Dry eye

1. DRY EYE
DR K HARIPRIYA

2. Definition
 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. Tear film

4. Introduction
 Dry eye is recognized as a
disturbance of the Lacrimal Functional
Unit (LFU), an integrated system
comprising the lacrimal glands, ocular
surface (cornea, conjunctiva and
meibomian glands) and lids, and the
sensory and motor nerves that
connect them

5.  This functional unit controls the major
components of the tear film and
responds to environmental,
endocrinological
and cortical influences.
 Its overall function is to
-preserve the integrity of the tear film,
-transparency of the cornea,
-quality of the image projected onto the
retina

6.  Trigeminal sensory fibers arising from
the ocular surface run to the
superior salivary nucleus in the pons,
efferent fibers pass
nervus intermedius
pterygopalatine ganglion.
Here, postganglionic fibers arise, which
terminate in the lacrimal gland,
nasopharynx, and vessels of the orbit.

7.  Another neural pathway controls the
blink reflex, via trigeminal afferents
and the somatic efferent fibers of the
seventh cranial nerve.

9. SSWS

10. Effect of environment
 Milleu interior
Low blink rate ,aging
Wide lid aperture
Low androgen pool
Systemic drugs
 Milleu exteror
Low relative humidity
High wind velocity
Occupational environment

11. Aqueous Tear-Deficient Dry Eye
(Tear Deficient Dry Eye; Lacrimal
Tear Deficiency)
Sjogren syndrome:
 It is an exocrinopathy in which the
lacrimal and salivary glands are targeted
by an autoimmune process.
 The lacrimal and salivary glands are
infiltrated by activated T-cells, which
cause acinar and ductular cell death and
hyposecretion of the tears or saliva.
 Inflammatory activation within the
glands leads to the expression of
autoantigens at the surface of epithelial
cells

12. Sjogrens syndrome
 The precise triggers leading to
autoimmune acinar damage are not
known in full, but risk factors include
genetic profile, androgen status, and
exposure to environmental agents,
ranging from viral infections affecting
the lacrimal gland to polluted
environments.
 A nutritional deficiency in omega-3-
and
other unsaturated fatty acids has
been reported in patients with SS

13. Sjogrens syndrome
Two types
 Primary SS consists of the occurrence
of ADDE in combination with
symptoms
of dry mouth
 Secondary SS consists of the features
of primary SS together with the
features
of an overt autoimmune connective
disease, such as rheumatoid arthritis,

14. Non-Sjogren Syndrome Dry
Eye
Primary lacrimal gland deficiencies:
Age-related dry eye
Congenital alacrima
Familial dysautonomia

15. Age-related dry eye
 Ductal pathology
Peri ductal, inter acinar fibrosis
Paraductal blood vessel loss
Acinar atrophy
 Low grade dacryoadenitis

16. Congenital Alacrima
 rare cause of dry eye in youth.
 It is also part of certain syndromes,
triple A syndrome
 Protien ALLADIN

17. Familial dysautonomia
 Developmental , progressive neuronal
abnormality of the cervical
sympathetic and parasympathetic
innervations of the lacrimal gland and
a defective sensory innervation of the
ocular surface
 Generalized insensitivity to pain is
accompanied by a marked lack of both
emotional and reflex tearing,

18. NSDE
Secondary lacrimal gland deficiencies
 Lacrimal gland infiltration
 Sarcoidosis
 Lymphoma
 AIDS
 Lacrimal gland ablation
 Lacrimal gland denervation

19. NSDE
Obstruction of the lacrimal gland ducts:
 Trachoma
 Cicatricial pemphigoid and mucous
membrane pemphigoid
 Erythema multiforme
 Chemical and thermal burns

20. NSDE
Reflex hyposecretion
 Reflex sensory block
Contact lens wear
Diabetes
Neurotrophic keratitis
 Reflex motor block
Cranial nerve damage
Multiple neuromatosis
Exposure to systemic drugs

21. Evoperative dry eye
 Intrinsic causes
 MGD
 Disorders of lid aperture
 Low blink rate

22. Extrinsic causes:
 Occular surface disorders
Vitamin A Deficiency
Topical Drugs and Preservatives
Allergic conjunctivitis

24. Inspection
 Signs of associaed systemic diseases
 Indications of personnel habits
 Ocular disease(lid malposition)

25. Evaluation of tear film
 Tear meniscus height
 TBUT
 Meniscometry : Tear meniscus radius,
height and cross sectional area
1MM, CONVEX-NORMAL
<0.3 MM IS abnormal
 Tear film lipid layer interferometry
color comparison table
kinetic analysis

26. TESTS OF TEAR
PRODUCTION
SCHIRMER TEST
 BASIC
 SCHIRMER 1
 SCHIRMER 11
 Inference - > 15 mm - normal, 6 to 10
mm - borderline dry, < 6 mm -
impaired secretion.

