HMCS Vancouver Pre-Deployment Brief - May 2024 (Web Version).pptx
Dry eye presentation latest-Dr Dildar Singh
1. Dry eye disease : A
review of diagnostic
approaches and
Treatments
Saudi journal of ophthalmology (2014)28,173-
181
HPuireLisne,MntDe,dP hBDy; S–aDmr.u eDlilCd.aYriuS,MinDg,hPhD
Moderator - Dr. K.Kanthamani
2. “Dry eye is a multifactorial disease of the tears and
ocular surface that results in symptoms of discomfort,
visual disturbance and tear film instability with potential
damage to the ocular surface. It is accompanied by
increased osmolarity of the tear film and inflammation of
the ocular surface”.
3. Dry eye is a disturbance of the lacrimal functional unit, an
integrated system that comprises of lacrimal glands, ocular
surfaces (conjunctiva, cornea, meibomian glands), lids and
sensory & motor nerves that connect them.
8. 1. Chronic meibomitis
2. Blepharitis
3. Debris in tear film
4. Chronic papillary conjunctivitis
5. Tear marginal meniscus < 0.3 mm
6. Interpalpebral hyperemia
7. Gland orifice metaplasia
SIGNS
9. - Although both ADDE and EDE present with similar signs of
reduced stability and increased tear film osmolarity.
- ADDE chiefly refers to a failure of lacrimal secretion and
EDE is due to excessive water loss from the exposed ocular
surface in the presence of normal lacrimal secretory
function.
10.
11. Diagnostic assessment
An ideal diagnostic method should be preferably non-invasive,
objective, specific, reproducible and sustainable in terms of
cost and time.
a) Subjective evaluation
b) Objective evaluation
12. Subjective evaluation :
• The symptoms and history of DE patients vary widely;
therefore, validated questionnaires have been developed to
ensure consistency in recording symptomatic information.
• Previously it was believed that DE can be diagnosed largely on
the basis of symptoms; however, recent studies have
questioned this opinion as there is often a lack of correlation
between the severity of the symptoms and signs of DE.
13. Objective evaluation :
a) tear film assessment
c) the Schirmer test as the most commonly used diagnostic
tests for initial assessment of dry eye.
d) Lacrimal river width
e) Tear ferning test
f) Lactoferrin contents
g) Tear penetration pressure test
14. SCHIRMER TEST
SCHIRMER'S TEST I
If wetting >10mm = normal eye
If wetting <3mm = very severe dry eye
If wetting 3-5 mm = severe dry eye
If wetting 5-10mm = moderate dry eye
If wetting is 10mm = mild dry eye
SCHIRMER'S TEST II
If Wetting<10mm -- >irratate the nasal
mucosa with cotton bud & note the wetting
after 2 min.
If no Wetting or <1mm Sjogren's
syndrome
If Wetting increases by 1mm Non-Sjogren's
syndrome
SCHIRMER'S TEST III – no diagnostic
15. LACRIMAL RIVER WIDTH TEAR FERN TEST
A drop of tear is collected from the
lower meniscus and dropped onto a
microscope slide and allowed to dry by
evaporation.
16. Apart from these traditional clinical tests, we will discuss
more about the less invasive evaluations based on the
recently developed technologies related to :
a) tear hyperosmolarity
b) tear film instability
c) inflammation.
17. Tear osmolarity
• Increase in tear osmolarity is common to all types of DE
• Normal Osmolarity value 305 mOsms/l
> 308 mOsms/l (mild DE)
>312 mOsms/l (moderate to severe DE)
18. Tear film osmolarity can be measured in three ways:
c) electrical conductivity or impedance
19. Assessment of tear stability
• Tear break-up time (TBUT), introduced by Norn , remains
the most frequently used diagnostic test to determine tear
film instability.
• Non-invasive tear break-up time (NIBUT) involves the
observation of an illuminated grid pattern reflected from
the anterior tear surface.
20. NIBUT can be measured by:
a) corneal topography
b) interferometry
c) aberrometry
d) functional visual acuity assessment
e) confocal microscopy
24. • Coloured fringes that arise from interference between
light reflected from the surface of the lipid layer and
from the interface between the lipid layer and the
aqueous layer of the tear film.
• used to observe the nature, thickness and rupture of
the lipid layer.
26. • non-invasive assessment of the visual disturbances
caused by higher order aberrations arising from tear
film instability and break-up.
• Aberrometry could be utilized for not only detecting
DE but also for monitoring the efficacy of
treatments.
27. D) Functional visual acuity
• measure of visual acuity during sustained eye
opening without blinking
• defined as the monocular recognition acuity at a
specific time point
• decreases significantly in both non-Sjögren’s
syndrome (NSS) and Sjögren’s syndrome (SS) dry eye
patients
28. Optical coherence tomography
• Anterior segment OCT can measure the tear film
thickness and tear meniscus parameters which indicate
total tear volume.
• lower tear meniscus height and radius were the best
indicators of DE with a cutoff meniscus height of 1.64 mm
and radius of 1.82 mm.
29. E) Non Contact Confocal Microscopy
• non-contact, tandem-scanning confocal microscope
demonstrating real-time images to observe the tear
film.
