
Management
1:50 pm - 2:45 pm
Sinusitis: Nothing
to Sneeze at
Break & Visit
Exhibits
Workshop Presented By Diopsys
1:50 pm - 2:45 pm
2:45 pm - 3:15 pm
3:15 pm - 4:05pm
Sinusitis: Nothing
to Sneeze at
Break & Visit
Exhibits
Ocular
Emergencies
1:50 pm - 2:45 pm
2:45 pm - 3:15 pm
Hands-On
Workshop
Break & Visit
Exhibits
OD, DO, FAAO
3:15 pm - 4:05 pm Ocular
Emergencies
2:45 pm - 3:15 pm
OD, DO, FAAO
3:15 pm - 4:05 pm Ocular
Emergencies
Workshop Presented By Diopsys
4:05 pm - 5:00 pm
ALT, SLT, LPI,
ECP: Glaucoma
Laser Alphabet
Soup
4:05 pm - 5:00 pm
ALT, SLT, LPI, ECP:
Glaucoma Laser
Alphabet Soup
4:05 pm - 5:00 pm
Hands-On
Workshop
Program Location: The Westin Riverwalk – 420 West Market Street, San Antonio, Texas 78205
presents:
Sunday, November 22nd
Morning Lectures
7:30 am
-
8:00 am
Registration, Continental Breakfast, & Visit Exhibits
Lecture presented by Anthony Litwak, OD, FAAO:
8:00 am
-
9:45 am
Advanced Interpretation of the OCT
9:45 am
-
10:15 am
10:15 am
-
12:00 pm
My Favorite Cases
12:00 pm
-
1:00 pm
Lunch & Visit Exhibits
Afternoon Lectures
Lectures presented by Bruce Onofrey, RPH, OD, FAAO:
1:00 pm
-
2:45 pm
Management of Ocular Infection - The Next Generation of Treatments
2:45 pm
-
3:15 pm
3:15 pm
-
4:00 pm
AREDS II and U
4:00 pm
-
5:00 pm
Professional Responsibility Course for Texas Optometrists
Program Location: The Westin Riverwalk – 420 West Market Street, San Antonio, Texas 78205
1
The Essence of Fundus Autofluorescence in Hereditary and Acquired
Retinal Disease
Sherry J. Bass, OD, FAAO
I.
Principles of Fundus Autofluorescence
a. Definitions
i. An imaging technique that uses a bandpass filter from 535 to 580
nm for excitation and a bandpass filter of 615 nm to 715 nm as a
barrier filter to image lipofuscin distribution in the RPE
b. Normal fundus autofluorescence
i. Uniformity of autofluorescense (isoautofluorescence) throughout
the entire fundus except for the optic nerve head, retinal blood
vessels and macula.
ii. Optic nerve head is dark (hypoautofluorescent) due to absence of
the RPE and lipofuscin
iii. Blood vessels are dark (hypoautofluorescent) due to absorption
from blood
iv. Foveal signal is reduced due to absorption by the luteal pigment
(lutein and zeazanthin)
v. Parafoveal signal is greater than the fovea but still slightly less
than the rest of the retina likely due to the presence of increased
melanin deposition and lower density of lipofuscin
c. Abnormal Patterns in Hereditary Retinal Disease
i. Hyperautofluorescence
1. Marks lipofuscin accumulation
2. Sign of stressed, metabolically active photoreceptor and
RPE cells
ii. Hypoautofluorescence
1. Sign of photoreceptor and RPE degeneration/death
II.
Current Clinical Applications of Fundus Autofluorescence in Hereditary
Retinal Disease
a. Identification of disease
i. “normal” ophthalmoscopy
b. Monitoring of disease progression
i. Changes in autofluorescent patterns over time
c. Identification of specific patterns of autofluorescence in specific diseases
i. Macular involvement
ii. Posterior pole abnormalities
iii. Mid and Far Peripheral Abnormalities
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III.
Fundus Autofluoresence (AF) Findings in Hereditary Retinal Diseases
a. Retinitis Pigmentosa
i. A heterogeneous group of complex retinal degenerations that affect
the rods initially and then the cones
ii. Mutations have been identified on a number of genes, mostly RHO
(Rhodopsin) in dominant RP, over 60 genes in recessive RP and
primarily RPGR in sex-linked RP.
iii. Some forms are severely progressive and others are mildly
progressive
iv. Attenuated arterioles in the affected retina is the most consistent
finding
v. Types of retinitis pigmentosa
1. Diffuse retinitis pigmentosa
a. Bull’s Eye Ring abnormalities around the macula
i. A large ring signifies early disease
ii. A small ring signifies more advanced
disease
b. Hyperfluorescent abnormalities
i. Signifiy borders of stressed photoreceptors
and RPE cells that have increased metabolic
activity.
c. Hypofluorescent abnormalities
i. Signify areas of degenerated outer retina
d. Comparison of fundus photography and fundus
autofluorescent images
i. Dissociation of color fundus photos and
fundus autofluorescnce
ii. More abnormalities are evident in fundus
2. Peripapillary/ Pericentral retinitis pigmentosa
a. A pericentral ring along the arcades and
peripapillary region are affected
b. Hyperautofluorescent abnormalities
i. At the edge of the affected areas
ii. Bull’s eye macular hyperautofluorescent
ring
c. Hypoautofluorescent abnormalities
i. In affected areas, representing photoreceptor
and RPE degeneration
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d. Comparison of fundus photography and fundus
3. Sector retinitis pigmentosa
a. Specific sectors of the retina are affected
i. Typically inferior
ii. The remainder of the retina appears normal
b. Autofluorescent Abnormalities
i. Hyperautofluorescent abnormalities
1. Hyperfluorescence at the edge of the
affected area with hypofluorescence
ii. Hypofluorescent abnormalities
1. Hypoautofluorescnece in
degenerated areas but the rest of the
retina remains intact
c. Comparison of fundus photography and fundus
i. Autofluorescent abnormalities are greater
that abnormalities seen on ophthalmoscopy
and fundus photography, especially in areas
mildly affected by disease
4. Retinitis Punctata Albescens
a. RP with scattered diffuse white spots
i. Autofluorescent abnormalities
1. Hyperautofluorsecent ring in the
macula
2. Diffuse uniform areas of
hypoautofluorescence in the
periphery
b. Cone and Cone Rod Dystrophy
a. Hyperautofluorescent central and peripheral
abnormalities
b. Seen at the edges of macular lesions marking
metabolically active, stressed cells
c. `Bull’s eye hyperautoflourescence signifying rod
component of disease
d. Central hyperautofluoresence signifying loss of
foveal cones
ii. Hypoautofluorescent abnormalities
1. May be scattered areas in the periphery as the cone
dystrophy progresses to a cone-rod dystrophy
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iii. Comparison of fundus photography and fundus autofluorescent
images
c. Stargardt’s Disease
i. A recessive form of macular degeneration that typically has its
onset in the early teens but as early as age 4
ii. May be associated with fundus flavimaculatus flecks
1. Pisciform or fish-tailed shape
2. Can progress outward from the macula over time
iii. The disease is caused by mutations on the ABCA4 gene on
chromosome 1.
1. Three types have been identified that mirror
autofluorescent abnormalities
a. Type 1: Normal ERG
i. Minimal central areas of
hypoautofluorecence conbined to the macula
b. Type II: Abnormal photopic ERG
i. More extensive areas of central
hypoautofluorescence
c. Type III: Abnormal photopic and scotopic ERG
i. More peripheral hypoautofluorescence in
addition to the central areas of
hypoautofluorescence
iv. Hyperfluorescent abnormalities
1. Fundus flavimaculatus flecks are composed of lipofuscin
and hyperautofluoresce ; may hypoautofluoresce around the
edges as outer retinal cells degenerate
v. Hypofluorescent abnormalities
1. Typically seen in the macula, representing outer cell
degeneration which explains the reduced visual acuity
vi. Comparison of fundus photography and fundus autofluorescent
images
1. Areas that appear normal on ophthalmoscopy and mildly
affected by disease may show hyperautofluorescence or
hypoautofluorescensse.
d. Best’s Vitelliform Disease
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i. An autosomal dominant disease that affects the retinal pigment
epithelium
ii. Is caused by mutations in the bestrophin gene responsible for
lipofuscin metabolism
iii. Is characterized by different stages
1. Vitelliform lesion (Egg-yolk) stage
a. Composed of lipofuscin
b. Normal visual acuity
2. Scrambled egg stage
a. Breakup of lipofuscin leads to breaks in Bruch’s
membrane
i. Risk of development of CNV
1. Hemorrhage
2. Exudation
3. Serous detachment
iv. Autofluorescent abnormalities
1. Hyperautofluorescent abnormalities
a. Vitelliform lesion will uniformly
hyperautofluoresce
b. Sacttered lipofuscin will hyperautofluoresce as the
vitelliform lesion breaks up
2. Hypoautofluorescent abnormalities
a. Degeneration of photoreceptors and RPE as lesion
deteriorates
b. Retinal hemorrhage and disciform scar from CNV
lesions will block underlying autofluorescence
v. Comparison of fundus photography and fundus autofluorescent
images
IV.
AF findings in Acquired Retinal Disease and Congenital (but not hereditary)
Retinal Disorders
i. Ophthalmic artery occlusions
1. Pattern of hypo and hyperautofluorescence and how it
differs from the patterns seen in hereditary disease
2. Note that CRA occlusions do not affect AF but ophthalmic
artery occlusions typically do ( because the CRA does not
supply the RPE )
3. Case presentation
ii. Central serous retinopathy-wide spectrum of AF findings from
completely normal to profound AF abnormalities
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1. Acute Disease
a. Pattern of hypo and hyperautofluorescence and how
it differs from the patterns seen in hereditary disease
b. Case presentation
2. Chronic Disease
a. Pattern of hypo and hyperautofluorescence and how
it differs from the patterns seen in hereditary disease
b. Large descending tracks of both hyper AF and hypo
AF are common
c. Case presentation
iii. Age-related macular degeneration
1. Pattern of hypo and hyperautofluorescence and how it
a. Drusen
b. Geographic AMD
c. Exudative- Wet- AMD
d. Comparison with OCT
e. RPE rips in wet AMD reveal hyper AF at “rolled”
RPE edge
2. Case presentations
iv. Toxoplasmosis
1. Clinical characteristics
2. Patterns of hypo and hyperautofluorescence and how it
3. Old lesions surrounded by hyper AF rings suggest new
activity and need to followed carefully or treated
4. Comparison with SD OCT quite useful
5. 3 mirror lens exams may reveal vitritis and supports
acitivity
v. Histoplasmosis
3. Peripapillary AF is usually hypo but hyper AF may
indicate recent activity
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vi. AZOOR and MEWDS
3. 3-As in most disorders, hyper AF is encountered first and
may become hypo AF when the RPE dies
4. In AZOOR, large changes in AF may occur in 4-8 wks and
hence questionable cases of acitivity should be followed
carefully
5. Treatment in AZOOR with Imuran should be considered if
the the macula is threatened
6. Comparison with SD OCT quite helpful
7. MEWDS is nearly always self- limited- lesions may
increase in number for the first month and then typically
fade8. As in nearly all conditions, hyper AF precedes hypo AF
9. Case presentations
vii. Harada’s Disease
3. Hypo AF alone suggests dead RPE and no activity
4. In contrast, hyper AF indicates metabolically sick RPE and
treatment with steroids PO may be indicated
viii.
ix.
White fundus lesions
1. Solitary Idiopathic Choroiditis- typically hyper AF
2. Osseous Choristoma
3. Scleral choroidal calcification
4. patterns and how they differ from hereditary degens
Dark fundus lesions
1. CHRPE – virtually always hypo AF
2. Choroidal nevus- essentially always disappears with AF- iso
3. Malignant melanoma –
4. Above lesions essentially never show symmetry between
eyes as do hereditary retinal degenerations
x.
Angioid streaks and other cracks in Brooks membrane
1. Streaks radiate from disc and also surround disc
2. older cracks typically are hypo AF
3. newer streaks are generally hyper A
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4. some symmetry between eyes but not mirror images
5. some streaks are completely invisible to ophthalmoscopy
V. Summary and Conclusions
a. Hereditary Retinal Degenerations are often quite symmetrical OD/ OS
b. Lesions due to any etiology are sometimes invisible to ophthalmoscopy
c. Comparing and contrasting SD OCT findings and AF images very helpful
d. Remember that some AF abnormalities are invisible to BIO as well
e. Although AF is not the standard of care at the present time, it may be soon.
1
Retinal and Optic Nerve Grand Rounds:
Challenging Cases You Don’t See Everyday
Sherry J. Bass, OD, FAAO
SUNY College of Optometry
[email protected]
Disclosures: Nothing to Disclose
A. Central Serous Choroidopathy
a. Two Clinical Presentations
i. One or more discrete isolated leaks at the level of the RPE
ii. Diffuse RPE dysfunction: broad areas of hyperfluorescence on FA that
contain one or many leaks.
b. Signs of an OLD Central Serous Choroidopathy
i. Decreased VA in affected eye
ii. Window defects on fluorescein angiography
iii. No leakage
iv. A U-Shaped area of retinal pigmentary changes
v. CSC “Drip”
vi. No fluid
c. Signs of a Recurrent Central Serous Choroidopathy
i. Sudden decrease in VA
ii. Ring of fluid in or near the macula
iii. VA may improve with more “plus”
iv. Late stage leakage noted on fluorescein angiography
d. Treatment of Recurrent CSC
i. Tincture of time
ii. Focal laser
iii. PDT
iv. Bevacizumab (Avastin)
v. Why not steroids?
vi. Kenalog injection
B. Idiopathic CNV After LASIK
a. Reported to occur in patients who have had LASIK and who also have a history
of AMD
b. POHS
c. Degenerative myopia
d. Rare (0.06% in one study) in patients with no history of any ocular pathology
e. Differential Diagnosis of Serous Detachment in a Young Patient
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i. No CNV
1. Central serous choroidopathy
2. Fluorescein angiography is the key
3. No nets in acute CSC
ii. CNV
1. POHS
2. High myopia
3. Trauma
4. Angioid Streaks
5. Idiopathic
6. Best’s disease
7. Laser photocoagulation scars
f. Etiology after CNV
i. Flap creation
ii. Temporary increase in IOP
iii. Can stress retina
iv. Photoablation
1. Is a “punch to the eye”
2. Contracoup waves that stress the retina
3. Cause breaks in Bruch’s membrane
C. Coat Disease
a. Vascular response in the peripheral retina
b. Unilateral (95%); Males (76%)
c. Telangiectatic microaneurysms
d. Exudation
e. Capillary drop-out
f. Neovascularization
g. Vitreal Hemorrhage
h. Retinal Detachment
i. Differentials
i. Sickle Cell Disease
ii. Familial Exudative Vitreretinal Response (FEVR)
iii. Hemangioma
iv. Retinopathy of Prematurity
v. Norrie’s Disease
vi. Eale’s Disease
vii. Incontinentia Pigmenti
j. Molecular Genetics
i. Fascioscapulamuscular dystrophy (FSHD) Genetic Marker
1. Genetic marker on chromosome 4q35
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2. Gene not yet identified
3. Marker consists of deletions or short fragments in this region (band
pattern)
4. Almost all patients with FSHD exhibit this pattern
ii. Molecular Genetic Results
1. A normal band is 36-38 kb
2. This patient’s bands were 24-27 kb.
k. Diagnosis: FSHD
D. Diffuse Unilateral Subacute Neuroretinitis (DUSN)
a. Term coined by Don Gass, MD
b. Unilateral loss of vision in youngsters
c. Fundus looks like unilateral retinitis pigmentosa, but etiology is inflammatory not
hereditary
d. ERG is flat in affected eye
e. Etiology believed to be similar to a nematode parasite related to but different than
toxocara
E. IRVAN: Idiopathic Retinal Vasculitis, Aneurysms and Neuroretinitis
a. Bilateral retinal vasculitis
b. Unknown etiology (idiopathic)
c. Characterized by
i. Multiple aneurysms at arterial bifurcations
ii. Neuroretinitis
1. Optic disc leakage on fluorescein angiography
iii. Capillary non-perfusion
iv. Progressive ischemia leading to
1. Neovascularization
2. Vitreal hemorrhage
3. Tractional retinal detachment
v. Vascular changes are believed to be due to VEGF over-expression
vi. IRVAN is a diagnosis of exclusion after other infectious and inflammatory
etiologies of vasculitis and aneurysms have been ruled out
1. Requires referral to PCP for extensive blood work-up and
evaluation , for example:
a. Diabetes
b. Sickle cell disease
c. Blood dyscrasias
d. Anticardiolipid antibodies; anticoagulant testing
e. Sarcoidosis
f. Infectious diseases, e.g.
i. Lyme disease
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ii. TB
iii. Syphilis
iv. Rubella
v. CMV
vi. HIV
vii. IRVAN responds favorably to PRP and anti-VEGF injections
viii. Long-term prognosis is unknown
F. Retinal Toxicity
a. Psychotropic drug use in the past caused degenerative retinal changes in the
posterior pole
b. Differential diagnosis of numular (scalloped) lesions in retina
i. High Myopia
1. Also affects the posterior pole greater than the periphery
ii. Gyrate Atrophy
1. Disease affecting the production of ornithine transferase which
affects the metabolism of ornithine in the body
2. Causes nummular lesions in the periphery of the retina initially not
the posterior pole
3. Toxicity
a. Poor excretion of the toxic agent causes continued retinal
destruction
b. Affects posterior pole
G. Vitreomacular Traction Syndrome (VMT)
a. A vitreoretinal disorder producing traction on the macula
b. Can cause macular pucker or folds or the macula can look normal
c. Can mimic a juvenile foveal retinoschisis
d. SD-OCT
i. very valuable in demonstrating vitreal traction
e. Management
i. Monitor
1. Spontaneous resolution into a PVD can occur
ii. If VA drops to 20/60 refer for vitrectomy
iii. Jetrea (Ocriplasmin)
1. Intravitreal injected substance that dissolves the adhesion
2. Works best on small adhesions
a. 1500 microns or less (one disc diameter)
b. No associated ERM
H. Retinoschisis (Degenerative)
a. A split in the retina at the outer plexiform layer
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b.
c.
d.
e.
f.
g.
Usually bilateral (38-82% of cases)
Differentiated from retinal detachment because of visibility of underlying choroid
Can be elevated with blister-like borders or flat with pigmentary changes
Associated with absolute field loss in affected area
Monitor-can progress to RD (10%)
Most frequently occur in the inferotemporal quadrant followed by superior
temporal quadrant
I. Accutane Toxicity
a. Differential Diagnosis of Bull’s Eye Retinopathy
i. Stargardt disease
ii. Cone dystrophy
iii. Benign concentric macular dystrophy
iv. Fenestrated sheen maculopathy
v. Toxic maculopathy
1. Plaquinil (Hydrochloroquine)
2. Isotretinoid-related maculopathy
b. Importance of a comprehensive drug history
c. Important tests to perfrom
i. Structure
1. SD-OCT
2. Fundus autofluorescence
ii. Function
1. Full flash ERG
2. Multifocal ERG
3. 10 degree visual fields
J. Chronic Pigment Epithelial Detachment (PED)
a. Separation of the RPE from Bruch’s membrane
b. Macular edema
c. Reduced VA
d. Can be associated with
i. CSC
ii. AMD
e. Monitor or Treat?
i. Make sure pt. is not using:
1. Steroids
2. Erectile Dysfunction (ED) medications
ii. Treatment ?
iii. Lucentis for Age-Related Macular Degeneration Pigment Epithelial
Detachment Study
1. 3 or 6 0.5 mg injections for 1 year
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2. Resolution of edema vs. edema and PED
3. Results
a. 42% decrease in volume after 1 month but was not
maintained over one year
iv. Some success with PDT and anti-VEGF has been reported
K. Presumed Ocular Histoplasmosis (POHS)
a. Inflammatory disease causing a chorioretinitis caused by exposure to ocular
histoplasmin spores in the air
i. Associated with residence in river valleys
ii. Chickens
iii. Triad of Findings
1. Punched out chorioretinal lesions
2. Peripapillary atrophy
3. Macular CNV
b. Differentials
i. Punctate Inner Choroidopathy (PIC)
1. More vitritis than POHS
ii. Multifocal Choroiditis
c. Treatment of macular CNV
i. Anti-VEGF
L. Astrocytoma (Astrocytic Hamartoma)
a. Mass composed of astrocytes
b. Can appear on the optic nerve, in the retina or in the brain
c. Is associated with Tuberous Sclerosis
i. Can be an isolated finding
d. Look for ash-leaf shaped skin lesions
e. Look for tuberous growths on the fingers
f. Differentials
i. Disc drusen
g. Management
i. MRI to r/o intracranial astrocytomas
M. Diabetic Papillopathy
a. Sudden ischemic event causes swelling of the optic nerve head
b. Usually unilateral
c. Occurs in uncontrolled diabetes
d. Usually in young Type I diabetics
e. VA can be normal or reduced
f. VF loss-usually arcuate-can occur
g. Is not a “papillitis”-not inflammatory
h. Is not a “papilledema”-no increase in intracranial pressure
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i. Monitor
i. Condition usually resolves on its own in a few weeks
ii. Unlike AION where VA resolution is more rare
iii. Includes resolution of VA loss and visual field loss
iv. Perform other tests to rule out infectious/inflammatory etiology of disc
swelling
N. Cerebellar Hemangioblastoma
a. Cerebellar Mass (Cyst)
i. Made up of vascular tissue
ii. Cyctic nature causes compression on the cerebellum and chiasm
iii. Herniated ventricles and increased intracranial pressure cause papilledema
iv. Most common CNS lesion seen associated with Von-Hippl Lindau disease
1. Cystic lesions are found elsewhere in the body
a. Kidney
2. Genetic testing available
v. Can be an isolated finding as seen in this patient
vi. Look for signs of cerebellar dysfunction and pituitary compression
1. Balance problems
2. Hormonal problems
O. Decreased Visual Acuity in Early Glaucoma
a. Supported by small C/Ds
b. Supported by well-preserved visual field OD except for central loss
c. It is rare but has been reported
i. Pickett JE, Terry SA, O’Connor PS, O’Hara M. Early loss of central visual
acuity in glaucoma. Ophthalmology 1985 Jul; 92(7): 891-6.
d. Will occur in early papillomacular bundle involvement also affecting the fovea
e. When you can’t explain central VA loss, do a 10 degree visual field test.
f. This is a case of glaucoma without cupping
9/20/2015
A PRACTICAL APPROACH TO HEADACHE MANAGEMENT
A Practical Approach
To Headache Management
Leonid Skorin, Jr., OD, DO, MS, FAAO, FAOCO
Consultant, Department of Surgery
Community Division of Ophthalmology
Mayo Clinic Health System in Albert Lea
Assistant Professor of Ophthalmology
Mayo Clinic College of Medicine
Ubiquitous symptom
73% of adults experienced headache in past year
10 million outpatient visits per year
Only 15% actually sought medical help
ESTIMATED PREVALANCE OF MIGRAINE SUFFERERS
IN THE UNITED STATES
HEADACHE CLASSIFICATION
HEADACHE DIAGNOSIS
P - Provokes, Palliates
Q - Quality
R - Region
S - Severity, Associated signs/symptoms
T - Timing
1. Onset
2. Frequency
3. Duration
International Headache Society criteria
1. Primary headache disorders
Migraine
Tension-type
Cluster
2. Secondary headache disorders
Headache is symptomatic of an underlying condition
such as temporal arteritis, brain tumor, stroke
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Pathophysiology
MIGRAINE CLASSIFICATION
Migraine without aura (common migraine)
Vascular
Migraine with aura (classic migraine)
Neural
Unified or neurovascular
Serotonin (5-HT) neurotransmission
Complicated migraine
1. Ophthalmoplegic migraine
2. Basilar migraine
3. Migraine equivalents
MIGRAINE WITHOUT AURA (COMMON MIGRAINE)
MIGRAINE WITH AURA (CLASSIC MIGRAINE)
MIGRAINE EQUIVALENTS
ACEPHALGIC MIGRAINE
EPISODIC, TRANSIENT DYSFUNCTION OF AN ORGAN OR
SYSTEM
NO ACCOMPANYING HEADACHE
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Physical Techniques
MIGRAINE TREATMENT
Nonpharmacologic
1. Eliminate trigger factors
2. Stress management
3. Biofeedback
4. Acupuncture

