Transcript Slide 1

Interactive Grand Rounds
Blair Lonsberry, MS, OD, MEd., FAAO
Diplomate, American Board of Optometry
Clinic Director and Professor
Pacific University College of Optometry
[email protected]
Disclosures and Special Request
Paid consultant for:
• Alcon Pharmaceuticals, Bausch and Lomb, Carl Zeiss
Meditec, NiCox, Sucampo
Special Request:
Interactive remotes don’t work on your TV, so please don’t
take them home! 
Commitment to change:
- write down three things that you “learned” from this
presentation that you can incorporate into your practice
to improve patient care
CASE 1
Case History
• 38 black male, complaining that the vision in
his right eye is blurry.
– Got the current Rx 3 weeks previously, and
started out good but in last couple of days
OD vision has become blurry
• Medical Hx: no current health concerns and
no medications
Entrance Skills
 Va’s: OD: 6/7.5 (20/25), OS: 6/6 (20/20)
 Pupils: PERRL
 CVF: full to finger count
 EOM’s: FROM
 Amsler: central metamorphopsia OD
 HVF: 10-2 (see VF)
Which of the following OCT’s goes with
this patient?
1
2
3
4
CASE 2
Case
• 55 yr white female complains of fluctuating
vision
– Worse at near
– Spends 8-10 hours/day on the computer
• Medical Hx:
– Hypertension for 10 years
– Joint pain
• Medications:
– HCTZ for HTN
– Celebrex for her joint pain
Exam Data
• VA (corrected):
– 6/7.5 (20/25) OD, OS
•
•
•
•
PERRL
EOM’s: FROM
CVF: FTFC
SLE:
– TBUT 5 sec OD, OS
– Positive NaFl staining and
Lissamine green staining of conj
and cornea
– Decreased tear prism
Additional Testing/Questions
• Schirmer: < 5 mm of wetting in 5 minutes OD,
OS
• RF and ANA: normal for patients age
• SS-A: 2.0 (normal < 1.0), SS-B: 1.9 (normal
<1.0)
• Additional symptoms reported:
– Patient experiences dry mouth and taking Salagen
• Diagnosis: Sjogren’s Syndrome
Differential Diagnosis of Dry Eye
Signs and Symptoms of Dry Eye
Signs:
– Ocular Surface Damage
•
•
Corneal Staining (Fluorescein and/or Rose
Bengal)
Conjunctival Staining (Lissamine Green )
– Decreased Tear Quantity
•
•
•
Schirmer Score
Phenol Red Thread Test
Tear Meniscus Height
– Decreased Tear Quality
•
•
Tear Break Up Time (TBUT)
Tear Osmolarity
Symptoms:
–
–
–
–
–
–
Grittiness
Burning
Irritation
Stringy discharge
Blurring of vision
Ocular Surface Disease Index (OSDI)
Treatment
• We initiated:
– Omega-3 supplements (3-4 grams per day)
– Recommended warm compresses and lid washes qhs
– Testosterone cream 3% applied to upper lid bid
• Patient had significant improvement in symptoms with the use of the
topical testosterone cream.
– However, she was still symptomatic at the end of the day and she
still had significant staining on her cornea and conjunctiva
– Initiated FML tid for 1 month, restasis bid after 2 weeks
• 2 months later patient reported further improvement in her
symptoms
• No conjunctival staining was noted and only slight SPK
• Schirmer values improved to OD: 9 mm, OS: 10 mm
Transdermal Testosterone Cream
• Recent studies suggest that androgen deficiency
may be the main cause of the meibomian gland
dysfunction, tear-film instability and evaporative
dry eye seen in Sjogren patients
• Transdermal testosterone promotes increased tear
production and meibomian gland secretion,
thereby reducing dry eye symptoms (Dr. Charles
Connor).
• arGentis and Allergan have conducted trials to see
if topical androgens are effective in treating dry eye
SJOGREN’S SYNDROME:
OLD/NEW CLASSIFICATION
• Old:
– 1o Sjogrens: occurs when sicca complex manifests by
itself
• no systemic disease present
– 2o Sjogrens: occurs in association with collagen
vascular disease such as
• RA and SLE
• significant ocular/systemic manifestations
• New:
– The diagnosis of SS should be given to all who fulfill
the new criteria while also diagnosing any concurrent
organ-specific or multiorgan autoimmune diseases,
without distinguishing as primary or secondary.
