WELCOME
DRY EYE
( Etiopathogenesis )
Chairman:
Prof. Md Abdul Quader
Professor and Head, Dept of Cornea, NIO&H.
&
Chairman, Academic Committee, NIO&H.
Moderator:
Dr. Tarzeen Khadiza Shuchi
Assistant Professor , Department of cornea, NIO&H
Presenter:
Dr.(Lt Col) A K M Monzur Morshed
FCPS Part II student
Def:
“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.”
Lacrimal Function Unit
Tearing apparatus
Production- lacrimal gland
Clearance- lacrimal passages
Ocular surface
Conjunctiva
Cornea
Eyelids
Sensory and motor nerves
Precorneal tear films
• 0.1 µm
• Outermost layer
Lipid Layer • Produced by meibomian gland
&Glands of zeis
•7 µm
Aqueous •Two modes of secretion
•[Link] primarily from lacrimal gland
layer •[Link] secretion accessory lacrimal gland
and conjunctival epi.
0.2 µm
Mucous Innermost layer.
Produced by conj. Goblet cells &
Layer stratified sq epi.
Tear film constituents
Outer Lipid Layer Function
Prevent evaporation of tear
Comes from:
Maintain tear film thickness
Meibomian gland
Act as surfactant
Gland of Zeiss
Allow spread of the tear film
Gland of Moll
Sealing the apposed lid margins during sleep
Tear film constituents
Middle Aqueous layer Function
Comes from:
Lacrimal gland Optical clarity of cornea
Accessory lacrimal gland Metabolic waste product wash away
Nutrition and oxygen to corneal epithelium.
of Krause
Antibacterial activity by lysozyme, lactoferrin,IgA
and Wolfring
Maintenance and renewal of the ocular surface
Tear film constituents
Inner mucin layer Function
Comes from: Wetting of corneal epithelium
Conjuctival goblet cells
Lubrication
Gland of Manz Traps foreign particles, cellular debris, and
Crypts of Henle microbes which, with blinking, are moved to the
medial canthus where they exit the eye
Lacrimal drainage
Flow along lacrimal passage by active
lacrimal pump mechanism
Classification
On the basis of physiological consideration and clinical observation
(Holly &Lamp 1977)
Aqueous Soluble
Impaired Lid
deficiency : surfactant Lipid Functions: Epitheliopathy:
KCS, (mucin) abnormality: Exposure Anesthetic
congrnital deficiency : Chronic Keratitis, Cornea, epithelia
alacrima, hypovitaminosis A, blepharitis Symblepharon, irregularity
paralytic SJS,drugs ,chemical Pterygium
hyposecretion burns
Classification
Diagnostic classification scheme on 2007 International Dry Eye
Workshop (DEWS)
Dry eye
Aqueous tear deficiency (ATD)
Evaporative dry eye
Aqueous tear deficiency (ATD)
Sec
ond Lacrima
ary l
deficien
cy
Sjög
ren
Primary
syn age
Non- Lacrima
dro Sjögren l duct
related
syndro obstruct
me hyposec
me ion
ration
Pri
mar
y Reflex
block
Aqueous tear deficiency (ATD)
Primary Sjogren syndrome:
An autoimmune disorder
lacrimal and salivary glands are infiltrated by activated t-cells
Resulting in symptoms of dry eye and dry mouth.
Aqueous tear deficiency (ATD)
Secondary Sjogren syndrome
Sjogren syndrome associated with
other autoimmune diseases such as
rheumatoid arthritis
or systemic lupus erythematosus.
Non-Sjogren aqueous-deficient DED can result from
lacrimal gland insufficiency ,
lacrimal duct obstruction,
or reflex hyposecretion
Sjögren's syndrome
Systemic autoimmune disease that affects the entire body.
Dry eye
Classsic
clinical
triad
parotid gland Dry
enlargement mouth
Aqueous tear deficiency (ATD)
Non Sjogren's syndrome
Primary age related hyposecretion
Lacrimal gland deficiency :
Congenital alacrima
Post radiation
Surgical removal
Lacrimal gland duct obstruction:
Old trachoma
SJS
Chemical burns
Reflex hyposecretion:
Parkinson disease,
th
Evaporative Dry Eye
Meibomian
oil Vitamin A
deficiency deficiency
Topical
Disorders of Contact
lid apertures
Intrinsic Low blink lens wear Extrinsic Drug
preservative
rate
Ocular
surface
Drug action disease
Tear fluid regulations
Hormonal regulation
Androgen
Estrogen
Progesterone
Neuronal regulation Lacrimal
Secretomotor Glands
Nerve Impulses
Tears Support and Maintain Ocular Surface
Neural Stimulation
Normal tear film
Neuronal response
Emotional response: Reflex secretion:-
Irritation of cornea and conjunctiva
From hypothalmous
Ophthalmic and maxillary division of vth nerve
Lacrimatory nucleus of facial
nerve through reticular Sensory nuclei of vth nerve
formation internuncial neurons
lacrimatory nucleus of facial nerve
Lacrimal Gland.