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Peripheral Nerve Stimulation


Eon Mini IPG
Stimulation of occipital nerves for intractable chronic
migraine: changes the pain signal
41% reduction in overall disability
 89% of patients would recommend to others
 27% reduction in number of headache days
 68% improved quality of life
Trigeminal Nerve Stimulation


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
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Cefaly – FDA approved
Uses TENS technology
Electrical impulses through an electrode patch to stimulate
the trigeminal nerve
20 minutes a day, 18 years or older
Three programs:
 Treatment – blocks flow of pain
 Prevention – increases endorphins in CNS
 Anti
Anti--stress – general relaxation
Homeopathic

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Feverfew – herb, 5050-100 mg daily, ((parthenolide
parthenolide))
Can cause oral ulcers, tongue irritation, lip swelling.
Riboflavin – Vitamin B2 – 400 mg daily
Increases energy efficiency of mitochondria.
Vitamin B Complex – B6 25 mg, B12 400 mcg,
folic acid 2 mg: 50% < HA
Butterbur – herb, 75 mg BID x 4 months: 50% <HA
Use the brand Petadolex.
Petadolex.
Magnesium 600 mg daily: 50% < HA
Start with 200 mg daily, slowly increase to 600 mg.
Massage, acupressure
Acupuncture + OTC painkillers: 44% < HA
Trigger point injections
Muscle stretching exercises
Osteopathic manipulation
Chiropractic spinal manipulation
Botulinum Toxin Injection


Peripheral effect – muscle relaxant
Central effect – inhibits release of trigeminal
cellcell-mediated neurotransmitters
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MIGRAINE TREATMENT
MIGRAINE TREATMENT
Symptomatic (Abortive)
Symptomatic (Abortive)
2. Prescription medication
a. Combination drugs with narcotic
b. Ergotamine tartrate
c. Dihydroergotamine: Migranal
d. Narcotics: Stadol NS
e. Midrin
1. Over-the-counter medication
a. Aspirin
b. Acetaminophen
c. Non-steroidal anti-inflammatory drugs
Motrin Migraine Pain
Advil Migraine
d. Combination drugs: Excedrin Migraine
Selective Serotonin Receptor Agonists
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Imitrex (sumatriptan)
sumatriptan)
Zomig (zolmitriptan)
zolmitriptan)
Amerge (naratriptan)
naratriptan)
Maxalt (rizatriptan)
rizatriptan)
Axert (almotriptan)
almotriptan)
Frova (frovatriptan)
frovatriptan)
Relpax (eletriptan)
eletriptan)
Treximet (sumatriptan/naproxen)
sumatriptan/naproxen)
Selective Serotonin Receptor Agonists




Prophylactic Therapy - Anticonvulsants
MIGRAINE TREATMENT
Prophylactic (Preventive)
a. Beta blockers
b. Tricyclic antidepressants
c. Nonsteroidal anti-inflammatory drugs
d. Calcium channel blockers
e. Monoamine oxidase inhibitors: Nardil
f. Anticonvulsants: Depakote, Depakene, Topamax
Efficacy: if first triptan does not work, try
another – may require trial and error
Onset: injection – 10
10--15 minutes
nasal spray – 15 minutes
troche – no faster than oral tablets
Route: nasal spray or injection for N/V
Duration: longest acting – Frova and Amerge