27. Tear composition assays
 Tear Osmolarity

28.  Rose Bengal staining – The dye has
an affinity for dead or devitalized
epithelial cells and for areas devoid of
mucus.
 Van Bijsterveld scoring system –
divide the ocular surface into three
zones:
 • Nasal bulbar conjunctiva, Cornea
Temporal bulbar conjunctiva.
 Each zone is then given a score of ‘0’
(no stain) to ‘3’ (confluent stain).
Scores in each eye is totaled. A score
of 3.5 or greater indicates positive for
keratoconjunctivitis

29. Newer technologies
 MEIBO METRY
Casual Lipid level (expressed as
arbitrary optical density units) is
calculated as (C-B), where C is the
casual reading, B is the reading from
the untouched tape
 MEIBO GRAPHY /MEIBO SCOPY
Finoff transilluminator
Most reliable test in patients with
ectodermal dysplasia syndrome

30.  Brush Cytology Technique
1) squamous metaplasia,
2) detecting inflammatory cells
3) expression of several surface
markers on the ocular surface
epithelium
 Flow cytometry in impression cytology
HLA DR expression by epithelial cells,
gold standard for inflammatory
assesment

31.  Ferning Test (TFT )
TO DIAGNOSE Quality of tears (electrolyte
concentration), KCS, Hyperosmolarity
The patterns of crystallization (ferning) are
classified in 4 classes:
Type 1: uniform large arborization,
Type 2: ferning abundant but of smaller size;
Type 3: partially present incomplete ferning;
Type 4: no ferning.
Types 1 & 2 are reported to be normal and
Types 3 & 4 reported to be abnormal

32.  Fluorophotometry (Fluorimetry)
 Tear Function Index
TFI is the quotient of the Schirmer test
value and the Tear clearance rate
(TCR).
A TFI of less than 40 is 100% sensitive
for patients with SS dry eye

33. MANAGEMENT
 A. Tear supplementation: lubricants
 B. Tear Retention
 C. Tear stimulation: secretagogues
 D. Biological tear substitutes
 E. Anti-inflammatory therapy
 F. Essential fatty acids
 G. Environmental strategies

34. A. Tear supplementation:
lubricants
 Hypotonic or isotonic buffered solutions
containing electrolytes, surfactants, and
various types of viscosity agents.
 Ideal artificial lubricant should be
preservative-free, contain potassium,
bicarbonate, and other electrolytes and
have a polymeric system to increase its
retention time.
 Physical properties
Neutral to slightly alkaline pH.
Osmolarities 181 to 354 mOsm/L.

35. Tear supplementation:
lubricants
 Electrolytes
potassium, bicarbonate
 Osmolarity
 Viscosity agents: prolong ocular
surface contact, increasing the
duration of action and penetration of
the drug
 Eye ointments and gels

36. B. Tear Retention
1. Punctal Occlusion
Types
 absorbable and nonabsorbable. The former
are made of collagen or polymers and last for
variable periods of time (3 days-6 mnths).
 The nonabsorbable “permanent” plugs
include silicon plugs, consists of a surface
collar resting on the punctal opening, a neck,
and a wider base
 Herrick plug is shaped like a golf tee and is
designed to reside within the canaliculus.
 cylindrical Smart plug: expands and
increases in diameter in situ, due to
thermodynamic properties of its hydrophilic
acrylic composition.

37. Punctal Occlusion
Indications
patients who are symptomatic of dry
eyes have a Schirmer test (with
anesthesia) result less than 5 mm at 5
minutes, and show evidence of ocular
surface dye staining

38. Contra indications
 Allergy to the materials used in the
plugs to be implanted,
 punctal ectropion,
 pre-existing nasolacrimal duct
obstruction,
 clinical ocular surface inflammation,

39. Complications
 Extrusion
 Internal migration of a plug,
 Biofilm formation
 Infection
 pyogenic granuloma formation

40. Tear Retention
 Moiature chamber spectacles
 Contact lenses

41. Tear Stimulation:
Secretogogues
 Diquafosol
 Rebamipide
 Gefarnate
 Ecabet sodium

42. D. Biological Tear Substitutes
 Serum
 Salivary Gland Autotransplantation:
 Indicated only in end-stage dry eye
disease with an absolute aqueous tear
deficiency (Schirmer-test wetting of 1
mm or less), a conjunctivalized
surface epithelium
 persistent severe pain despite punctal
occlusion and at least hourly
application of unpreserved tear
substitutes.

43.  Due to the hypoosmolarity of saliva,
compared to tears, excessive salivary
tearing can induce a microcystic
corneal edema, which is temporary,
but can lead to epithelial defects.

44. E. Anti-Inflammatory Therapy
 1. Cyclosporine
 2. Corticosteroids
 3. Tetracyclines
 a. Properties of tetracyclines and their
derivatives
 1) Antibacterial properties
 2) Anti-inflammatory
 3) Anti-angiogenic properties

45.  Essential fatty acids
 Environmental strategies:
Use of room humidifiers
Avoid extreme/harsh environmental
conditions.

46. Treatment recommendations by
severity level
Level 1:
 Education and environmental/dietary
modifications
 Elimination of offending systemic medications
 Artificial tear substitutes, gels/ointments
 Eye lid therapy
Level 2:
 Anti-inflammatories
 Tetracyclines (for meibomianitis, rosacea)
 Punctal plugs ,Secretogogues
 Moisture chamber spectacles

47. Treatment recommendations by
severity level
Level 3:
 Serum
 Contact lenses
 Permanent punctal occlusion
Level 4:
 Systemic anti-inflammatory agents
 Surgery (lid surgery, tarsorrhaphy;
mucus
 membrane, salivary gland, amniotic
 membrane transplantation)

48. THANKYOU