30. Evaluation of ocular surface and
inflammation
Confocal microscopy
Meibomian gland evaluation
Corneal and conjunctival
staining
Conjunctival impression cytology or brush
cytology
Other tests
31. 1) Confocal Microscopy
• Corneal in vivo confocal microscopy (IVCM) is a novel,
noninvasive, high-resolution tool that allows imaging the
cornea at the cellular level and provides images
comparable to histochemical methods and used for non-invasive
impression cytology in DE evaluation.
32. • IVCM enables the study of:-
a) corneal epithelium
b) corneal stroma and keratocytes
c) endothelial cells,
d) corneal nerves
e) corneal immune and
inflammatory cells
f) conjunctiva
g) meibomian glands
33. 2) Meibomian gland evaluation
• source of lipids in the lipid layer of the tear film
• MGD is the most common cause of evaporative dry eye
• Meibomian glands can be assessed by :-
a) slit lamp
b) Meiboscopy
c) Meibography
d) Meibometry
34. 3) Corneal and conjunctival staining
• Invasive procedure which enables the assessment of
ocular surface damage by instilling a dye:
a) sodium fluorescein
b) rose bengal
c) lissamine green
35. Sodium fluorescein
• A vital dye which has no intrinsic toxicity.
• Detects epithelial defects & irregularities.
• Filter paper strips or 0.25% - 2% solution.
• Sodium fluorescein emits green light(520nm) when
excited with with blue light (490nm).
36. Rose bengal
• Rose bengal is a vital stain taken up by dead and devitalised
epithelial cells.
• Also stains mucous threads, filaments & strands .
• Does not diffuse into the epithelial defects or penetrate
corneal stroma like fluorescein.
• It is toxic resulting in decreased cell vitality, motility & cell
death.
• Causes ocular discomfort –prior anaesthesia is needed.
Score 0 - absent
Score 1-just present
Score 2-moderate staining
Score 3-gross staining
37. • Dark green, water soluble
• Degenerated cells, mucus, dead cells
• Less irritating
Lissamine green
38. 4) Conjunctival impression cytology or brush cytology
• harvesting conjunctival epithelial,Goblet, and inflammatory
cells from the bulbar mucosa
• cytokines IL-1a, mature IL-1b, and IL-1Ra are found in a
significantly greater percentage of conjunctival cytology
specimens from eyes with SS
• dry eye group was found to have a significant difference in the
CD4/CD8 ratio
• Elevated matrix metalloproteinases levels in DE
40. • Artificial tears provide palliative relief to eye irritation in
patients with aqueous tear deficiency, but do not
prevent the underlying inflammation
• Mild-to-moderate DE disease- Combinations of
artificial tears, oral omega-3 essential fatty acid
supplements, mucin secretagogues,short-term steroids,
and daily cyclosporine A
41. Severe- autologous serum, oral tetracyclines, prosthetic
lens, and systemic immunesuppressants
Severe forms associated with systemic diseases- surgical
intervention, including tarsorrhaphy and amniotic
membrane transplant.
42. Additionally, a stepwise guide to approach the
best combination of medications to avoid
symptoms of DE was also recommended
Anti-inflammatory
treatments
Surgical treatment
Supplementary treatments
43. Anti-inflammatory treatments :
• Cyclosporine A Controls inflammation
Increasing tear secretion
Tear film stability
Restoring epithelial damage
Reducing disease recurrences
• Steroids Decreases inflammation
(corticosteroids ) Apoptosis of lymphocytes
44. • Hormonal therapy
(androgen and estrogen)
Increase tear production TBUT,
lipid layer thickness.
• Antibiotics
(azithromycin and tetracycline,
doxycycline, and minocycline)
Decrease ocular surface
inflammation,
Normalize lipid production by
the meibomian glands.
45. Supplementary treatments :
• Essential Fatty Acids (EFAs)
Omega-3 FAs Anti-inflammatory
Omega-6 FAs Proinflammatory.
Topical administration of resolvin E1, an omega-3 FA
derivative increased tear production, helped maintain ocular
surface integrity, decreased cyclooxygenase 2 expression
and decreased immune cell infiltration in experimental dry
eye.
46. • Nerve growth factor (NGF) Increase ocular surface
sensitivity,
Inhibit inflammatory reactions,
Regulate tear film production,
Reducing the apoptosis
of corneal epithelial cells
triggered by hyperosmolarity .
• Autologous serum Autologous and umbilical cord
serum contains substances
that support the proliferation,
differentiation, and maturation
of the normal ocular surface
epithelium and therefore, finds
application in the treatment of
severe DE.
• Acupuncture
47. Surgical treatment
• Punctal occlusion Reduces drainage, preserves natural
tears and prolongs the effect of
lubricants.
• Salivary gland procedures
• Subcutaneous abdominal artificial tear pump-reservoir
- treatment of severe dry eye.
48. • Understanding of the pathogenesis and specific cellular
responses involved in different forms of DE could result in the
development of other treatment strategies for a better
management and long lasting results.
• Development of additional treatment options in the form of
compounds targeting specific components would provide
hope for the millions of individuals who daily experience this
deleterious condition.