Topiramate (Topamax
Topamax))
 50% reduction of headache by 6 weeks
 Adverse effects: paresthesia
paresthesia,, weight loss
 Acute angle closure glaucoma within one month of
starting therapy. Edema and forward rotation of
ciliary body – tx
tx:: atropine and prednisolone
 Acute myopia: forward movement of irisiris-lens
diaphragm
 Reversible visual field defects independent of
elevated intraocular pressure
4
9/20/2015
5
Disease Prevalence
Sinusitis: Nothing to Sneeze At
• Affects 35 million Americans – making this
disease more common than arthritis or
hypertension
• Most common health complaint leading to
office visit – 25 million outout-patient visits
• Prevalence is increasing
Pathogenesis
Paranasal Sinuses
• Ostiomeatal complex: obstruction is key element
in disease
- composed of maxillary sinus ostia, anterior
ethmoidal cells and ostia, middle meatus
Predisposing Factors
Pathogenesis
• Mucocillary activity: removes
microorganisms, pollutants and irritants
• Nasal airflow: lower O2 leads to growth of
organisms, impaired local defenses, altered
leukocyte function and mucous membrane
swelling
•
•
•
•
•
•
•
Viral upper respiratory tract infection
Allergic rhinitis
Genetic predisposition
Anatomic ostial compromise
Air pollution and smoking
Nasal polyposis
Pregnancy
Sinusitis Symptoms
•
•
•
•
•
•
•
•
•
•
Nasal obstruction, congestion, discharge
Postnasal drip
Facial pressure, headache, toothache
Cough
Halitosis
Pharyngitis
Hyposmia – diminished sense of smell
Ear fullness
Fatigue, malaise
Fever
Physical Examination
Anterior Rhinoscopy – Nasal speculum
• Evaluate and inspect: nasal cavity, nasal
vestibule and anterior septum
• Look for mucosa color, congestion, secretions,
septal deviation and polyps
Technique
• Use bright, focused light source
• Vasoconstriction with Afrin
Anterior Rhinoscopy
• Technique
- Hold speculum in left hand
- Left index finger presses against side of cheek
to act as anchor
- Insert blades 1 cm
- Open vertically, NOT horizontally
- Position right hand on patient’s head
Sinus Palpation
Maxillary
• simultaneous finger pressure over both
maxillae
• palpation under the upper lip for fullness
• percussion of maxillary teeth with tongue
blade
Sinus Palpation
Transillumination
Frontal
Maxillary
• finger pressure directed upward toward
1. place light source over the middle of the
infraorbital rim to judge light transmission
between sides through the hard palate
floor of the sinus
• palpation directly over sinus
Ethmoid and sphenoid: unable to evaluate
Transillumination
Transillumination
Frontal
Maxillary
2. place light source in patient’s
mouth and note red pupillary
reflex, note crescent of light
on the lower eyelids, note
patient’s sense of light in the
eyes when they are closed
1. place light source below supraorbital rim,
under the floor of the frontal sinus at the
upper inner angle of the orbit
3. inspection over the anterior
wall of the maxillary sinus is
not dependable
• Nasal Endoscopy
• Cultures: endoscopically guided
Treatment
• Analgesics for pain: NSAIDS or acetaminophen
• Steam and saline
• Topical decongestants: use for 3 – 5 days;
otherwise, can develop rhinitis medicomentosa,
rebound vasodilation
• Oral decongestants: use for 3 - 5 days, use with
caution in patients with cardiovascular disease,
hypertension or benign prostatic hypertrophy
Radiography
Radiographic hallmarks of sinusitis
1. mucoperiosteal thickening 8mm (adults)
or 4 – 5 mm (children)
2. airair-fluid level
3. opacification of sinus
Treatment
• Mucoevacuants: guaifenesin – thins sinus
secretions, eases mucus drainage
• Antibiotics: amoxicillin, trimethoprimtrimethoprimsulfamethoxazole, erythromycin; for
treatment failure use levofloxacin 500mg daily
for 10
10--14 days
• Mucoregulators: acetylcysteine – promotes
synthesis of normal mucus
Treatment
• Topical steroids: beclomethasone (Beconase,
Vancerase), triamcinolone (Nasacort),
mometasone (Nasonex) – relieve symptoms of
allergic and nonallergic rhinosinusitis, suppress
inflammation
Treatment
Surgery
Caldwell--Luc: strip maxillary sinus mucosa
• Caldwell
• Functional endoscopic sinus surgery
Not recommended
• Antihistamines: can cause overover-drying of mucosa
• Zinc preparations: can cause permanent anosmia
• Oral steroids: prednisone – use in chronic cases
Complicated Sinus Disease
Fungal Sinusitis: cerebro
cerebro--rhino
rhino--orbital
phycomycosis
Subperiostial orbital abscess or orbital cellulitis:
surgical emergency, can lead to blindness,
intracranial complications
Orbital Cellulitis
Complicated Sinus disease
Mucocele or Pyocele
Case 1
•
•
•
•
•
•
16
16--yearyear-old white male
Chemotherapy for leukemia
Antibiotics for persistent sinusitis
Endoscopic sinus surgery
Maxillary antrostomy, ethmoidectomy
All cultures negative
•
•
•
•
Three days later – infraorbital pain
Proptosis OS
Edema left upper eyelid
Blurred disc borders, retinal hemorrhages
•
•
•
•
Orbital decompression
Ethmoidectomy with biopsy
Culture – phycomycetes
Started on Amphotericin B
Case 1
Case 1
Case 1
• Six days later – from 20/20 to 20/400 OS
• Complete external ophthalmoplegia
non-reactive pupil
• Dilated, non-
• Macular edema, venous stasis retinopathy
• CT scan – proptosis
sinus inflammation
Case 1
Case 1
• 70% of mucor pts have diabetes, most of
these also have ketoacidosis
• Treatment: antifungal therapy, surgical
debridement of involved tissues, control of
underlying disease
• Prognosis is poor with 62% mortality
• Pathology is essential, BUT absence of
evidence is not evidence of absence
Case 2
• 60
60--yearyear-old male comes in for routine exam
Case 2
FAT scan confirmed ptosis, OD lower,
conjunctival hyperemia
• Others mentioned OD “droopy”
• PERRL, full ROM, HVF – normal
• OD 3 mm proptotic
• Orbital palpation – periorbita hard and full
• Transillumination – right frontal sinus
opacified
Case 2
Coronal MRI - Pansinusitis
Case 2
Case 2
Coronal MRI – Frontal Sinus Mucocele
Case 3
Treatment
23--yearyear-old female
• 23
• Oral antibiotics for one week
• Sharp pain behind OD for two weeks
• Dull bibi-frontal headaches for four weeks
• Surgery to remove inflammatory material
• Vision unchanged after surgery
• Proptosis decreased
• PERRL, full ROM
• Red cap – 20% desaturation OD
• Transillumination – opaque right frontal and
maxillary sinuses
Case 3
HVF 3030-2 – Right constricted
Case 3
Case 3
MRI - Pansinusitis
Case 3
Post--treatment VF 30Post
30-2
Treatment
• Clindamycin 300 mg daily x 8 weeks
• Guaifenesin/phenylephrine caps BID
• Traimcinolone inhaler daily both nostrils
Case 4
38--yearyear-old male – slow progressive LOV OS
• 38
• VA OD 20/20, OS 10/400
• 3+ RAPD OS, color vision defect OS
• Globe palpation – resistance to backward
movement OS
• VF – overall significant depression OS
Case 4
Proptosis, hyperemia OS
Case 4
Fundus – OD normal, OS optic atrophy
Case 4
GDX – NFL loss OS
Case 4
Case 4
Coronal CT – right and left ethmoid, frontal opacity,
left frontal extension into orbit, left maxillary opaque
Axial CT – mucocele left sphenoid sinus
- OS proptosis, optic nerve compression
Case 4
Treatment
• Surgery to remove mucoceles and
inflammatory tissue
• Visual acuity stayed the same OS
• Patient felt he had brighter vision OS
• Slight visual field improvement OS
Mucocele Surgery
ALT, SLT, LPI, ECP:
Glaucoma Laser Alphabet Soup
LASER ALPHABET SOUP
•
•
•
•
ALT – Argon Laser Trabeculoplasty
SLT – Selective Laser Trabeculoplasty
LPI – Laser Peripheral Iridotomy
ECP – Endoscopic Cyclophotocoagulation
ALT
•
•
•
•
•
Standardized laser protocol 1979
Mechanical effect – thermal burn
Cellular & biomechanical cascade
Lowers IOP by 20–
20–30% (5(5-8 mmHg)
Reduces diurnal IOP elevation by 25%
ALT Technique
• Target junction between pigmented and
non
non--pigmented TM
• Spot size 50 μm, 0.1 sec duration
• Power 600 – 800 mW
• Blanching of TM or vaporization bubble
Success Rate for ALT
•
•
•
•
POAG: 80–
80–97%; 1 year: 77
77--81%
PXE: 97%; 1 year: 5050-70%
Pigment: 95%; 1 year: 4444-80%
Average: 50% at 5 years
180 vs. 360 Degree Treatment
180 Degrees
• Less post
post--op iritis
• Less risk of IOP spike
• Remaining 180 degrees treated later
360 Degrees
• Better initial IOP lowering
• Longer duration of effectiveness
• Less delay to do filter if ALT not effective
Glaucoma Laser Trial
•
•
•
•
•
•
Compared ALT to Timolol 0.5%
ALT – 44%; Timolol – 30% at 2 years
ALT – 32% still controlled IOP at 5 years
Initially tx with ALT – needed less meds
ALT at 7 years – lower IOP; less VF loss
ALT as firstfirst-line therapy
Complications of ALT
•
•
•
•
•
Early IOP spike (pre(pre-treat with Iopidine)
Iritis – 59% (post(post-op steroids)
PAS – 46% by 3 months (do not treat PTM/CB)
Hyphema – 2-5% (avoid vessels)
Corneal burn
SLT
Mechanism of Action
•
•
•
•
Selective photothermolysis of TM melanin granules
Short 3 nsec pulse – confines heat to target tissue
No widespread tissue destruction – remodels TM
Macrophages recruitment – clears pigment from TM
Success Rate For SLT
•
•
•
•
•
•
POAG: 90%, 6 months; 2 years: 75%
Not affected by degree of pigment in TM
Selective uptake – even light pigment responds
Heavy pigment – pressure spike
Takes 4 – 6 weeks to see effect
Repeatable
SLT Technique
•
•
•
•
•
•
Q-switched frequency doubled Nd:YAG
Spot size 400 μm, 3 nsec duration
Power 0.8 to 1 mJ per pulse
Can treat 360°
360°
Adjust to just before vaporization bubble
Compared to ALT: SLT has shorter pulse
duration and produces several thousand
times lower fluence laser energy
Complications of SLT
• Iritis – 47% (post(post-op NSAIDS)
• IOP spike (pre(pre-treat with Iopidine)
LPI Indications
Comparison of ALT with SLT
•
•
•
•
•
Acute angle closure
Chronic angle closure
Intermittent angle closure
Incomplete surgical iridectomy
Occludable or narrow angle
LPI Laser Protocol
•
•
•
•
Argon – pigment dependent
Nd:YAG – mechanically tears tissue
Treat superior iris – prevents monocular diplopia
Treat iris crypt – thinner tissue
CP1101264-47
Complications of LPI
•
•
•
•
•
Pupil distortion – seen with Argon
IOP spike > 10 mmHg in 2020-30%
Hemorrhage – 2020-40% of Nd:YAG
Corneal epithelial/endothelial burn
Anterior capsule disruption – Nd:YAG
Complications of LPI
•
•
•
•
•
Iritis – treat with steroids
Lenticular opacities – Argon
Retinal/macular burn – Argon
Monocular diplopia
Patency failure - Argon
ECP Technology
•
•
•
•
•
•
•
•
•
Laser endoscope – 810 nm
Endoscopy unit
20
20--gauge handpiece with optical fibers
110°
110° panoramic field of view
Depth of focus 1mm to 30 mm
ECP Technique
• Limbal vs. pars plana approach
• Endoscope under iris, watch video monitor
• 0.25 – 0.30 watts, continuous mode
ECP Technique
ECP Contraindications
Whiten and shrink ciliary processes
Try to treat 360°
360°
Post--laser: steroids every 2 hours
Post
Stop glaucoma meds: 6 – 8 weeks
• Active uveitic glaucoma
• IOP > 40 mmHg
Success Rate for ECP
Questions
follow-up 13 months
• 90% mean follow• 68% require at least one fewer glaucoma
medication
• Can combine with cataract surgery
• Comparable results to trabeculectomy and
shunt valve
• Repeatable
Introduction
• Ocular trauma is America’s number 1 cause
Ocular Emergencies
of preventable blindness
CP1167371-1
• 2.5 million eye injuries in the U.S. each year
• 40,000 are legally blinded in the injured eye
• 80% of all eye injuries occur in males
• Average age 30
• Non-whites – 40-60% higher risk
• Occupational eye injuries – 1,000/day
• Total costs (medical expenses, lost wages,
legal action) surpass $1 billion a year
CP1167371-2
History
History
Essential documentation (cont)
Essential documentation
• Which eye was injured
• Where and when the injury occurred
• How did the injury happen (record in
patient’s own words)
• Was any first aid or emergency
treatment rendered
• Was patient wearing safety glasses
or eye shield
CP1167371-3
Examination and Testing
Ocular Examination
• Any previous history of eye injuries or
eye disease
• General medical history
• Immune status (tetanus immunizations)
• Any allergies
• Recent food and fluid intake (if general
anesthesia is contemplated)
Document extent of ocular injury with
drawings or photographs
CP1167371-4
Additional Studies
• Scleral depression
• Visual acuity
Pinhole
• Pupils
• Ocular alignment – motility
(cranial nerve or orbital injury)
• Confrontation visual fields
Avoid if hyphema,
open globe, orbital
fracture, lid
laceration
• Ultrasonography
• Slit lamp examination
• Tonometry – defer in open globe injury
• Ophthalmoscopy
CP1167371-5
Intraocular foreign
bodies
• Conventional x-rays
CP1167371-6
1
Additional Studies
Additional Studies
MRI Scanning
CT Scanning
• Slower, more expensive
• Readily available
• No contrast
• Claustrophobia
needed
• Do not use with metal
• Safe with metal
• Great for bony
• Superior for soft tissue injury
fractures
• Can use with pregnant patient
CP1167371-8
CP1167371-7
Foreign Body
Foreign Body
Instrumentation
Technique
• Extent of
corneal injury?
• Evert upper
eyelid
• Double eversion
– Desmarres lid
retractor
CP1167371-9
CP1167371-10
Corneal Abrasion
Foreign Body
Small abrasions – no patching
• Acular 0.5%, 1 drop qid x 3 days
• Antibiotic eye drops qid x 3 days
• Cycloplegia
• See patient in couple days
Check anterior
chamber
• Foreign
body
• Iritis
• Hyphema
CP1167371-11
Moderate abrasions
• Acular 0.5%, 1 drop qid x 3 days
• Antibiotic eye drops qid x 3 days
• Cycloplegia
• Bandage soft contact lens
• See patient next day
CP1167371-12
2
Large Abrasions – Pressure Patch
Pressure Patching
• Antibiotic ointment
• Cycloplegia
• Pain medications
Ultram (tramadol) 50 mg qid
Darvocet-N 100 q 4 hr
Tylenol #3 q 4 hr
• See patient next day
CP1167371-14
CP1167371-13
Pressure Patching
Pressure Patching
CP1167371-15
Disadvantages of Pressure Patching
•
•
•
Blunt Trauma
Iridodialysis – iris torn off ciliary spur
• Inability to apply antibiotic, cycloplegic
•
•
•
CP1167371-16
after patch is applied
Patient is rendered monocular
Allergy to tape
20% of patients will remove eye pad before
the next office visit
Cannot be used in 1-eyed patients
Cannot be used in contact lens induced
abrasions
Cannot be used if pre-existing ocular
infection
CP1167371-17
CP1167371-18
3
Hyphema
Blunt Trauma
• 5% develop secondary
Zonular rupture
Lens subluxation or dislocation
glaucoma
• 25% rebleed
(2-5 days after injury)
• 30% have rise in IOP
during acute phase
• 75% have angle
recession
• 7% will have corneal
blood staining
CP1167371-19
Hyphema Grading
CP1167371-20
Hyphema Treatment
• Bed rest, elevate head 30˚
• Cycloplegia with Atropine 1%
• Eye shield
• No ASA or NSAIDs
• Topical steroids for uveitis
• Aminocaproic acid (antifibrinolytic agent)
Grade 0 –
microhyphema
Grade I –
<25% filled
Grade II –
25-50% filled
Grade III –
50-75% filled
Inhibits plasminogen to plasmin
50 mg/kg q 4 hr x 5 days
Maximum 30 grams daily
Grade IV –
total (“8-ball”)
CP1167371-21
Hyphema Treatment
CP1167371-22
Surgery for Hyphema
• Prednisone 20 mg bid x 5 days
• Antiglaucoma medication
• Antiemetics
• IOP >50 mg Hg for 5 days
• IOP >35 mm Hg for 7 days
Tigan (trimethobenzamide)
250 mg po or 200 mg pr tid
Phenergan (promethazine)
25-50 mg po or pr tid
• Non-ASA analgesics
• IOP >25 mm Hg for 5 days if total
• IOP not responsive in 24 hours
• Sickle cell anemia
CP1167371-23
CP1167371-24
4
Orbital Blowout Fracture
Rebleed
Signs and Symptoms
• Large hyphemas
• Diplopia
• Orbital emphysema
• Enophthalmos
• Proptosis
• Subconjunctival or lid hematomas
• Infraorbital nerve dysesthesia or
• Young patients
• Blacks and
Hispanics
• Patients on
ASA, NSAIDs
anesthesia
• Corneal blood
staining
• Nausea, vomiting in trapdoor fractures
CP1167371-26
CP1167371-25
Medical Treatment
• Ice, do not blow nose
• Afrin NS tid
• Antibiotic prophylaxis
Augmentin 500 mg bid x 10-14 days
Duricef 500 mg bid x 10-14 days
Keflex 500 mg tid x 10-14 days
CP1167371-27
CP1167371-28
Surgical Repair
Blunt Trauma
• Vertical diplopia that
does not resolve in
10-14 days
• Positive forced
duction test
• Enophthalmos of
2 mm
• Floor fracture 50%
as seen on CT scan
CP1167371-29
CP1167371-30
5
Penetrating/Perforating Trauma
Definitions
• Penetrating – entrance wound only
• Perforating – entrance and
exit wounds
• Laceration – full-thickness
wound – sharp object
• Rupture – full-thickness
wound – blunt object
• Lamellar – partial-thickness wound
CP1167371-32
Signs and Symptoms
CP1167371-33
• Poor vision
• Seidel sign
• Peaked pupil
• Hypotony
• Hyphema
• Extruded intraocular tissue
CP1167371-34
Penetrating Trauma
CP1167371-35
Eyelid Injuries
Lacerations and perforations
CP1167371-36
CP1167371-37
6
Periorbital Lacerations
Periorbital Lacerations
CP1167371-38
CP1167371-39
Animal Bites
Animal Bites
• 4 million bitten each year
• Children bitten on face
• 80% by domestic dogs
• Avulsions, lacerations,
puncture, crush
• Pasteurella multocida,
staph aureus
CP1167371-40
CP1167371-41
Animal Bites
Treatment
• Augmentin
Adults 500 mg q 8 hr x 10-14 days
Children 40 mg/kg/day x 10-14 days
• Keflex
Adults 500 mg qid
Children 50-100 mg/kg/day
CP1167371-42
CP1167371-43
7
Treatment
• Tetanus prophylaxis
If <3 doses of tetanus toxoid
If >5 years since last dose
If immunization status unknown
• Rabies prophylaxis
Acute encephalomyelitis – fatal
Skunks, raccoons, bats, fox
Begin within 48 hours
CP1167371-44
8
Advanced Interpretation of the OCT
Anthony B. Litwak, OD, FAAO
VA Medical Center
Baltimore, Maryland
Glaucoma 101
 Glaucoma is a disease of the ganglion cell axons
 Damage occurs at the level of the lamina cribrosa
 Selective damage to the superior and inferior poles of the optic nerve
 Relative preservation of the temporal and nasal poles
Glaucoma Discriminates
 Glaucoma Often Asymmetrically Damages Between Above and Below and
Between the Two Eyes
 Look for Notches in the Neuro-Retinal Rim Tissue
 Occurs in 30% of Glaucoma Patients
 Inferior Temporal Pole Most Common Site of Notching
 Associated With a Corresponding VF Defect
Compare Neuro-Retinal Rim Tissue Between Superior and Inferior
 Vertical Extension of Cupping Supra or Infra Temporal
 Normal Ratio of Neuro Rim Tissue Is :
 2.0 Inferior: 1.5 Superior: 1.0 Temporal
 Glaucoma Should Be Suspected When the Amount of Temporal Neuro-Retinal
Rim Tissue Is Greater Than or Equal to the Inferior or Superior Rim Tissue
Does Size Really Matter?
 Is there a C/D ratio that defines glaucoma?
 Do You Think This Nerve Has Glaucoma?
A Big Cup Does Not Necessarily Mean Glaucoma
 There is No Demarcation Line Separating a Physiological Cup From a
Glaucomatous Cup
 Physiological Cup Size Is Directly Related to Overall Disc Size
 Large Discs Will Have Large Physiologic Cups
 Small Discs Will Have Small Physiologic Cups
 Physiologic Disc and Cup Size Is Genetically Determined
 Physiologic Cup of .7 Or Greater Occurs in 2% of Normals
 A Small Disc With a Medium Size Cup Should Be As Suspicious As a Large Cup
in a Medium Size Disc
How to Evaluate Disc Size
 Use a 60 D Lens at the Slit Lamp