Diagnosis: New Criteria
•
•
Sjogren’s International Collaborative Clinical Alliance
(SICCA) was funded by the National Institutes of Health to
develop new classification criteria for SS
New diagnostic criteria requires at least 2 of the following 3:
– 1) positive serum anti-SSA and/or anti-SSB or (positive
rheumatoid factor and antinuclear antibody titer
>1:320),
– 2) ocular staining score >3, or
– 3) presence of focal lymphocytic sialadenitis with a focus
score >1 focus/4 mm2 in labial salivary gland biopsy
samples
Ocular Surface Score (OSS)
• The ocular surface score (OSS) is the sum of:
– 0-6 score for fluorescein staining of the
cornea and
– 0-3 score for lissamine green staining of both
the nasal and temporal bulbar conjunctiva,
– yielding a total score ranging from 0-12.
Antibodies to SS-A and SS-B
• Sjogren’s syndrome A and B
• Typically tested by ELISA and immunoblot
• Associated Conditions:
– Uncommon in the normal population and in
patients with rheumatic diseases other than
Sjogren’s syndrome and SLE
– Present in 75% of patients with “primart”
Sjogren’s but only 10-15% of patients with
RA and secondary Sjogren’s syndrome
Antibodies to SS-A and SS-B
• Indications:
– Should be measured in patients with a clinical
suspicion of Sjogren’s or SLE
• Interpretation:
– Presence of AB’s is a strong argument for the
diagnosis of Sjogren’s Syndrome in a patient
with sicca syndrome
Dry Eye and Lid Disease?
• It is estimated that 67-75% of patients who have
dry eye have some form of lid disease
– it is often the most overlooked cause for dry eye
symptoms
• Important to address the lids in any treatment
plans for patients with dry eye
QUICKIE
CHRPE vs Nevus
25
Nevi Trivia
• 31% of choroidal nevi show slight enlargement
over time without the transformation to a
melanoma (Ophthalmology 2011)
• The prevalence of choroidal nevi in the white U.S.
population ranges from 4.6% to 7.9%
– If it is assumed that all choroidal melanomas arise from
preexisting nevi, then the published data suggest a low rate
(1/8845) of malignant transformation of a choroidal nevus in the
U.S. white population. (Ophthalmology 2005)
• Choroidal melanoma risk for metastasis, ranging
from 16% to 53% (at 5 years of follow-up)
depending on the size of the tumor at the time of
diagnosis. (Arch Ophthalmol 1992)
Nevi Trivia
• Studies suggest that the presence of orange pigment is
significantly correlated with the risk of subsequent growth
– when orange pigment is difficult to clinically discern
(especially with the natural coloration of the fundus and
in amelanotic nevi), FAF offers the best currently
available method to enhance its visibility. (Optometry
2009)
• Aggressive surveillance for survivors of ocular melanoma
appears to carry a relatively high risk of secondary cancers
from the radiation exposure, particularly for young women.
(JAMA Ophthalmology 2013).
TFSOM—“To Find Small Ocular
Melanoma”
Thickness: lesions >2mm
Fluid: any subretinal fluid (suggestive of serous retinal
detachment)
Symptoms: photopsia, vision loss
Orange pigment overlying the lesion
Margin touching optic nerve head
• None of these factors = 3% risk of a nevus converting to
melanoma in five years.
One of these factors = 8% risk of conversion in five years.
Two or more factors = 50% risk of conversion in five years.
For any changes noted during the course of follow-up, refer
the patient to a retinal practice or an ocular oncology
service.
Case
• 65 yr old white male
– Notices spot in vision in his left
eye
– Diabetes for 15 years
• Vision:6/6 (20/20) and 6/12 (20/40)
• Dilated exam:
– Large lesion noted in left eye (not
noted in exam 6 months
previously
– See photo
Ocular Tumors
Astrocytic Hamartoma
Retinoblastoma
Amelanotic Melanoma
Metastatic Choroidal Tumor
Choroidal Melanoma Metastases
• 80 to 90% of metastases from uveal
melanoma occurred in the liver, less common
sites being the skin and lung.
– Gragoudas ES, Seddon JM, Egan KM, et al. Longterm results of proton beam irradiated uveal
melanomas. Ophthalmology. 1987;94:349–53.
