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Outline
I.
Defining Dry Eye
A. NEI Dry Eye Workshop
B. CANDEES
C. Symptomology
II.
Case History
A. Identifying patients at risk
1. gender
2. age
3. systemic conditions
4. medications
5. allergies
6. contact lens wear
7. environment (occupation/sports/hobbies)
B. Questionnaires
III.
Tear Tests
A. Tear Quantity
1. 1. Meniscus Evaluation
2. Schirmer Test (I & II)
3. Cotton Thread Test
B. Tear Distribution/Flow
1. blink (rate, completeness)
2. lid margin (uniformity, scarring)
3. meniscus (presence, uniformity, viscosity)
C. Tear Stability/Quality
1. Reflex
2. Debris
3. Viscosity
4. Lipid layer
5. Meibomian glands (secretions, frothing, lid margins)
6. Ophthalmic dyes (sodium fluorescein, rose bengal, lissamine green)
7. Tear Break Up Time (TBUT)
a. barrier filter
b. full beam method (FBM) vs scanning method (SBM)
c. ethnic diversity
8. Dry eye test (DET)
9. Tear Thinning Time (TTT)
10. Non-invasive Break up Time (NIBUT) (Tearscope, grid)
11. Lid Wiper epitheliopathy (LWE)
D. Tear Outflow
1. Lid Apposition
2. Punctum
3. Tear Meniscus
4. Jones Test (1 & 2)
IV.
Documentation
A. Grading Scales (CCLRU, Efron)
V.
Does your patient have dry eye ?
A. Evaporative vs Tear deficient dry eye
B. Establishing severity
VI.
Sjogren’s Syndrome (SS)
A. Description of disease : An autoimmune disorder with hallmark clinical
presentation of dry eyes and dry mouth.
B. Diagnosis
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1. history
2. dry eye signs: Schirmer, stains
3. dry mouth signs: spit into cup
4. blood work: anti-Ro, anti-La
C. Epidemiology: female 90%, two main onset ages: 20-40, then > 60 yr
D. From an Optometric Point of View :
These patients present as contact lens failures or patients with sore and
uncomfortable eyes. Do not dismiss these complaints without a full workup.
Many Sjogren’s patients tell stories of attending multiple practitioners’ offices
before being diagnosed.
VII.
Pathophysiology of Sjogren’s
The initial stimulation to inflammation is not known. Retroviruses and EpsteinBarr viruses have been implicated.
The lacrimal and salivary glands are infiltrated by T cells. These form clusters that
on histology appear as focal sites. The focus score is used to diagnose the
disease.
The glands begin to secrete less and less. Part of the reason is the death of the
acinar cells but there are many apparently healthy acinar cells within the gland
that do not secrete. The reasons for this breakdown in function are not well
understood.
The lack of tear film on the ocular surface causes friction and damage to cells
seen as staining.
The lacrimal gland begins to create cytokines that flow to the ocular surface and
create part of the inflammatory response. This further causes a breakdown in
cellular function.
The lacrimal and salivary glands also create antinuclear antibodies named Ro and
La and these are secreted into the blood stream. They serve as markers for the
disease. These markers can also be seen in other autoimmune diseases such as
lupus.
VIII.
Clinical Work Up of Sjogren’s
A. History: Any dry eye questionnaire but include any history of dry mouth and
autoimmune disease.
B. Ocular tests: Schirmer 1, fluorescein staining of cornea, rose bengal or
lissamine green staining of bulbar conjunctiva, assessment of meibomian
glands.
C. Mouth testing: Observation of caries, tooth loss, dry tongue and gums, spit
into cup for 5 minutes.
D. Blood work: test for anti-Ro and anti-La, ANA, R
E. Minor salivary gland biopsy
IX.
Diagnosis of Sjogren’s
A. Dry eye symptoms for 3 months or more
B. Schirmer less than 5 mm in 5 minutes
C. Staining scores of 4/9 or greater
D. Less than 1 mm per minute of salivary flow
E. Anti-Ro and Anti-La markers in blood
F. Determine whether primary or secondary
X.
Management
A. drops and ointments
B. lid hygiene
C. water, fluoride rinses, sugar free gum
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D. rheumatological followup re : risk of lymphoma
E. moisture seekers newsletter
XI.
XII.
Conclusion / Closing remarks
References
Korb et al. The Tear Film : Structure, function and clinical examination,
Butterworth-Heinemann 2002
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