Make a Thin Vertical Beam
Adjust Beam Height
Read Disc Diameter off Scale on Slit Lamp
Vertical Disc Diameter > 2.2 mm Is a Large Disc
Vertical Disc Diameter < 1.8 mm Is a Small Disc
Expected Physiologic Cup Size
Based on Measured Vertical Disc Diameter
Using a 60 Diopter Lens At The Slit Lamp
NFL 101
 Patterns of Diffuse NFL Loss
 Focal NFL Defects
Cirrus™ HD-OCT
 Cirrus OCT – RNFL Thickness
Does the OCT Do It Better?
 Caveat #1
- It is difficult to create a normal data base with a structure like the optic
nerve that varies significantly in regards to size, shape and number of
ganglion cell axons
Cirrus Database
 284 patients
 Image quality 6 or above
 Age 19-84


Refractive range -12 to +8 diopters
Ethnicity 43% Caucasian, 24% Asian, 18% African America, 12% Hispanic, 1%
Indian
Factors That Affect Normative Database
 AGE
 RNFL and Neuro rim tissue slightly decreases with age
 The current software does account for age by comparing patients in similar age
groups
 DISC SIZE
 Disc Area range 1.06 – 3.38 mm2 (ave 1.83 mm2)
 Small - disc area < 1.63 mm2
 Medium - disc area 1.63-1.97 mm2
 Large – disc area > 1.97 mm2
 Larger Discs will have larger c/d ratios
 Larger Discs generally have greater neuro rim tissue
 The current software does match disc size for optic nerve parameters but not
RNFL
 Disc area <1.33 mm2 or > 2.50 mm2 is not compared to the normative database
because there are too few in the database
 RIM AREA
 Rim area range 0.75-2.38 mm2 (ave 1.31)
 We are born with different number of ganglion cell axons (700,000-1.5 million)
 No way to account for this in the database
Caveat #2:
 There are structures (ie blood vessels, astrocytes and glial cells) that contribute
to the measured RNFL by the OCT
Caveat #3:
 Your OCT is not shipped with a brain, so use yours
Cirrus Optic Nerve and RNFL Analysis
OPTIC DISC CUBE SCAN
The 6mm x 6mm cube is captured with
200 A-scans per B-scan, 200 B-scans.
CALCULATION CIRCLE
AutoCenter™ function automatically centers the 1.73mm radius peripapillary calculation
circle around the disc for precise placement and repeatable registration.
The RNFL thickness map shows the patterns and thickness of the nerve fiber layer.
The RNFL deviation map is overlaid on the OCT fundus image to illustrate precisely
where RNFL thickness deviates from a normal range
Distribution of Normals





White represents upper 5% of normal database
Green represents middle 90% of normal database
Yellow represents lower 5% of normal database
Red represents lowest 1% of normal database
Gray not compared to the normal database
Quantitative Optic Nerve and Nerve Fiber Layer Parameters
Average RNFL Thickness
 Represent the average thickness drawn along the 1.73 mm radius calculation circle
around the optic nerve
 Measures the thickness of ganglion cell axons
 But along includes blood vessels, astrocytes and glial cells
 Global index (will miss focal loss)
RNFL Symmetry
 Compares the entire TSINT of the RNFL between and right and left eye
Rim Area
SmartCube™ Defines Disc at Bruch’s Membrane End
Minimizes effect of peripapillary Atrophy on measurements
Cirrus Optic Nerve Head Calculations
The disc edge is determined by the termination of Bruch’s membrane.
The rim width around the circumference of the optic disc is then determined by measuring the
shortest distance from the edge of Bruch’s membrane to inner edge of neuro-retinal tissue in the
optic nerve.
Rim Area
 Rim area range 0.75-2.38 mm2 (ave 1.31) in normative data base
 We are born with different number of ganglion cell axons (700,000-1.5 million)
 No way to account for this in the database other than to average values
Disc Area
 Disc Area range 1.06 – 3.38 mm2 (ave 1.83) in normative data base
 Small - disc area < 1.63 mm2
 Medium - disc area 1.63-1.97 mm2
 Large – disc area > 1.97 mm2
 Disc Area is always Gray color coded
 Larger Discs will have larger c/d ratios


Larger Discs generally have greater neuro rim tissue
The current software does compare disc area to the optic nerve parameters but not to
RNFL parameters
C/D Ratio
 Average and Vertical C/D ratio are reported
 Dependent on Disc Area
 Dependent on the number of ganglion cell axons in our retina
 C/D ratio will increase as ganglion cell axons are lost
 Vertical C/D ratio is probably more important than average C/D ratio

Cup Volume
 Partially Dependent on Disc Area
 Can increase as glaucoma excavation progresses
 Poorer Reproducibility compared to other optic nerve parameters
Thickness Profiles
Neuro-retinal Rim Thickness profile, OU
- compared to normative data
RNFL Peripapillary Thickness profile, OU
- compared to normative data
Quadrant and Clock Hour RNFL Analysis
Should We Look Elsewhere for Glaucoma Damage other than the Optic Nerve?
 The ganglion cell complex (ILM – IPL)
 Ganglion Cell Analysis
 Measures thickness for the sum of the ganglion cell layer and inner plexiform
layer (GCL + IPL layers) using data from the Macular 200 x 200 or 512 x 128
cube scan patterns.
 RNFL distribution in the macula depends on individual anatomy, while the
GCL+IPL appears regular and elliptical for most normals. Thus, deviations from
normal are more easily appreciated in the thickness map by the practitioner, and
arcuate defects seen in the deviation map may be less likely to be due to
anatomical variations.
Advantage of Ganglion Cell Analysis
 More reproducible measurement than peripapillary RNFL
 Less physiological variation compared to peripapillary RNFL
 Less major blood vessels to create pseudo-thickness measurements
 Better symmetry between superior and inferior and between eyes than
peripapillary RNFL

Clinical Correlation is Paramount
Errors in Interpretation


Green always represents Non-Disease
Red always represents Disease
Red Disease Does Not Always Mean Glaucoma
 Clinical Correlation is Key
Does Green Always Mean Normal?
 Symmetry is a Beautiful Thing!
 Lack of Symmetry Should Raise Suspicion!
Cirrus Guided Progression Analysis (GPA)

RNFL Thickness Change Maps demonstrate change in RNFL between exams.
Up to 6 progression maps are compared to baseline. Areas of statistically
significant change are color-coded yellow when first noted and then red when the
change is sustained over consecutive visits.
• TSNIT values from baseline and current exams are plotted.
• Areas of statistically significant change are color-coded yellow when first noted
and then red when the change is sustained over consecutive visits.
•
•
•
•
Average RNFL Thickness values are plotted for each exam.
Yellow marker denotes change from both baseline exams.
Red marker denotes change sustained over consecutive visits.
Rate and significance of change are shown in text
Cirrus GPA™ Analysis
• RNFL SummaryLegend summarizes GPA analyses and indicates with a check
mark if there is possible or likely loss of RNFL
• RNFL Thickness Map Progression (best for focal change)
• RNFL Thickness Profiles Progression (best for broader focal change)
• Average RNFL Thickness Progression (best for diffuse change)
Updated Guided Progression Analysis (GPA™)
Optic Nerve Head information now included
 Average Cup-to-Disc Ratio plotted on graph with rate of change information.

RNFL/ONH Summary includes item “Average Cup-to-Disc Progression”.

Printout includes an optional second page with table of values, including Rim
Area, Disc Area, Average & Vertical Cup-to-Disc Ratio and Cup Volume. Each


cell of the table can be color coded if change is detected.
Miscellaneous updates to the report design.
Updated Guided Progression Analysis (GPA™)
OCT Clinical Pearls
 Normal data bases for optic nerve and RNFL are difficult to construct
 Blood vessels, astrocytes and glial cells can taint optic nerve and RNFL
measurements
 If you simply evaluate the OCT printout in isolation, you will make interpretation
errors
 Understand that GREEN does not always mean NORMAL and RED does not
always mean ABNORMAL
 Symmetry is a beautiful thing, lack of symmetry should be cause for concern
Summary
 OCT is amazing technology that enhances glaucoma diagnosis
 Understand the potential for interpretation errors and you will make fewer
 OCT can uncover glaucoma damage before visual field loss occurs
 OCT can add another technique to judge for glaucoma progression
 Software updates and improved normal databases will improve OCT
interpretation
 The doctor should always correlate the data from the OCT printout with clinical
data before making management or treatment decisions in glaucoma.
My Favorite Cases
Anthony B. Litwak, OD, FAAO
VA Medical Center
Baltimore, Maryland
Dr. Litwak is a speaker and on advisory boards for Alcon and Zeiss Meditek
Case RS
62 yobm
No family history of glaucoma
BVA 20/20 OU
There is no APD
SLE nl
TA 21 OU
Gonio reveals open angles OU
See optic nerve, NFL, Visual fields.
The ganglion cell complex (ILM – IPL)
Ganglion Cell Analysis
Isolates ganglion cell layer to remove variance of RNFL
Measures thickness for the sum of the GCL and IPL layers using data from the SmartCube ® (Macular
cube scan)
RNFL distribution in the macula depends on individual anatomy, while the GCL+IPL appears regular
and elliptical for most normal individuals
Advantage of Ganglion Cell Analysis
More reproducible measurement than peripapillary RNFL
Less physiological variation compared to peripapillary RNFL
Less major blood vessels to create pseudo-thickness measurements
Better symmetry between superior and inferior and between eyes than peripapillary RNFL
How Strongly Do You Feel That This Patient Has Glaucoma?
1. 0-20 %
2. 20-40 %
3. 40-60 %
4. 60-80 %
5. 80-100 %
You obtain three IOP readings: 21, 19, 25 OD and 21, 18, 24 OS. What is your management plan?
1. Treat right eye only
2. Treat left eye only
3. Treat both eyes
4. Order MRI of head and orbits
5. Follow without treatment with serial visual fields
How Strongly Do You Feel This Patient is at Risk for Becoming Visually Impaired from Glaucoma?
1. No risk
2. Very little risk
3. Low risk
4. Moderate risk
5. High risk
What is your target IOP?
Guidelines For IOP Target Values
No Damage – 20% Reduction Of Baseline IOP based on OHTS
Mild Damage - 20-30% Reduction Of Baseline IOP
Moderate Damage - 30-40% Reduction Of Baseline IOP
Severe Damage - 40-50% Reduction Of Baseline IOP
Don’t Like Math?
Generally set 3 target pressures:
1. Patient with high risk ocular hypertension – elevated pressure but no glaucoma damage
Treat with 1-2 meds max
2. Patients with definite glaucoma damage, but in the mild-moderate stage of damage
Target pressure < 18 (consistent)
Will use multiple meds and laser to achieve, but not filtering surgery
3. Patients with definite damage in the moderate to severe stage of damage
Target pressure < 15 (consistent)
Will use multiple meds and laser to achieve and will consider filtering surgery in select cases early and
will not delay filtering surgery in cases of progression on MMT
What is it going to take to achieve this target pressure?
1. One med
2. Two meds
3. Three meds
4. Two meds and ALT/SLT
5. Three meds and ALT/SLT
6. Filter
What’s It Going to Take?
20-30% reduction - 1 or 2 meds
30-40% reduction – 2-3 meds +/- ALT/SLT
40-50% reduction - 2-4 meds +/- ALT/SLT +/- filter
The patient reports a history of mild SOB but is not taking any breathing medicines, which medication
would you start for this patient?
The patient's IOP (Tmax) goes from 25 to 19 while taking Travatan QHS.
15. Which medication would you add next?
You have set a target IOP of
The patient is taking Travatan qhs and Alphagan bid with an IOP reading of 15, however the patient
has developed redness and itching. What is your next step?
1. Continue present meds and Rx Patanolol
2. D/C Travatan and start Trusopt
3. D/C Alphagan and start Trusopt
Alphagan is D/C and the redness and itching improve.
What is your next step?
IOP (Tmax) is 17 on Travatan and Trusopt.
Glaucoma Management
Start with a prostaglandin
Add Beta-blocker as second line
Change beta-blocker to Cosopt or Combigan
Add Alphagan or CAI as third drug
OR consider ALT/SLT
Filtering surgery
Only if the benefits overweigh the risks
SLT is performed 360 degrees OD only.
would you repeat the visual field?
Six weeks later the IOP (Tmax) is 14 OD and 18 OS.
When
CASE CR
35 yohf
Neg PMH
+FOH mother and grandmother with glaucoma
VA 20/20 OD, 20/20 OS
SL unremarkable
TA 19-26 OD, 18-26 OS
CCT 554/561
Gonio: 4+ open OU, s PAS or angle recess
1. 0-20 %
2. 20-40 %
3. 40-60 %
4. 60-80 %
5. 80-100 %
1. No risk
2. Very little risk
3. Low risk
4. Moderate risk
5. High risk
Should we treat or observe?
1. Does the patient have nerve damage?
If yes then in most cases – TREAT
If no, then access risk factors to determine the benefits of treatment vs observation
Level of IOP
CCT
Age
FOH
Race
POAG Endpoints by Central Corneal Thickness
and Baseline IOP (mmHg) in Observation Group*
Decided to treat
Based on elevated IOP
Strong family history
Hispanic race
Young age
Follow up
Pt started on timolol .5% bid ou
IOP range 14-19 OD 16-20 OS
What should you do?
How Strongly Now Do You Feel This Patient is at Risk for Becoming Visually Impaired from Glaucoma?
1. No risk
2. Very little risk
3. Low risk
4. Moderate risk
5. High risk
Glaucoma as the Disease Progresses
Visual Field changes occur late in the disease
What should you do now?
Reset TP < 15 OU
Added travatan qhs ou
Changed timolol to cosopt bid ou
IOP 12, 15, 17 OD 13, 14, 17 OS
What should we do?
Add Alphagan?
ALT/SLT?
Would you filter?
30-2 vs 10-2 Testing Points
Case WC
69 yobm
PMH: HTN
-FOH
VA: 20/20 OD, 20/20 OS
Pupils -APD
CF:FTFC OU
SL: Unremarkable
TA: 18 OD 19 OS
Gonioscopy 4+ open with 1+ pigment
See DFE and VF
1. 0-20 %
2. 20-40 %
3. 40-60 %
4. 60-80 %
5. 80-100 %
1. No risk
2. Very little risk
3. Low risk
4. Moderate risk
5. High risk
What is your next step in the management of this patient?
1. Start topical glaucoma therapy
2. Repeat visual field
3. Do blue yellow perimetry
4. Do frequency doubling perimetry
5. Take disc photos and observe
6. Measure CCT
7. Do diurnal curve
8. Do GDx, HRT or OCT
9. Order MRI of orbits and chiasm
Additional Data Gathering
IOP ranges between 16-21 OD and 16-20 on multiple readings
Pachymetry shows CCT 498 OD and 510 OS
According to the Baltimore Eye Study, what percentage of patients who presented with optic nerve
damage or visual field loss from glaucoma had an initial IOP below 21 mm HG?
1. 10%
2. 20%
3. 30%
4. 40%
5. >50%
Baltimore Eye Study
Over
5000 individuals received complete eye exams in a community in east Baltimore
was diagnosed based on the appearance of the optic nerve and visual fields
Glaucoma
Multiple
baseline IOP readings were taken
of patients had a single IOP measurement was < 22 mmHG in newly diagnosed, untreated glaucoma patients
24% of patients had two IOP readings < 22 mm HG
16% of patients had three IOP readings < 22 mm HG
55%
Pseudo NTG
–Diurnal Fluctuation
POAG
Pigmentary
PXG
Uveitic
Intermittent angle closure
–Previous on oral or topical steroids
–On oral IOP lowering agents
–Thinner corneal thickness
Oral Medications Which Lower IOP
Propranolol
(Inderal) (80mg/day)
(Lopressor) (100mg/day)
Atenolol (100 mg/day)
Clonidine (Catapres) (.2mg/day)
Calcium Channel Blockers
Metoprolol
Corneal Thickness and NTG
Thinner
corneas will read lower Goldmann applanation IOPs
corneal thickness 555 nm
POAG 556 nm
NTG 521 nm
31% of NTG patients would be classified as POAG if corneal thickness was accounted for
Japan 503 nm
Refractive surgery patients read 2-3 mm HG lower
Average
Normal Tension Glaucoma Study
Does
Lowering IOP In NTG Delay Glaucomatous Progression
Have Fixation Threatened, Documented VF Progression Or New Disc Hemorrhage
145 Patients Had One Eye Randomized To 30% IOP Reduction (#61) Vs Observation (#79)
Step Therapy With Pilocarpine, ALT And Filter
No Adrenergic Agents (Beta-blockers, Epinephrine Drug)
Xalatan, Alphagan And Topical CAI’s Were Not Available
Patients Followed With Serial VF’s And Optic Disc Photographs
Must
Normal Tension Glaucoma Study
57%
Had IOP Lowered 30% Without Filtering Surgery
12% Of Treated Eyes Versus 35% Of Untreated Eyes Progressed
89% Progressed By Visual Field Progression And 11% By Optic Disc Change
48% Of Filtered Patients Developed Cataract
New Medications May Reduce The Need And Complications Of Filtering Surgery
Should All NTG Patients Be Treated?
How to Treat Normal Tension Glaucoma
Prostaglandin
Non-selection
beta blockers contraindicated?
Alpha
agonist
CAI
Oral CAI
Pilocarpine
ALT
Filtering surgery
Topical
Should Beta-blockers Be Used In Normal Tension Glaucoma?
One
Study Showed Non-selective Beta-blockers Impairs Blood Flow To Ciliary Body
Not Know The Effect On Optic Nerve Blood Flow
May Decrease Cardiac Output
Theoretically Beta 1 Selective Blockers May Have Less Effect On Optic Nerve Blood Flow
Betoptic Showed Less Visual Field Progression Than Timoptic In One Study
Final Verdict Has Not Been Reached
Do