CASE 3
Case
• 23 WM
– Eye pain OD
– Severe, started 2 days ago
– Photophobia and redness
• POHx:
– Had similar problem and was given drops
and felt better
• PMHx:
– Told to get back into shape and to reduce
stress
• Meds:
– Ibuprofen for lower back pain
Assessment
• VA:
• 6/6 (20/20)-,
• 6/6 (20/20)+
• Entrance skills
unremarkable
• SLE:
– OD:
•
•
•
•
2+ injection,
2+ cell,
Mild flare,
Fine deposits
– IOP: 18, 14 mm HG
• DFE: unremarkable
Uveitis
• Uveitis frequently is nonspecific
but can be associated with:
– systemic disease,
– occur following trauma, or
– be the result of a primary
ocular disorder such as:
• Fuchs's heterochromic
iridocyclitis or
• glaucomatocyclitic crisis (ie,
Possner-Schlossman
syndrome)
Helpful Mnemonic
• Mnemonic for acute forms of nongranulomatous uveitis: BLAIR G
– B: Behcet’s disease
– L: Lyme disease
– A: Ankylosing spondilitis
– I: Irritable bowel syndrome (Crohn’s)
– R: Reactive arthritis
– G: Glaucomatocyclitic crisis
Uveitis: Clinical Features
• The clinical features of anterior uveitis are
readily recognizable
– complaints of:
• photophobia,
• pain,
• blurred or variable vision
• A change in the blood-aqueous barrier
results in the liberation of protein and
cellular matter into the anterior chamber
and the vitreous.
Uveitis: Clinical Findings
• Clinical findings of:
– circumlimbal hyperemia,
– cells and flare in the
aqueous and anterior
vitreous, and
– keratic and trabecular
precipitates
Uveitis: Treatment
– “Classical treatment”:
• Pred forte: every 1-2 hours, ensure
taper
–Pred forte: prednisolone acetate
formulation which allows
penetration through cornea to
anterior chamber
– Newer treatment option:
• Durezol
Treatment Options
• Durezol:
– Difluprednate
• only difluorinated steroid
– Steroid emulsion
– BAK free
– Increased “potency” so dosing needs to be less
than “classical treatment” with Pred Forte
• rough recommendation is 1/2 dosing of
Pred Forte
Cycloplegics
• Common cycloplegic agents include:
– cyclopentolate 1-2% tid for mild-tomoderate,
– homatropine 5% BID
– scopolamine 0.25%
– atropine 1% bid-tid for moderate-to-severe
inflammation
• most common is the use of Homatropine 5%
bid
• be careful using atropine as there is potential
for severe systemic side effects
– also makes the iris essentially immobile
Cycloplegics
• Cycloplegia:
– used for reduction of pain,
– break/prevent the formation of
posterior synechiae
– also functions in the reduction of
inflammation
Treatment
• Topical administration is most common
though periocular injections and
systemic meds are useful for posterior
uveitis and difficult cases
• Dosing is dependent upon severity of the
inflammation
– typically you want to hit the uveitis hard and fast!
• E.g 1 gtt q 2hrs until the inflammation is gone!
• If you have a minimal anterior chamber reaction
then steroid may not be necessary at all
Treatment
• NOTE: it is crucial to taper your
steroid treatment!
– You will have a rebound inflammation if you
simply remove your patient from their
steroids…
– The taper will be dependent upon how long
you have had them on the steroid to get rid of
the inflammation!
– Typically, a slow taper is better in order to
prevent rebound inflammation
– If the patient has been on the steroid for less
than a week a faster taper can be considered.
Treatment
• NSAIDs:
– do not play an important role in
the treatment of an acute uveitis
Treatment: Additional Therapies
• Immunosuppressive agents (cytotoxic)
– reserved for sight-threatening uveitis that
have not responded to conventional
treatment
• e.g. cyclophosphamide
• Antimetabolites (e.g. methotrexate) have
been found useful in JIA related iridocyclitis
and scleromalacia
• Cyclosporin has a very specific effect on the
immune system and has been found useful in
posterior and intermediate uveitis
Follow-up
• Every 1-7 days in acute phase
depending upon severity and every
1-6 months when stable.
• On each f/u visit the AC reaction
and IOP should be evaluated
– DFE should be performed for flareups, when VA affected, or every 3-6
months.
Follow Up
• If AC reaction improving, then
steroid drops can be slowly tapered.
– cycloplegia can also be tapered as the
AC reaction improves.
– slow taper recommended for chronic
granulomatous uveitis.
CASE 4
Case
• 65 year old Caucasian patient presents with
sudden onset loss/blurring of vision in the
right eye
• PMHx: HTN for 15 years, takes “water pill”
• VA’s: 6/18 (20/60) OD, 6/7.5 (20/25) OS
• Pupils: PERRL –APD
• CVF: Inferior defect right eye, no defects
noted in the left eye
Vision Loss Without Pain:
Diabetes/Diabetic Retinopathy
 Microvascular complications resulting in
capillary closure & abnormal permeability
 S&S include;
◦ blurring of vision (maculopathy and refractive
error shifts),
◦ sudden drop in vision (vitreous heme),
◦ dot and blot hemes,
◦ exudate,
◦ cotton wool spots,
◦ neovascularization (iris, retina and disc)
VEGF and DME
Aug. 10, 2012: FDA approves Lucentis to treat
diabetic macular edema
• The drug’s safety and effectiveness to treat DME
were established in two clinical studies involving
759 patients who were treated and followed for
three years.