A Randomized Trial of Brimonidine versus Timolol in Preserving Visual
Function: Results From the Low Pressure Glaucoma Treatment Study AJO
2011; 151:671-681.
Randomized,
double masked, multicenter clinical trial
Normal tension glaucoma patients (IOP < 22)
Randomized to monotherapy with brimonidine .2% or timolol .5% bid ou
Followed with serial visual fields and IOPs for four years

Low Pressure Glaucoma Treatment Study
99
brimonidine and 79 timolol patients
Mean IOP lowering was similar for both treatment groups
Used two different visual field analysis to judge for progression: Pointwise linear
regression (Progressor software) and glaucoma change probability maps
Visual Field Analysis

Brimonidine group showed less visual progression than timolol on
Progressor software (9.1% vs 39.2%), Glaucoma change probability maps
(8% vs 44%), 3 omitting method (5% vs 27%)
Adverse Reactions/Drop Out Rates
of brimonidine vs 10% of timolol dropped out prior to 1st year of study
Most common cause was ocular allergy (28% of brimonidine group)
2.5% of timolol vs 8% of brimonidine group had a systemic adverse reaction
5% brimonidine vs 1% timolol died from unrelated to meds causes
55% (54/99) brimonidine vs 29% (23/79) of timolol dropped out of study
Unequal drop out rate may bias results of study
36%
Final Analysis of the Low Pressure Treatment Study
 Is timolol contraindicated in NTG?
 Is brimonidine neuroprotective?
 Does the drop out rate of brimonidine change the way you use it for COAG
patients?
NTG Clinical Pearls
Common
form of glaucoma
by careful inspection of the optic nerve and NFL and screening VFs (FDT)
Be sure to establish baseline IOP (Diurnal helpful)
Similar in characteristics to POAG with some slight modifications
IOP lowering is beneficial in patients with NTG
Avoid non-selective beta blockers ?
Use prostanglandin, alpha agonist, topical CAI’s, ALT and filtering surgery to achieve a 30%
reduction
NTG is Not A Diagnosis of Exclusion and Does Not Require A Neurological Massage
Diagnosed
When do you do additional testing to R/O other etiologies?
Evidence
of disc pallor
field loss respects the vertical midline
Greater temporal than nasal visual field loss
Visual field loss out of proportion to optic nerve damage
–Be sure to rule out unreliable visual field tester
Over 95% of NTG do not require a neurological massage
Visual
Should We Abolish the Term “Normal Tension Glaucoma”?
We
Do Not Fully Understand the Pathophysiology of NTG or High Tension Glaucoma
in Risk Factors, Optic Nerve, NFL and Visual Field Appearance
50% of Glaucoma Patients Will Exhibit an IOP Reading <21 Mm HG
Lowering IOP Slows Down the Rate of Progression Whether Patients Have NTG or High Tension
Glaucoma
Overlap
Managemen
Management
Manag
ntt off Infectious
Inf
Eyee D
E
Disease
Diseas
sese
ee-The
-The Next
N
Generation of Treatments
Bruce E. Onofrey
ey,
ey
y, OD,
D,, RPh
Ph,, FAAO
Ph
Professor, U. Houston
UEI
KWIIK CAS
KWIK
CASE 2:
Take a guess
S: 17 Y/O Female
Fema with c/o
c itching
itchin
in
ng
g , watering
wate
terin
ing red
r OD
O
X 24 hours associated with flu
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u-like symptoms.
O: “Mixed” conjunctivitis
j
NO
O Pre
ree-Auricular
node
Mucous like discharge with
y
erythema
OD
Pseudomembranee OD
Cornea: Multiple
p infiltrates
Unilateral presentation
Enterrovir
Enteroviruses
oviirruseees:
s:
The “REAL
L “PINKEYE”
Entero
roo-from
the ggut
EHC
E C--Epidemic
Epidemicc Hemorrhagic
Ep
Conjunctivitis
j
C
Called Apollo
llo 11 dise
diseasee aft
after
er
outbreak in Africa from 1969
outb
6969
9
70
Enterovirus
s type
y 70
yp
Minimal corneal signs
g
Big PA nodes common
Viral
ral conjunctivitis
unctiviti is the
#11 Cause
Ca
of ACUTE
AC
ACU
CUT
INFECTIO
INFECTIOUS
NFE IOU
NF
IOUS
S
Conjunctivitis (in adults)
Adenovirus
Enterovirus
Adenoviral Signs@@@@
F
Follicular
ular
conjunctivitis
conjunctiviti
conju tivitiisVariablee most common in
lower fornix
Mild to moderate
e chemosis
Lid swelling
g with mild ptosis
“Watery” discharge
Lymphadenopathy
in
66%
Adenovirus Family
DNA
Viruses
At least 35 different serotypes
Type
yp
8 Classic EKC
Types
T
10, 13, 19, and 37
7 NEW
EKC
N
NEW VIRUS =
INFLAMMATION
REMEMBER
ADENOVIRAL
DENOVIR L
DISEASE
EASE IS
BILATERAL
****EVENTUALLY******
CLASSIC PRESENTATIONS
ARE ONLY FOUND IN TEXTBOOKS
DO
DOES
OES SELF
SEL
ELF
F-LIMITING
F
-LI
LIMITING
MIT
DISEASE NEED TREATMENT?

SELF-LIMITING DOES NOT MEAN
HARMLESS
INFECTIVE PROCESS IS THE SELF
LIMITED FACTOR
INFLAMMATION IS NOT
TREAT TO PREVENT
INFLAMMATORY DAMAGE
TREATMENT
REAT
OF BOTH
SYMP
SYMPTOMS
MP
PTOMS
PTO
OMS AND PREVENTIO
PRE
PREVENTION
EVENT
TIO
ON
O
OF INFLAMMATORY DAMAGE
Cool
compresses
p
and ASA
Lubrication
Decongestants
g
Steroids
s (in
((infiltrates,
nfiltrates,
ltrates, membranes,
mem
inflammation)
n))@
@@@@
@@
@@@
Membrane removal
Antibiotics??
NOOOOOOOO!!!!!
A
Is there a Cure for the
Common Cold of the eye?
NOT QUITE
• Spit and swish: Povidone 5%
ophthalmic solution
• Don’t spare the steroids
CURE?
THE CURE?
Currently in Animal Testing
FORESIGHT
Decreaas infection from 18 to 7
Decrease
days
y
Fewer complications
Tabbara K, Jarade E. Ganciclovir effects in adenoviral
keratoconjunctivitis. Invest Ophthalmol Vis Sci.
PHARMACEUTICALS
Topical FST100 Dexamethasone 0.1%
Containing Povidone-Iodine 0.4% Reduced the
Clinical Signs and Infectious Viral Titers in a
Rabbit Model of Adenoviral Conjunctivitis
KWIK
WIK CASE #3
#
LIKE FATHER, LIKE SON
CHLAMYDIA FACTOIDS

3 Week old newborn with sudden onset
mucopurulent mixed conjunctivitis
Father with unilateral “GIANT” follicular
conjunctivitis
Marked pre-auricular nodes in both patients
Chalmydia
Chalmyd
halmydia
Treatment
#
#11
CAUSE OF C
CHRONIC
NIC CONJ
CONJ. AND
OPHTHAMIA NEONATORUM
STD
Mother should be checked p
prior to birth
Onset in 2nd week post
p stt-p
partum
Potential conjunctival
j
scarring
Systemic complications
KWIK CASE 3A

Both
topical
p
and systemic
y
Treat parents
p
and friends also
T
The family th
that gets treated together
stays
y together
g
Erythromycin
y
y n ophth
p th
h. Oint
Zithromax
Z
x1
10mg/kg/day
0mg/kg/
X 1 day, then
5mg/kg/D
g g X 4 days
y
Adults: 1 gm SINGLE DOSE

24 Y/O
O SCL
Lp
patient
Crusty
y lid lesion OD
Red painful
R
pai
p
aiin
nful eyee OD
O X 48
hours
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s-”getting
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“Mixed” conjunctivitis
j
No CL X 24 hours
3rdd tim
ttime this year “pink
eye”
y
(+PA node on R side)
Disinfectants and infection
•
•
•
•
•
•
•
•
Broad anti-infective efficacy
Ionic
Some stain
Uncomfortable
Toxic
Not all eye approved
Skin infections
Pre-op
H es Fam
Herpes
Family
mily of
Viruses@@@@
Herpes
p
simplex
p
Herpes
p zoster
E
Epstein
Epste
ein Barr
Barrr
rrr--Infectious
Inf
In
mononucleosis
CMV
V-Cytomegalovirus
-
Herpes Simplex
T
Type
I Above
A
waist
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g
g
T
Typee II below
ww
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ai
aisst-most
sstt-most
t m severe
in eye iinfection
nfectio
nfection
onon
n-Saccral
n
-S
Sa
a
ganglia@@@@
g
g @@
@@@
50% reoccurrence within 2 years
Multiple
p triggers@@@@
gg @@@@
@@@
90% carry antibodies by age 10
Herpes Simplex
Primary
y
disease
Recurrent disease
Conjunctivitis
Keratitis
Stromal
disease
Kerato
to-uveitis
to
-
@@@
@@@@
@
@@
@@
@
@
Primary H. simplex
P
Pr
Pre
reee-auricular
-au
auricu
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Vesicles
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No dendrite
Se
Self
S
lflf
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limiting
im
mittiing
g
disease
dis
diseas
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asse
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- TTreat
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aggressi
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prevent
recurrence
Str
Stromal
l H. simple
simplex
simp exA whole new ball game

Mechanissm is
Mechanism
M
primarily
p
rimarily
inflammation@@@@
@ @@
@@@
Stromal
Strom
S
mal infiltrates
infiltratee are
the critical sign
g
Balanced u
B
use
se of
topical ssteroid
ster
terrooi
oid
id (FML)
(F
with anti
antii-viral
ant
-vi
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cover@@@@
@@@@
Consider oral
C
acyclovir at this point
poi
in time (HEDS II)
Recurrent H. simplex

Pre
P
rere-au
aauricular node
rare
V
Virus inv
involves
volves
es
deeper
eeper tissu
tissues
tissue with
each episode
p
5
50% get
et recurrence
recurre
within 2 years
y
S
Steroids willl
exacerbate
infectious H.
H
simplex
p disease
Contr
Contra
C
rara
aa-indicated
-in
ndicated in
n
purelyy in
infectious
disease
Topica
Topi
all v
a
vss S
Syste
temic
emic
Topical
Systemic
Steroid
d vss no steroid
TX Mechanisms
ms-not
ms
a Name
Know Your HEDS 1 and 2
#1: Topical for Everyone
ZIRGAN: THE NEW
Trifluorothymidine
ne:
e: THE OLD

T E FORMER dr
THE
drug
ru of
choice for topica
topical
al
management
managem
ment of Herpes
H
simplex ocular
ocu
ular
disease.@@@@@
@@@
@@@
Rapid
p absorption
p
T
Toxicity occurs when used
over 21 days
y
Dosage
ggee-5
-55-8X dailyy
Viroptic
c 1%
%-7.5cc
- ccc-Burroughs
Selective
Toxicity
y
Gel formulation
A
Adenoviral
Adeno
noviral
effective?
5
5X/D
till re
rreee-epith
-eep
pitth
th,
then TID X 3D
HX of HEDS I and II
Multicenter
study of H. Simplex
1992
9292
2-1996
5
The Herpetic
rpetic Eye Disease
Disea Study
y 1 and 2
(HEDS I and II) and
an
a it’s
it s impact
i
on the
th
current TX of H. Simplex Eye Disease
separate
parate st
study
dy gr
groups too evaluate
benefits
ts of H.
H simplex
s mple
mplex TX modali
modalities
and prevention
vention b
benefits
ben
benee
of oral
antiviral therapies
p
HEDS 1 TX studies (active
(
disease)
H
HEDS II Preve
Prevention studies
(prophylaxis)
The KWIK HEDS 1 RESULTS
The KWIK HEDS 2 RESULTS
1
1.
STEROIDS
STER
ROI
OIIDS
DS FOR STROMAL
HERPES
S - YES
2
2. ORAL
OR
AN
ANTI
NT
TITI
I-VIR
VIRALS
V
RAL
AL
LS forr
STROMAL
STRO
OMAL HERPES
HE
HERP
ERP
ER
ERP
PES
P
ES
S – DO
DOES NOT
D
HASTEN RESOLUTION
3
3.. O
ORAL AN
ANTIVIRALS
NTIVIRA
VIRA
RA
ALS
A
S FOR
FO
IRIDOCYCLITIS
IRIDOCYCLI
RID
ITIIS
ISS-- S
S
SMALL
SM
MAL
MALL
LL T
TES
TEST
GROUP, BUT
GROUP
BU STATISTICAL
BENEFIT
1.
USE OF ORAL
L ANTI
ANT
NT
TII-VIRALS
I--VIRAL
V
IN
HERPETIC DISEASE
USE OF ORAL
L ANTI
ANT
NT
TIII-VIRALS
-VIRAL
V
IN
HERPETIC DISEASE
EPITHELIAL HERPES
Combine
Comb
mbinee wit
with topic
topical to
maximize therapy
py
Acyclovir
y
400mgg 5X dailyy
Valacyclovir
y
r 500mgg TID
Famcyclovirr 250mg TID
Oral anti-virals DO NOT prevent
conversion from epithelial to stromal
Herpes
2. Prophylactic use of ORAL antivirals DO prevent REOCURRENCE
of ALL forms of H. simplex
DISCIFORM HERPES
T PICA STEROID
TOPICAL
STERO
OID WITH
ORAL ANTIVIRAL
Acyclovir
y
400mgg 2-5X
- daily
Famcyclovir
y
r 125mgg BID
SLOWWWW TAPER
CONT
CONTINUE
NTINUE
PROPHYLACTIC
PROPH
HYLACTI
H
YLAC
ORAL
ORALS
LONG TERM (YEARS)
USE OF ORAL
L ANTI
ANT
NT
TIII-VIRALS
-VIRAL
V
IN
HERPETIC DISEASE
USE OF ORAL
L ANTI
ANT
NT
TIII-VIRALS
-VIRAL
V
IN
HERPETIC DISEASE
DISCIFO
DISCIFORM
D
ORM
M HERPES
HERP
W/KERATO
O-UVEITIS
-
HERPES
ERPES ZOS
ZOSTER
OPHTHALMICUS
TOPICAL
OPIC
STEROID
ROID WITH
ORAL ANTIVIRAL
Acyclovir
y
400mgg 5X dailyy
Valacyclovir
y
r 500mgg TID
Famcyclovir
y
r 250mgg TID
ORAL acetazolamide
TOPICAL
AL STE
STEROID
OID WITH
ORAL ANTIVIRAL
Acyclovir
y
800mg
g 5X daily
y
Valacyclovir
y
r 1000mgg TID
Famcyclovir
y
r 500mgg TID
Glcc drops as needed
NOW FOR SOMETHING TOTALLY
SIMILAR
Asbell rabbit study
• Oral valacyclovir reduces risk of
recurrent H. simplex after eximer PRK
• Response is highly dose dependant
• 150mg/kg X 14 days 0% reactivation
• Debridmenent did not reactivate virus
• Eximer produced reactivation
• Pre-TX?? Better results??
AND SOMETHING SOMEWHAT
DIFFERENT
Scoper study
• 42 Dry eye patients with H. Simplex
stromal keratitis
• Thermal punctalplasty
• Topical cyclosporin A
• 3 groups:
• Punctalplasy
• Cyclosporin A
• Both
Results
• Non-treated group: 6-7 months of disease/yr
• TX with EITHER thermal cautery or topical
cyclosporin: 1.1 months/yr of active disease
• TX with both: 0.8 months/yr
• Learning point:
Differential
ntial DX
D of In
Infection
n
The Tests
Cultures
Diff
fff Q
ffQuick
Gram
Stain
• OSD patients with H. simplex require
aggressive management
• Topical cyclosporin A is safe and effective in
H. simplex patients
Gram Stain (FA
G
(FAST)
D
Differentiates
Dif
ifferentiates
fferentiates
rent
bacteria
cteria by differen
differences
dif
in cell wall morphology@@@@
p
gy@@@@
D
Designates
Designa
atess bacteria as Gram (+) orr (()@@@@
Bacterial Ulcer Guidelines
Always
y
culture if yyou have the means
P
Patients
atients tha
that gget
et better
bette never sue
ueue
those that don’t
’tt-DO
Consider the 1-2
-2-3
-3-4 rule
Fluor
Fluoroquinolone
F
uorro
oquin
ino e mono
nono
o-therapy is not
fool
ol-proof
-p
Grade the ulcer
erer
r-Location,, location,
n, etc
Step TX based on cultures
Fourth
thh-Generation
ion
n Fluoroq
Fluor
Fluoroquinolone
quin
Chemical
Structures
Evolution of the Quinolones
Nalidixic
Acid
O
Norfloxacin
Lomefloxacin
Ciprofloxacin
Ofloxacin
N
COOH
N
N
H3CN
HN
Limited spectrum
of activity
F
F
HN
Extended spectrum
Enhanced activity against
Gram-negatives
American Pharmaceutical Association; 2000.
CH
C
H3
H
H3C
COOH
• 1.5 H2O
COOH
N
HN
OCH3
N
H
H
Extended spectrum
Enhanced activity against
Gram-positives, streptococci,
anaerobes, atypical
mycobacteria
Improved pharmacokinetic
properties
NEW Molecule
Moxeza: Longer duration
Zymaxid: Higher concentration
N
F
H
OCH
H3 N
Gatifloxacin
Moxifloxacin
TWO MOXY’s
’ss-What’s the difference
The Latest
Besivance:
OCH3
HN
N
O
COOH
N
H
N
O
O
F
O
COOH
N
N
N
C2H5
F
Gatifloxacin
Moxifloxacin
O
O
COOH
H3
C
Sparfloxacin
Grepafloxacin
Levofloxacin
Vigamox
g
Moxeza