– patients were randomly assigned to receive monthly
injections of Lucentis at 0.3 milligrams (mg) or 0.5 mg,
or no injections during the first 24 months of the studies
– after 24 months, all patients received monthly Lucentis
either at 0.3 mg or 0.5 mg
• Results:
– 34-45% of those treated with monthly Lucentis 0.3 mg
gained at least three lines of vision compared with 1218% of those who did not receive an injection.
Vision Loss Without Pain:
Vein Occlusion
• Associated with:
–
–
–
–
hypertension,
coronary artery disease,
DM and
peripheral vascular disease.
• Usually seen in elderly patients (60-70), slight
male and hyperopic predilection.
• Second most common vascular disease after
diabetic retinopathy.
Branch Retinal Vein Occlusion:
Signs/Symptoms
 BRVO: sudden, painless,
visual field defect.
◦ patients may have normal
vision.
◦ quadrantic VF defect,
◦ dilated tortuous retinal
veins with superficial
hemes and CWS
◦ typically occurs at A/V
crossing (sup/temp)
BRVO
 BRVO more common than CRVO and has more
favorable prognosis
◦ Overall 50-60% of BRVO patients will maintain VA of
6/12 (20/40) or better
 Visual loss results from:
◦
◦
◦
◦
◦
◦
◦
Macular edema
Foveal hemorrhage
Vitreous heme
Epiretinal membrane
RD
Macular ischemia
Neovascularization complications
Study Design (n=397) BRVO
BRAnch retinal Vein Occlusion study safety/efficacy
Macular Edema Secondary to BRVO
1:1:1 Randomization
Sham
(n=132)
Ranibizumab
0.3 mg
(n=134)
Ranibizumab
0.5 mg
(n=131)
Monthly Injections (last at 5M)
Rescue Laser (if eligible beginning at Month 3)
12M
PRN ranibizumab for all patients
Rescue Laser (if eligible beginning at Month 9)
Ranibizumab
0.5 mg
Ranibizumab
0.3 mg
Ranibizumab
0.5 mg
Month 6
Primary
Endpoint
Mean Change from Baseline BCVA
BRVO
Mean Change from Baseline
BCVA (ETDRS Letters)
Sham/0.5 mg (n=132)
0.3 mg Ranibizumab (n=134)
0.5 mg Ranibizumab (n=131)
+18.3*
20
+18.3
18
+16.4
16
14
+16.6*
+11.6
+12.1
12
10
+10.2
8
+7.3
6
+3.1
4
2
0
07
2
4
Day 0–Month 5
Monthly Treatment
6
Month
8
10
Months 6–11
PRN Treatment
The gain of additional 3 lines occurred at a rate of 61% of 0.5 AVT grp, 55% for
0.3 AVT & 29% placebo
12
Central Retinal Vein Occlusion:
Signs/Symptoms
CRVO: thrombus occurring at
lamina is classical theory but
new evidence indicates that the
occlusion is typically in the optic
nerve posterior to the lamina
cribrosa
◦ decreased VA ranging from
near normal to hand motion
with majority 6/60 (20/200)
range
◦ dilated tortuous vessels,
with numerous retinal
hemes and CWS
Central Retinal Vein Occlusion
• Visual morbidity and blindness are primarily from:
– persistent macular edema,
– macular ischemia and
– neovascular glaucoma
• CRVO’s can be ischemic or non.