Active ingredient:
g
0.5%
% Moxafloxacin

DITTO

Indication

DITTO

3cc

BID

NO
Bacterial conjunctivitis
j

Bottle size
5cc
Dose
TID
Generic
YES
Kid
Kids
ds Conjunctiviti
Conjunctivitis
njunctivitis
isss-NO
-NO
N
drops alone if…..
For MRS
MRSA
RSA
A-Forget
A
-Fo
Forget
rget the
Fluoroquinolones
Back to the OLD Drugs
g
Trimethoprim
p m
Recurrent
(not just for kids)
Tobramycin
y
Fever
Vancomycin
Sore
throat
Generally
y ill
T
Treat with
Polytrim/fluoroquinolone
Polytrim/fluo
oroquinol ne and
effective oral anti H. Flu
DON’T Forget Your
Differential DX-The Bad Signs
The STYE that Wasn’t
When topicals are NOT
ENOUGH!
•
•
•
•
32 yowm swollen upper lid
Very painful
Warm to touch
+ HX frequent “Styes”
or active otitis media
•
•
•
•
•
•
•
Decreased Acuity
Proptosis
Diplopia-Extraocular paralysis
Febrile
Elevated WBC’s
Get blood cultures
Consider orbital CT scan
Orbital Cellulitis is a Life/SightThreatening Condition
• Patient must be hospitalized
• Parenteral IV therapy is mandatory
• Drug based on culture/sensitivitiy
reports
• HX of trauma or insect bite is
common
THE END
• MANY MANY THANKS!
• QUESTIONS?
AREDS 2 and U
Bruce E. Onofrey, OD, RPh, FAAO, FOGS
Professor, University of Houston UEI
a Novartis company
DISCLOSURES
• I’M AN ADVISOR TO :
• KEMIN PHARMA
• ALCON
• B AND L
• ALLERGAN
Age-Related Eye Disease Study (AREDS):
Rationale and Significance
PART 2
a Novartis company
1
AREDS 2 The Age Related Eye Disease
Study-Part 2
•JAMA, May 2013
• Lutein (+) Zeaxanthin and Omega 3 fatty acids
for age related macular degeneration: AREDS
2
•The QUESTIONS:
• 1. Does adding lutein (+) zeaxanthin, the
Omega 3 fatty acids DHA (+) EPA or both to
the original AREDS formula decrease the risk
of developing advanced AMD?
QUESTION #2
• Does removal of betacarotene or reduction in the
amount of zinc increase the
risk of developing AMD?
QUESTION #3
•JAMA, JULY 2013
• Does L/Z supplementation affect the rate of
cataract surgery or cataract associated vision
loss?
2
AREDS: NEI Trial Overview
Feature
Description
Objective
To evaluate the effect of high-dose
vitamin supplementation, age-related
macular degeneration (AMD)
progression and visual acuity.
Design
Double-masked, randomized, placebocontrolled trial
Population
3640 high risk patients (55-80 years)
Duration
6.3 years supplementation and follow up
Age-Related Eye Disease Study Research Group. A Randomized, Placebo-Controlled clinical Trial of High-Dose Supplementation With Vitamins C and E,
Beta Carotene, and Zinc for Age-Related Macular Degeneration and Vision Loss: AREDS Report No. 8. Arch Ophthalmol 2001;119(10):1417-36.
ARED (Age related eye disease) Study
results
Archives of Ophthalmology-October
2001
• Categories
• 1. NO AMD
2. Mild AMD
• 3. Moderate AMD
• 4. Advanced AMD
Daily Dosage: Placebo VS AREDS formula
Supplements were manufactured to have the following minimum contents:
Supplement
Dosage
Antioxidants
Beta-carotene
15 mg
Vitamin C
500 mg
Vitamin E
400 IU
Essential Trace Elements
Copper
Zinc
2 mg
80 mg
Age-Related Eye Disease Study Research Group. A Randomized, Placebo-Controlled, Clinical Trial of High-Dose Supplementation With Vitamins C and E,
3
AREDS Rationale: Beta-Carotene
• Why is it important?
▫ Body unable to synthesize1
▫ Antioxidant capability1
• What dose was studied?
▫ 15 mg/day (AREDS)2
• Where can I get it in my diet?
▫ Carrots, broccoli, spinach, kale3
▫ 15 mg beta-carotene = 1.6 cups of carrots3
▫ 15 mg beta-carotene = 47.1 cups of broccoli3
1.
Paiva SAR, et al. Β-Carotene and Other Carotenoids as Antioxidants. J Am Coll Nutr 1999;18(4):426–33.
2.
Age-Related Eye Disease Study Research Group. A Randomized, Placebo-Controlled, Clinical Trial of High-Dose Supplementation With Vitamins C
and E, Beta Carotene, and Zinc for Age-Related Macular Degeneration and Vision Loss: AREDS Report No. 8. Arch Ophthalmol 2001;119(10):1417-36.
USDA National Nutrient Database for Standard Reference, Release 18, Beta-carotene. Available at:
http://www.nal.usda.gov/fnic/foodcomp/Data/SR18/nutrlist/sr18w321.pdf. Accessed May 1, 2012.
3.
DON’T FORGET THE
CONTRAINDICATIONS - Beta
Carotene and Cancer
The three beta-carotene intervention trials: the Beta Carotene
and Retinol Efficacy Trial (CARET), Alpha-Tocopherol, BetaCarotene Cancer Prevention Study (ATBC), and Physician's
Health Study (PHS) have all pointed to a lack of effect of
synthetic beta-carotene in decreasing cardiovascular disease or
cancer risk in well-nourished populations. The
contribution of beta-carotene supplementation
to increased risk of lung cancer in smokers has
been raised as a significant concern. Risk
increase = approx 30% (avg of 3 studies)
DON’T SMOKE:
Cigarette smoking and retinal carotenoids: implications for agerelated macular degeneration.
Subjects were matched with respect to age, sex, dietary
patterns and overall pigmentation (i.e., eye, skin and hair
color). The
smoking group had a mean MP of
0.16 (SD = 0.12) compared to a mean MP of
0.34 (SD = 0.15) for nonsmokers (P < 0.0001).
MP density and smoking frequency were
inversely related (r = -0.498 P < 0.001) in a
dose-response relationship.
4
AREDS Rationale: Vitamin C
▫ Citrus fruits and juices3
▫ 500 mg vitamin C = 4 cups/32 fl oz of orange
juice3
1.
Jacob RA, Sotoudeh G. Vitamin C function and status in chronic disease. Nutr Clin Care 2002;5(2):66-74.
2.
Age-Related Eye Disease Study Research Group. A Randomized, Placebo-Controlled, Clinical Trial of High-Dose Supplementation With Vitamins C and E,
USDA National Nutrient Database for Standard Reference Release 18, Vitamin C. Available at:
3.
AREDS Rationale: Vitamin E
▫ 400 IU/day (AREDS)2
▫ Nuts, fortified cereals, sweet potatoes3
▫ 400 IU vitamin E = 182.6 sweet potatoes3
1.
2.
3.
Traber MG, Stevens JF. Vitamins C and E: Beneficial Effects From a Mechanist Perspective. Free Radic Biol Med 2011;51(5):1000-13.
Age-Related Eye Disease Study Research Group. A Randomized, Placebo-Controlled, Clinical Trial of High-Dose Supplementation With Vitamins C and
E, Beta Carotene, and Zinc for Age-Related Macular Degeneration and Vision Loss: AREDS Report No. 8. Arch Ophthalmol 2001;119(10):1417-36.
USDA National Nutrient Database for Standard Reference Release 18, Vitamin E. Available at:
AREDS Rationale: Zinc: Early studies suggested
ability to slow progression, but not VA loss in
AMD
▫ Essential trace element1
▫ 80 mg zinc/day (AREDS)2
▫ Red meat, poultry, mixed nuts2
▫ 80 mg zinc = 55.8 oz of red meat3
▫ 80 mg zinc = 50.3 oz of nuts3
1.
2.
3.
Grahn, BH, et al. Zinc and the eye. J Am Coll Nutr 2001;20(2 Suppl):106-18.
Age-Related Eye Disease Study Research Group. A Randomized, Placebo-Controlled, Clinical Trial of High-Dose Supplementation With Vitamins C and
E, Beta Carotene, and Zinc for Age-Related Macular Degeneration and Vision Loss: AREDS Report No. 8. Arch Ophthalmol 2001;119(10):1417-36.
USDA National Nutrient Database for Standard Reference Release 18, Zinc. Available at:
http://www.nal.usda.gov/fnic/foodcomp/Data/SR18/nutrlist/sr18w309.pdf Accessed May 1, 2012.
5
AREDS Rationale: Copper
▫
▫
▫
▫
Essential trace element1
Both an anti-oxidant and pro-oxidant2
Body unable to synthesize2
High zinc may cause copper deficiency3
▫ Seafood, Liver, Nuts, Legumes2
▫ 2 mg copper = 1/2 oz of liver5
▫ 2 mg copper = 5 cups of beans5
1.
2.
3.
4.
5.
Determinants of Copper Needs Across the Lifespan. Office of Dietary Supplements, National Institutes of Health. Available at: at: http://ods.od.nih.gov/News/Copper.aspx. Accessed August 31,
2011.
Copper Overview. University of Maryland Medical Center. Available at: http://www.umm.edu/altmed/articles/copper-000296.htm. Accessed August 31, 2011.
NIH Dietary Supplement Fact Sheet: Zinc. National Institutes of Health. Available at: http://ods.od.nih.gov/factsheets/Zinc-HealthProfessional / Accessed 21 July 2011
Age-Related Eye Disease Study Research Group. A Randomized, Placebo-Controlled, Clinical Trial of High-Dose Supplementation With Vitamins C and E, Beta Carotene, and Zinc for Age-Related
Macular Degeneration and Vision Loss: AREDS Report No. 8. Arch Ophthalmol 2001;119(10):1417-36.
USDA National Nutrient Database for Standard Reference Release 18, Copper. Available at: http://www.nal.usda.gov/fnic/foodcomp/Data/SR18/nutrlist/sr18w312.pdf Accessed May 1, 2012
AREDS 1: THE RESULTS
• 21 published reports
• Those likely to benefit from
AREDS formula:
- extensive intermediate-size
drusen
- at least one large drusen
- noncentral geographic atrophy
- advanced AMD
- vision loss in one eye
ARED Study results
Archives of Ophthalmology-October 2001
• 1. Patients over 55 years should have DFE to be
4.
8% decrease
of progression
evaluated
for risk of AMD.
• from
2. If extensive
intermed. 3
Drusen,
Catagory
to 4 at least 1 large
druse, non-central geographic atrophy in 1 or
Reduced
visualAMD
acuity
both eyes or advanced
and noloss by
contraindications-TX
19%
in Catagory 3 and 4
• 3. Vit C 500mg, Vit E 400IU, Beta carotene
15mg + Zinc 80mg and Copper 2mg (Oxides)
6
IMPORTANT TO NOT TAKE
AREDS TOO FAR
• DID NOT PREVENT AMD
• DID NOT REVERSE AMD
WHY AREDS 2?
• WHY L/Z?
• WHY OMEGA 3’S?
AREDS 1: Observations
• Lutein/zeaxanthin and omega-3 fatty acid: Intake
was independently linked with decreased
likelihood of:1,2
• Neovascular AMD (Lutein/zeaxanthin, Omega-3s)
• Geographic atrophy (Lutein/zeaxanthin, Omega-3s)
• Large or extensive intermediate drusen
• Omega-3 fatty acids were of particular benefit in
groups at higher risk for neovascular AMD and
geographic atrophy3
1.
2.
3.
Age-Related Eye Disease Study Research Group. The relationship of dietary carotenoid and vitamin A, E, and C intake with age-related macular degeneration in a
case-control study: AREDS Report No. 22. Arch Ophthal 2007;125(9):1225-32.
Age-Related Eye Disease Study Research Group. The relationship of dietary lipid intake and age-related macular degeneration in a case-control study: AREDS
Report No. 20. Arch Ophthalmol 2007;125(5):671-9
Sangiovanni JP, et al. 6{omega}-3 Long-chain polyunsaturated fatty acid intake and 12-y incidence of neovascular age-related macular degeneration and central
geographic atrophy: AREDS report 30, a prospective cohort study from the Age-Related Eye Disease Study. Am J Clin Nutr 2009;90(6):1601-7.
7
Significance of Lutein and Zeaxanthin
• Several carotenoids are present in human
serum, but only lutein and zeaxanthin are
present in macula and provide a yellow
color known as macular pigment1
• This macular pigment protects the macula
from the damaging photo-oxidative effects
of blue light1
• Body cannot synthesize2
• 5:1 ratio of lutein to zeaxanthin in the diet3
• Powerful Antioxidant4
Yellow macular pigment
composed of
lutein and zeaxanthin
– Reduces free radical damage in the eye
1.
2.
3.
4.
Lutein and Zeaxanthin. Alternative Medicine Review 2005;10(2):128-35.
Nutritional Supplements for Eye Health. Bausch & Laumb Website. Available at: http://www.preservision.co.uk/. Accessed 3 October 2011
Thurnham DI. Macular Zeaxanthins and Lutein—A Review of Dietary Sources and Bioavailability and Some Relationships with Macular Pigment Optical
Density and Age-Related Macular Disease. Nutr Res Rev 2007;20:163–79.
Subczynski WK, et al. Location of Macular Xanthophylls in the Most Vulnerable Regions of Photoreceptor Outer-Segment Membranes. Arch Biochem
Biophys 2010;504:61–6.
Lutein Antioxidant Supplementation Trial (L.A.S.T.)
and Macular Pigment Optical Density (MPOD)
– Mean age: 75
– Mean number of smoking pack
years: 7
• Treatment arms:
FloraGLO®
– 10 mg
lutein
– 10 mg FloraGLO® lutein +
antioxidants
– Placebo
Macular pigment optical density
• 90 patients with AMD (4 females,
86 males):
36%
improvement
0.6
*
0.5
1.
2.
*
0.3
0.2
0.1
0 Right eye Left eye
• Significant improvements from
baseline in visual function1
Lutein
– Greatest benefit in patients
with lowest baseline MPOD2
*
*
*
*
0.4
43%
improvement
Baseline
Right eye Left eye Right eye Left eye
Lutein +
antioxidants
Placebo
Final visit
*P<0.05
Richer S, et al. Double-Masked, Placebo-Controlled, Randomized Trial of Lutein and Antioxidant Supplementation in the Intervention of Atrophic AgeRelated Macular Degeneration: the Veterans LAST Study (Lutein Antioxidant Supplementation Trial). Optometry 2004;75(4):216-30.
Richer S, et al. LAST II: Differential Temporal Responses of Macular Pigment Optical Density in Patients with Atrophic Age-Related Macular
Degeneration to Dietary Supplementation with Xanthophylls. Optometry 2007;78(5):213-9.
*FloraGlo is a registered trademark of Kemin Industries, Inc.
Long-term FloraGLO® Lutein and Zeaxanthin
Supplementation Improves MPOD in patients with AMD
LUTEGA STUDY
• 172 subjects (50+, AMD)
• Double-masked, randomized:
MPOD CHANGES
QD Daily supplementation
Placebo
Lutein /
Absolute Change in ODU*degree²
–10 mg
FloraGLO®
1 mg Zeaxanthin /
255 mg Omega-3 QD
–10 mg FloraGLO® Lutein /
1 mg Zeaxanthin /
255 mg Omega-3 BID
– Placebo
• 4 evaluations over 12 months
Supplementation in Months
Jentsch S, et al. The Lutega-Study: Lutein And Omega- 3- Fatty Acids And Their Relevance For Macular Pigment In Patients with Age-related Macular
Degeneration (AMD). Invest Ophthalmol Vis Sci 2011;52:E-Abstract 3632.
*FloraGLO is a registered trademark of Kemin Industries, inc.
8
Increased MPOD is linked to Positive Effects
on Visual Performance
•
•
•
•
Glare tolerance1
Glare recovery1
Contrast sensitivity2
Amsler defect and
VA improvement3
• Chromatic aberration2
• Photophobia4
1.
2.
3.
4.
Stringham JM, et al. Macular Pigment and Visual Performance in Glare: Benefits for Photostress Recovery, Disability Glare, and Visual Discomfort. Invest
Ophthalmol Vis Sci 2011;52(10):7406-15.
Loughman J, et al. The Relationship Between Macular Pigment and Visual Performance. Vision Res 2010;50(13):1249-56.
Richer S, et al. Double-Masked, Placebo-Controlled, Randomized Trial of Lutein and Antioxidant Supplementation in the Intervention of Atrophic Age-Related
Macular Degeneration: the Veterans LAST Study (Lutein Antioxidant Supplementation Trial). Optometry 2004;75(4):216-30.
Wenzel AJ, et al. Macular Pigment Optical Density and Photophobia Light Threshold. Vision Res 2006;46:4615-22.
ICP11003SK
Omega-3 Fatty Acids (DHA/EPA)
• Important for proper visual
development and retinal function1
• Docosahexaenoic acid (DHA) is
found in the highest concentration in
the retina1
• Eicosapentaenoic acid (EPA) is
used in DHA biosynthesis1
1.
Essential Fatty Acids. American Optometric Association. Available at: http://www.aoa.org/x11853.xml. Accessed October 3, 2011
Omega-3 Fatty Acids (DHA/EPA)
• Benefits of DHA/EPA
– Intake is associated with a decreased risk of
progression from bilateral drusen to
geographic atrophy1
• Low levels of DHA and EPA
associated with chronic eye
conditions such as:2
–
–
–
–
1.
2.
Diabetic retinopathy
Age-related macular degeneration (AMD)
Retinopathy of prematurity
Dry eye disease
SanGiovanni JP, et al. The Relationship of Dietary -3 Long-Chain Polyunsaturated Fatty Acid Intake Inversely Associated With 12-Year Progression
to Advanced Age-Related Macular Degeneration: AREDS Report No. 23. Arch Ophthalmol 2008;127(1):110-2.
Essential Fatty Acids. American Optometric Association. Available at: http://www.aoa.org/x11853.xml. Accessed October 3, 2011
9
AREDS2*
Feature
Objective
Design
Population
Description
Assess effect of a alternative
combination of vitamins and minerals
on the progression of AMD and vision
loss
NEI 5 year, multi-center, randomized,
double-masked, placebo-controlled trial
4000 patients at higher risk of
developing AMD (Men and women;
50-85 years*)1,2
*Age limit 5 years younger than AREDS
1.
2.
Age-Related Eye Disease Study 2 Protocol. Available at: www.emmes.com/study/areds2. Accessed July 14, 2011.
AREDS2 Study Overview. Available at: http://clinicaltrials.gov/ct2/show/NCT00345176?term=AREDS2&rank=1. Accessed July 21, 2011.
PROTOCOL
•NO NORMALS
•1-3 MONTH RUN IN WITH AREDS (+)
PLACEBOS
•IF PATIENT COMPLIES WITH DRUG USE
AND SHOWS UP-RANDOMIZED TO TX
•ANNUAL EXAM (+) FUNDUS PHOTOS
•ANNUAL BLOOD TESTS FOR ANTIOXIDANT BLOOD LEVELS
AREDS2: To Evaluate…
Ingredients being studied in AREDS2:
•
FloraGLO® lutein (10mg)
•
OPTISHARP® zeaxanthin (2mg)
•
Omega-3 fatty acids (350 mg DHA, 650 mg EPA)
•
With and without β-carotene (15 mg vs 0 mg)
•
High vs low zinc levels (80mg vs 25mg)
Patients in the AREDS2 study are assigned to different
combinations of ingredients
*FloraGlo is a registered trademark of Kemin Industries, Inc.
* Optisharp is a registered trademark of DSM IP Assets B.V.
10
AREDS 2 WAS COMPLICATED
• 16 RANDOMIZED GROUPS
• NO NORMALS
• 2 LEVELS OF RANDOMIZATION
• SPECIAL RULES FOR SMOKERS
• CENTRUM SILVER FOR THOSE ON A MV
SUPPLEMENT
• STATISTICS LIMITED BY COHORT SIZE AND
DURATION OF STUDY
AREDS2 Study Design
Randomized Participants
~4000
Placebo
L/Z
DHA/EPA
• No smoker can be
in an arm with
beta-carotene
L/Z+DHA/EPA
ATS* Options
No
ATS*
ATS*
AREDS2 Vitamin /
Mineral Evaluation
No ß-C
Low Zn
• Background
multivitamin
supplementation
is allowed, but is
standardized
Original
ATS*
No ß-C & Low Zn
Age-Related Eye Disease study 2 Protocol. Available at: www.emmes.com/study/areds2 . Accessed July 14, 2011.
AREDS 2 Study Overview. Available at: http://clinicaltrials.gov/ct2/show/NCT00345176?term=AREDS2&rank=1. Accessed July 21, 2011.
*AREDS type supplements.
32 | ICP12167SK Ocular Nutrition | May 2012 | Business Use Only
NEI AREDS2 Dosage Options1
Lutein
(FloraGLO®)
Zeaxanthin
(OPTISHARP®)
•10 mg/day
•2 mg/day
• 5:1 ratio of lutein to zeaxanthin commonly found in
American diet2
1.
2.
Age-Related Eye Disease Study 2 Protocol. Available at: www.emmes.com/study/areds2 . Accessed July 14, 2011.
Thurnham DI. Macular Zeaxanthins and Lutein—A Review of Dietary Sources and Bioavailability and Some Relationships with Macular Pigment Optical
Density and Age-Related Macular Disease. Nutr Res Rev 2007;20:163–79.
FloraGLO is a registered trademark of Kemin Industries, Inc.
Optisharp is a registered trademark of DSM IP Assets B.V.
11
AREDS2: To Evaluate…
Endpoints:
Progression to advanced
AMD
•• Progression
to advanced
AMD
Progression to moderate
vision loss
•• Progression
to moderate
vision loss
Progression of lens
•• Progression
of opacity
lens opacity
••
••
Effective cognitive
Cognitive function
function
Effective
Cardiovascular
morbidity/mortality
Cardiovascular morbidity/mortality
LIES, DAMN LIES AND
STATISTICS
•SPINNING THE AREDS 2 DATA
Re-interpretation of results at ARVO 2013 by
lead investigator, Emily Chew et al
• Adding omega 3’s to AREDS: No benefit
• Adding L/Z to AREDS and evaluating the
effect on the total cohort (study population)
• 1. L/Z reduced advanced AMD by 10%
• 2. Neovasc. AMD 11%
• 3. Neovasc AMD 26% in low L/Z diets
• 4. Cataract progression 30% in low L/Z diets
• 5. Beta carotene doubles risk of lung cancer
in all participants, 0.9% VS 2% W-BC
12
Lutein + zeaxanthin intake (mg/day)
Consumption of Lutein/Zeaxanthin in the US is
LOW
•
10
8
6
AREDS2 Intake
4
Women
2
0
19-30
Men
31-50
Age
51-70
Figure courtesy of Kemin Health, Inc.
71+
The average American only gets between 1 mg to 2.3mg per day of combined
lutein and zeaxanthin in their diet which is below the AREDS2 intake of 10mg
CDC. National Health and Nutrition Examination Survey Data 2001-2002. Available at: http://www.cdc.gov/nchs/about/major/nhanes/nhanes01-02.htm. Accessed July 14, 2011.
37 | ICP11001SK Ocular Nutrition | October 2011 | Business Use Only
The Bottom Line on
ARMD/AREDS 1
•
•
•
•
•
DON’T BE Northern European
DON’T GET OLDER
DON’T SMOKE
DON’T GIVE SMOKERS ANTIOX
CONTROL VASCULAR DISEASE RISK
FACTORS
• SUPPLEMENTS DON’T REPLACE A BAD
LIFESTYLE
ADDITIONAL
RECOMMENDATIONS FROM
AREDS 2
• NEVER use beta-carotene in
ANYBODY
• INCREASE L/Z foods in patients diet-if
not, then supplement
• OMEGA 3’s have value, but NOT for
AMD
13
MY RESEARCH INTEREST
• WHY DO STUDIES HAVE TO LAST
SSSSSOOOOOOOO LONNNGG?
• WAY TOOOO EXPENSIVE
• STRUCTURE VS FUNCTION
• ADAPTIVE OPTICS (Dr. Porter)
• Supplement X 6 months-evaluate VA, 10-2VF,
OCT and retinal cone density and
morphology-supplement vs no supplement
• CAN AO’s predict vision loss
• Can we take a photo-objective test and
measure stability VS progression
QUESTIONS?
14
2015 Texas Professional Responsibility Course
“Eight Shades of Gray”
UNIVERSITY OF HOUSTON COLLEGE OF OPTOMETRY
JOE W. DELOACH, OD, FAA0
COURSEMASTER
Welcome to the Professional Responsibilities Course
sponsored by the University of Houston College of
Optometry. As you know, this course is a requirement for
Texas license holders. What you may not know is that all
fees associated with this course are devoted to permanent
projects that are important for the future of the profession.
Thank you for choosing UHCO for your continuing
education.
The development and production of the 2015 Professional Responsibility Course is underwritten by the Harris Lee Nussenblatt Lecture Series Endowment.
This endowment was established in 1992 by the Nussenblatt Family in memory of former Associate Professor Harris Nussenblatt, OD.
The Lecture Series focuses on issues related to professional ethics, public health and practice administration
1
Preface
The content of the Professional Responsibility Course is at the discretion of the Texas Optometry Board. This year, the Board requested only a few issues be addressed. The rest of the agenda will address the core concept of this course, professional ethics. UHCO and the Coursemaster thank the following leaders of our profession for their contribution and advice in developing this years program: Ron Hopping, Jeff Jones, Clarke Newman, Stacie Virden, Peter Cass, Laurie Sorrenson, Kevin Katz, and Bj Avery. Special thanks to Clarke Newman for his research and invaluable opinions and to Jeff Jones for supplying the title of the course.
AGENDA I – TEXAS OPTOMETRY BOARD
Drug prescribing information ◦New classification of Schedule II Drugs
◦Reference for pain management drugs