– Classical definition of ischemic is 10-disc area of nonperfusion found on angiography
– RAPD and ERG maybe better predictor
– VA’s typically worse in ischemic
– Increased number of cotton wool spots with decreased VA
maybe predictive
Central Retinal Vein Occlusion
 Ischemic CRVO may lead to iris
neovascularization and neovascular
glaucoma
◦ Estimated apprx 20% of CRVO’s are ischemic with
45% of those developing neo
 Regular examinations (1-2 wks) to monitor
for ischemia or neo development
◦ should include gonio as angle neo can precede iris
rubeosis
Study Design CRUISE (n=392)
CRVO
Central Retinal vein occlUsIon Study: Efficacy & safety
Macular Edema Secondary to CRVO
1:1:1 Randomization
Sham
(n=130)
Ranibizumab
0.3 mg
(n=132)
Ranibizumab
0.5 mg
(n= 130)
Monthly Injections (last at 5M): 6M tx period
12M trial
PRN Lucentis available for for all patients: 6M tx period
0.5 mg
Ranibizumab
0.3 mg
Ranibizumab
0.5 mg
Month 6
Primary
Endpoint
Mean Change from Baseline BCVA
CRVO
0.3 mg Ranibizumab (n=132)
Mean Change from Baseline BCVA
(ETDRS Letters)
Sham/0.5 mg (n=130)
0.5 mg Ranibizumab (n=130)
18
16
+14.9*
+13.9
+13.9
14
12
+12.7*
10
8
+7.3
6
4
+0.8
2
0
-2
07
2
4
Day 0–Month 5
Monthly Treatment
6
8
10
Months 6–11
PRN Treatment
12
Month
Pts with >/= 3 line improvement was noted in 48% of .5 AVT, 26 of .3 AVT & 17% of sham
Vision Loss Without Pain:
Artery Occlusion
• Primarily embolic in nature from cholesterol,
calcifications, plaques.
• Usually occurs in elderly associated with:
– hypertension (67%),
– carotid occlusive disease (25%),
– DM (33%) and
– cardiac valvular disease.
• Sudden loss of unilateral, painless vision
– defect dependent upon location of occlusion
Vision Loss Without Pain:
Artery Occlusion
• BRAO typically
located in
temporal retinal
bifurcations.
CRAO
• CRAO has profound vision
loss with history of
amaurosis fugax.
– Vision is usually CF
(count fingers) to LP
(light perception) with
positive APD.
– Diffuse retinal whitening
with arteriole
constriction, cherry red
macula.
Ophthalmic Emergency
 Treatment is controversial due to poor prognosis
and questionable benefit.
 Treat immediately before workup, if patient
presents within 24 hours of visual loss:
◦
◦
◦
◦
◦
Digital ocular massage,
systemic acetozolamide (500 mg IV or po),
topical ocular hypertensive drops (Iopidine, B-blocker),
anterior chamber paracentesis,
consider admission to hospital for carbogen Tx (high
carbon dioxide)
CASE 5
Case
• 30 WM presents with 2 weeks worsening vision OS
– Was seen by neurologist 2 years previously for flashes, head
CT was normal
– Flashes continued for the two years
– History of color blindness
– Patient presents with pressure behind the eye and tightness
with left eye movement for the past week
– No vision changes with activity or movement
– Denies history of trauma, redness, discharge or headache
• VA: 6/6 (20/20) and 6/9 (20/30)
• External exam reveals no ptosis or resistance to
retropulsion
Case
• PERRL with a left APD
• Hertel: Base of 102 and
measurements of 19 and 18
• EOM: FROM though notes
tight feeling in OS abduction
• IOP: 15 OU
• DFE: normal ONH
appearance and fundus
unremarkable
• HVF: inferior altitudinal
defect OS
Case
• One week f/u:
• Reports continued decreasing
vision OS
– Now 6/120 (20/400)
• Increased left APD
• Increased visual field defect
• ONH swelling OS
Question
Which of the following MRI scans goes with this
patient’s diagnosis?
1
2
3
4
Optic Neuritis
• Optic neuritis typically presents with a triad of
symptoms:
– loss of vision, dyschromatopsia and eye pain.
• The initial attack is unilateral in 70% of adult
patients and bilateral in 30%.
• Associated visual symptoms are reduced perception of
light intensity and Uhthoff's symptom (visual deficit
induced by exercise or increased body temperature)
• The mean age of onset of optic neuritis is in the third
decade of life
Optic Neuritis Treatment
• The ONTT showed that intravenous
methylprednisolone followed by oral
prednisone speeds the recovery of visual loss
• Oral prednisone was found to increase the risk
of recurrent optic neuritis.
– Thus, treatment with oral prednisone in standard
doses is no longer advised.
Case 6
Case History/Entrance Skills
•
•
•
•
•
•
•
31 YR HM
CC: referred from PCP for a possible uveitis
LEE: 3 years ago
PMHx: unremarkable
Meds: Omega-3 supplements
Entrance VA: 6/9 (20/30) OD, OS
Refraction:
– +0.75 -2.50 x 003 6/7.5+ (20/25+)
– +0.25 -2.75 x 004 6/7.5+ (20/25+)
• All other entrance skills unremarkable except for
difficulty doing confrontation visual fields
76
Health Assessment
• SLE:
– 1+ conjunctival injection in the right eye
– Anterior chamber: deep and quiet (no cells or
flare noted in either eye)
• IOP: 12 and 11 OD, OS
• DFE: see photos
77
OS
OD
78
OS
OD
79
OS
OD
80
81