◦Rules 280.5 and 280.10 listing types of drugs that may be prescribed Professional designation Importance of reading newsletter
Issues with EHRs
New Rule 277.10 – Remedial Plans
AGENDA II – SITUATION ETHICS
What are the challenges in ethical behavior
Examples of challenges in ethical behavior
2
New Drug Prescribing Information
Reclassification of Hydrocodone to Schedule II
Implementation Dates
October 6, 2014 – the actual adoption date
April 8, 2015 – the actual implementation date for the majority of the regulation changes
What this really means for Texas ODs
Optometrists in Texas cannot prescribe Schedule II narcotics and most all pharmacies are already using the adoption date as the implementation date. You must find alternate sources of pain management for your patients.
New Drug Prescribing Information
Misc. Issues
• To find or look up the classification of any controlled substance – reference www.dea.gov/druginfo/ds.shtml or www.deadiversion.usdoj.gov/schedules
• You can find a good deal of information on controlled substances, drug abuse and patient diversion tactics at http://www.pharmacy.texas.gov/sb144.asp
• To review the medications that you are allowed to prescribe under current Texas law, reference www.tob.state.tx.us, specifically Rules 280.5 and 280.10
Practice of License Holder
Professional Identification
The Statute: Section 351.362
Rules: Rule 279.10
Name(s) of the optometrists practicing at a location must be visible before entry into the reception area
Does not apply to doctors acting in a temporary capacity as defined in the rule as “no more than two consecutive months”
3
Practice of License Holder
Professional Identification
Legal identification per state law includes:
‐ Optometrist
‐ Doctor, Optometrist
‐ Doctor of Optometry
‐ O.D.
It is illegal to use any designation or advertising that could mislead the public into thinking you are any other health care practitioner other than an optometrist. This is not the Optometry Board’s law – this is a State law the Optometry Board must uphold. www.statutes.legis.state.tx.us/Docs/OC/htm/OC.104.htm
Texas Optometry Board Newsletter
The Optometry Board releases a newsletter once a year to all licensees. The newsletter identifies issues the Board feels are important to all practicing optometrists as well as explanations of all new Rules passed since the last newsletter.
You are legally obligated to stay abreast of and follow the law. “Ignorance” is not an excuse.
The newsletter is the easiest way to keep up with any new laws or rules and you are encouraged to read it “cover to cover”. If you are not receiving the newsletter, contact the Optometry Board.
Texas Optometry Board 512‐305‐8500
Electronic Medical Records
This is really easy folks. You cannot put statements into a record that do not accurately reflect the services you provided on that date of service.
Since wellness or routine care examinations can often reveal very little to no change from visit to visit, it is imperative your documentation, that will often look very similar year to year, be representative of the care delivered during that date of service.
Additional documentation such as review of history statements and/or attestation statements are a good means of making it clear your patient’s records are completely accurate and truthful (remember, most all EHRs have an internal audit feature that tracks the time and date of every entry!)
4
Examination and Medical Records All optometrists are encouraged to review the examination requirements found under Rule 277.7 that apply to the initial evaluation of a patient where an ophthalmic prescription is generated.
(1) An accurate identification of the patient;
(2) The date of the examination;
(3) The name of the optometrist or therapeutic optometrist conducting the examination;
(4) Past and present medical history, including complaint presented at visit;
(5) A numerical value of the monocular uncorrected or monocular corrected visual acuity in a standard acceptable format;
(6) The results of a biomicroscopic examination of the lids, cornea, and sclera;
Examination and Medical Records
(7) The results of the internal examination of the media and fundus, including the optic nerve and macula, all recorded individually;
(8) The results of a retinoscopy. A tape from an automatic refractor is acceptable;
(9) The subjective findings of the examination. A tape from a computer assisted refractor/photometer is acceptable if the instrument is being used to obtain subjective findings;
(10) The results of an assessment of binocular function, including the test used and the numerical endpoint value;
(11) The amplitude or range of accommodation expressed in numerical endpoint value including the test used in the examination;
(12) A tonometry reading including the type of instrument used in the examination; and
(13) Angle of vision: the extent of the patient's field to the left and right. he initial evaluation of a patient where an ophthalmic prescription is generated
Documentation Notes
Be aware that the Board Rules require that the examining optometrist PERSONALLY make and record the examination elements listed in orange (biomicroscopy, internal evaluation, subjective refraction)
Optometrists should also be aware that, although not a requirement of the Texas Optometry Board, the rule that the attending physician personally “make” the patient’s HPI is commonly cited, while the rest of the history may be delegated to an assistant/technician as long as the it is clear the physician has reviewed the information
5
NEW Rule 277.10 – Remedial Plans
This Rule gives the Board the authority to resolve typically more minor violations by mutual agreement to a remedial plan
If the licensee completes the requirements of the remedial plan, the violation is removed from the licensee’s record two years after completion of the remedial plan and is not reported to the national physician data bank
Remedial plans may be issued a maximum of once every two years
Remedial plans may be initiated by the Executive Director of Investigative Committee but must be approved by vote of the Board
Remedial plans may include a $1,000 administrative fee
And now…
Situation Ethics
Are Ethics a Real Issue?
We all face “ethical” decisions every day – it’s not limited to what most would consider as lying, immorality, religious beliefs or generally being a “good or bad person”
Ethical decisions can range from something terrible like deciding to rob a bank to something seemingly benign like not handing out bonuses to your staff because you really want to buy a new car
Our decisions are influenced by a host of internal and external influences
Not all decisions have a “right” answer – many are “shades of gray” (thanks Jeff!)
Much of the information in the next few slides can be found in the excellent reference [email protected]
6
“Ethics Unwrapped” identifies 22 moral standards that define how we make decisions. The next slides review eight standards considered most applicable to doctors.
Moral Standards
Role Morality
Actions or decisions are justified because of the unique role we play (as doctors) in or because we separate our personal beliefs from our work beliefs. EX: Selling patient ocular supplements when you wouldn’t take them yourself
Conflict of Interest
Actions or decisions are influenced by professional or economic interests
EX: “Stretching” medical necessity (is that specular microscopy REALLY necessary even though it will add to the month’s bottom line)
Moral Standards
Ethical Fading
“What was I thinking?” Decisions are based more on an emotional response than a rational response (“moral disengagement”)
EX: Insider trading with a pharmaceutical company
Incentive Gaming
Decisions or actions influenced by potential incentives, usually monetary.
EX: Incentive bonus systems – employed doctors and/or staff
(NOTE: Unwrapped authors define the new American Dream as “minimal effort for maximum gain”)
7
Moral Standards
Incrementalism
No one wakes up one day and decides to lose their morality. It is almost always a progressive lowering of the ethical bar, often based on prior success with lower standards.
EX: Stretching medical necessity progresses to billing fraud
Moral Equilibrium
Also called “moral licensing” – keeping score on our good behavior allows us to justify a certain degree of behavior we otherwise would not consider acceptable
EX: Indigent care efforts make it reasonable to overbill patients with insurance
Moral Standards
Moral Imagination
Success defined by many as winning. In the movie “Margin Call”, Jeremy Irons says “there are only three ways to win – be first, be smarter or cheat.” When winning rules our lives, our emotional barometer can lead our imagination to find ways to cheat and consider it part of doing business.
EX: Embezzlement
Moral Myopia
Possibly the most common and deadly – it is the “everyone is doing it” scenario. Blurring the right behavior is often fueled by potential for financial gain.
EX: The classic scenario of “run this test – you’ll get paid” forgetting the rule of medical necessity
Again, we must emphasize that not all seemingly straight forward “ethical” decisions are always so clear cut. While some actions are obviously unethical (billing for services not rendered) others can be “shades of gray” (individual decisions regarding medical necessity of care).
With that in mind, let’s look at some “situations” and how they can often be difficult to address
8
Situation Ethics – Case One
A fifteen year old patient, cheerleader at her school, presents with an obvious chlamydial conjunctivitis (Effects, at a minimum, 4% of all females 14‐19 y/o. Gottlieb – Pediatrics 12/2009). Are you obligated to inform the minor’s parents of this diagnosis and are you required to report this STD to the health department?
The Legal Ins and Outs
In Texas, a minor may consent to treatment of STDs by a physician without parental consent. The attending physician has the authority to decide if the parents have rights to the medical records. (Texas Family Code Title2; Subtitle A; Chapter 32; Subchapter A; Sec. 32.003). The question is does this apply to an optometrist?
In Texas, the attending health care provider is required to report the diagnosis of all STDs to the Texas Department of State Health Services (www.dshs.state.tx.us). This DOES apply to an optometrist. NOTE: It is widely believed that STDs are significantly under reported!
The Ethical Dilemma
FACT: Treatment and education are essential
Can you just call it an infection and let it go at that?
Can you say you’re not sure of a positive diagnosis and just treat as an infection of “unknown or non‐confirmed etiology”?
How do you discuss the situation with the minor in private?
Can you just refer the condition out to someone else?
Is it better to not report and break the law or report and potentially cause real problems for your patient?
9
So Who Can Get Me?
 The Texas Optometry Board
 The Texas Department of State Health Services
 The minor (the consent issue could be problematic and make it necessary to refer a minor wanting to consent to treatment to a physician as defined by Texas law)
 Yourself – remember your Oath?
“I WILL advise my patients fully and honestly of all which may serve to restore, maintain or enhance their vision and general health.”
Situation Ethics – Case Two
One of your highly valued employees is pregnant. She is conducting herself in a manner you feel is detrimental to her health and the baby’s health – smoking, gaining too much weight, drinking heavily on the weekends. What would you do?
There is no legal requirement or authority on your part. The controlling Texas case on this subject is Collins vs TX, (TX Court of Appeals, 1994). Legally, there must be clear and convincing evidence of mental illness or intent to harm before a woman may be committed to care against her will (FYI – Collins was using cocaine during her pregnancy)
Firing the employee is very complicated. Texas is an employment at will state but this means little when it come to protected classes like pregnant employees. If the employee pushed for wrongful termination, the suit would be long, painful, expensive and with potential for significant penalty to the employer from an unpredictable jury.
10
The Ethical Dilemma
Do you have rights as an employer to protect your practice and your employee by counseling the employee on her actions in general and how they may effect her work performance (smoking, drinking, obesity)?
More importantly, do you have a duty as an individual, friend, counselor or humanitarian to discuss the situation with the woman?
So Who Can Get Me?
Your employee ‐ Equal Employment Opportunity Commission and hungry legal counsel will be happy to assist with wrongful termination, gender discrimination, pregnancy discrimination (Pregnancy Discrimination Act of 2014)
Yourself – your duty of care obligations as a health care provider and humanitarian Situation Ethics – Case Three
A parent brings a child in for an examination. The parent is obviously intoxicated and in no condition to drive. What should you do?
11
In Texas, this is a no‐brainer. See Texas Child Endangerment – Drunk Driving Protection Act. The Act provides a separate mechanism for charging and punishing a person who drives while impaired with a passenger under the age of 15. The statute’s penalties are more severe than Texas’ traditional DWI penalties. The Ethical Dilemma
Should you consider the significantly damaging effects conviction of the parent would bring?
Would providing transportation or a taxi home remove your obligations to report?
Should you consider the mental trauma the child will go through seeing their parent taken away in cuffs?
How can you be sure the parent meets the definition of legally intoxicated?
So Who Can Get Me?
The courts. Failure to report carries potential jail time of 30 days to 5 years and fines ranging from $300 to $10,000, or both.
The parent – if your assumptions are wrong!
Yourself – could you live with injury to a child that could have been avoided if you would have reported the potentially dangerous situation?
12
Situation Ethics – Case Four
One of your employees is strongly suspected of stealing from one or more of your other employees. You feel the only way to get to the bottom of this is make the suspect take a polygraph test. What can/should you do?
The Employee Polygraph Protection Act of 1988 prohibits employers from “requiring, requesting, suggesting or causing” an employee to take a polygraph test – with exceptions. One of the exceptions is investigation of a crime in your business. There are requirements and regulations involved in these exceptions, a lot of them.
You cannot take any action against an employee for refusal to take a polygraph test
The Ethical Dilemma
How sure are you? If you are that sure, would it be better to find other ways to terminate the employee?
Can you threaten to polygraph everyone in hope the perpetrator will confess or run? (remember – illegal to “suggest” the polygraph!)
Provide extra security for your employee’s personal items – like individual lockers http://www.lockers.com/products/extra‐wide‐standard‐metal‐locker‐double‐
tier‐3‐wide‐6‐feet‐high‐15‐inches‐deep
13
So Who Can Get Me?
The “suspect” – if you try to push illegal polygraph testing
The “suspect” – if you take actions related to their employment that you cannot prove
Your other employees – unlikely legal action but you have an obligation to protect them
Situation Ethics – Case Five
Your associate is making false claims to Medicare by up‐coding office visits and performing medically unnecessary tests. What should/can you do?
The False Claims Act (FCA) allows for treble damages (damages being the fraudulent claim amount) PLUS $11,000.00 fine PER CLAIM Fraud is no longer just criminal activity – FCA states that providers “should know” what is medically necessary and should know all billing, coding and reimbursement laws and regulations. Not knowing can now be considered synonymous with fraud.
The False Claims Act specifically states providers are obligated to self report erroneous billing practices, especially fraudulent activity – even if discovered during a self‐audit (new annual Federal requirement for MC/MD providers)
14
The Ethical Dilemma
“Self reporting” means you will, at a minimum, pay back the fraud or abuse claims. If the violation is excessive, the addition per claim fine is possible if not likely. This can also easily open the door for a full audit as well as reporting you to all other Federal agencies for potential investigation (all other payers, IRS, DEA, EEOC…you name it, it is “tattle time” in Washington)
These actions can obviously have significant financial impact on you, your practice and the livelihood of your employees.
So Who Can Get Me
EVERYONE – CMS to start with then the potential reverse funnel to all other payers, IRS, DEA, EEOC. These actions by the Feds are unlikely if you fess up. BUT THE POTENTIAL RAMIFICATIONS OF NON‐DISCLOSURE ARE SEVERE IF NOT FINANICALLY FATAL
Situation Ethics – Case Six
A patient comes in at 5:00 on Friday with symptoms of flashing lights for the last day. You have plans for the evening, the symptoms do not sound very severe so you conduct a decent but not dilated retinal evaluation using your OptoMap but find nothing. You tell the patient to return in a month. Two weeks later you see them at the mall and they tell you they just had retinal detachment surgery. What would you do?
15
Dilated retinal evaluations, especially with symptoms of potential retinal disease present, is a standard of care issue no matter what time of day (See AAO Preferred Practice Pattern “Posterior Vitreous Detachment, Retinal Breaks and Lattice Degeneration” and AOA Optometric Clinical Practice Guideline “Retinal Detachment and Related Peripheral Vitreoretinal Disease”)
OptoMaps are wonderful but are not a legal substitute for a dilated retinal evaluation (Texas Optometry Board Rule 279.3 (a)(1)(B)
The Ethical Dilemma
Whether the patient actually had a retinal break at the time you evaluated them or not, your care was sub‐standard. The only issue remaining is patient management. Suggestions include:
Do not deny or admit to anything
Show great concern and compassion
Isolate but do not alter the medical record in any way
So Who Can Get Me
The patient – this would be a clear case of negligent care. No one could prove there was a retinal break when you examined the patient but they can easily prove you did not follow standard of care
Yourself – remember the Oath?
With full deliberation I freely and solemnly pledge that: I will practice the art and science of optometry faithfully and conscientiously, and to the fullest scope of my competence…
I WILL strive continuously to broaden my knowledge and skills so that my patients may benefit from all new and efficacious means to enhance the care of human vision
16
Situation Ethics – Case Seven
You diagnose a new patient as a significant glaucoma suspect and suggest additional testing. Your patient refuses to proceed with anything their vision insurance doesn’t cover and will not give you any medical insurance information. What would you do?
“Informed Consent” is the responsibility of the doctor. “Informed refusal” is the right of the patient. Doctors are very unlikely to be held responsible for the medical consequences of informed refusal if the standards for informed consent are met
Sec. 351.360. PROFESSIONAL STANDARD OF THERAPEUTIC OPTOMETRIST.
A therapeutic optometrist, including an optometric glaucoma specialist, is subject to the same standard of professional care and judgment as a person practicing as an ophthalmologist under Subtitle B.
The Ethical Dilemma
There really isn’t one. You have three choices:
Provide comprehensive, documented informed consent – this must include documentation of the risks and potential complications of non‐compliance. Continue to follow up with the patient with your best medical recommendations. ATTEMPT TO PIN DOWN WHY YOU HAVE A CARE REFUSAL ISSUE AND SOLVE THAT PROBLEM
Give the patient the option of seeing another eye care provider
“Divorce” the patient – let’s talk about that concept
17
So Who Can Get Me
With proper informed consent, no one. Anyone can attempt to sue you for anything but proper documentation usually prevails. This applies to this patient, the abusive contact lens patient, the patient who won’t take their medication and the like.
Situation Ethics – Case Eight
You are fairly certain you have the flu and are running a fever. You also have a full schedule and are behind on your lab bills. What would you do?
Texas Optometry Act 351.454(a) ‐ “An optometrist or therapeutic optometrist may not practice optometry or therapeutic optometry while knowingly suffering from a contagious or infectious disease, as defined by the Texas Department of Health, if the disease is one that could reasonably be transmitted in the normal performance of optometry or therapeutic optometry.”
OSHA/CDC regulations prohibit health care workers with known contagious disease from treating patients if there is likelihood of disease transmission
18
The Ethical Dilemma
The responsibility of the world on your shoulders – practice bills to pay, staff members rely on you for income, new house needs new furniture
Do you really have a contagious disease? Are you just convincing yourself it’s just s sinus infection? So Who Can Get Me
Honestly, more people than you think. A patient or employee COULD file a complaint against you with CDC or OSHJA – both really bad things
And remember show and tell?
This is not to be fooled with. If you have a contagious disease that could be communicated to another person through the normal activity of your business, stay home till you are well
Thank you for your attention and have a great 2015
[email protected]
www.tob.state.tx.us
19