Etiopathogenesis
Predisposing factors
Ageing
UV Medications
Dry Ocular
Contact lens
eye surgery
Menopause Allergy
Environmental
Other causes of dry eyes :
Aging
Hormonal changes during pregnancy and after
menopause
Poor blinking habits
Dry indoor environments
Diabetes
Scleroderma
Graft vs. host disease
Sarcoidosis
Significantly increases with age
Age
18
17
14
Prevalence (%)
48- 59 60-69 70-79 80-91
Prevalence of dry eye symptoms by age
Beaver Dam study Arch Oph 2000, 118:1264-1268
Age
More in women
30
Prevalence (%)
20
10 Men
Women
0
48-59 60-69 70-79 80-91
Prevalence of dry eye symptoms by age and sex
Beaver Dam study Arch Oph 2000, 118:1264-1268
Environmental factors
Climate: Dry, hot, windy, or sunny climates can increase tear
evaporation.
Air quality: Exposure to air pollution, cigarette smoke, or other airborne
pollutants can worsen dry eyes.
Heating and cooling: Air conditioning and dry heating systems can
aggravate dry eyes.
Allergies: Allergic conjunctivitis can cause dry eyes, itchiness, redness,
and discomfort.
Digital screens: Prolonged use of digital screens can lead to dry eyes
because it reduces blinking.
Altitude: High altitudes can cause dry air, which can worsen dry eyes.
Diseases can cause dry eyes:
Rheumatoid arthritis:
An autoimmune disease that can cause dry eyes.
Lupus:
An autoimmune disease that can cause dry eyes.
Thyroid disorders:
Both overactive and underactive thyroid conditions can cause dry
eyes.
Rosacea:
A skin condition that can cause dry eyes, redness, itchiness, and
burning around the eyes.
Contact lens wear
Decreased corneal sensitivity
Increased evaporation due to a reduced blink rate and/or incomplete
lid closure during blinking
Poor lens wettability may also contribute to increased evaporation
Refractive surgery
Disruption of dense sub basal nerve plexus
Loss of conjunctival goblet cells
Change in corneal shape may affect the relation ship between the
eyelids and ocular surface causing abnormal tear distribution .
Post LASIK dry eye 38-75% immediately which improve within
6-12 months .
Vitamin A deficiency
Causes xerophthalmia
Impaired goblet cell development
Lacrimal gland damage
Parkinson disease
Reduced blink rate
Resulting in increased evaporation
Digital Devices (Smart Phone)
Office workers who spent more than 4 hours watching visual
display terminal (VDT) experienced severe ocular symptoms.
Blue light emitted from the smartphone screen
adverse effect on the corneal epithelial cells in human.
Overexposure to blue light caused
deterioration of the tear film
increased levels of inflammatory markers
and reactive oxygen specie
Preoperative povidone iodine :
Goblet cell destruction reduced basal tear secretion
Loss of micro plicae and reduce mucin production ( MUC5AC production)
Less retention of fluid even with normal lacrimal gland function
Exposure time is also important 1 min exposure and 3 min exposure
shows similar microorganism eradication rather 1 min exposure causing no
epithelial damages.
Medications causing dry eye
Anticholinergics (eg, antihistamines, antispasmodics, tricyclic antidepressants,
diphenoxylate/atropine)
Beta-blockers, Preservatives (specially BZK)
Diuretics
Systemic isotretinoin
Amiodarone
Interferon, postmenopausal hormone replacement therapy (estrogen alone more so than
estrogen plus progestin)
Antiandrogenic agents
In contrast, one population study found that angiotensin-converting enzyme
inhibitors were associated with a lower risk of DE
M/A of Some drugs
Antidepressants, anti-anxiety, and anti-psychotic medications:
suppress the parasympathetic nervous system, which controls tear production.
Antihistamines:
block histamine receptors, which reduce tear production.
Beta-blockers and diuretics:
lower the pressure in eyes, which lower the amount of water in tears.
Retinoids:
reduce the amount of lubricating oils in tears.
Proton pump inhibitors (PPIs):
affect the absorption of vitamin B12, which can increase the risk of dry eye.
Isotretinoin:
shrinks sebaceous oil glands, which can cause dry eyes.
Basic Mechanism
Tear
film
instabili
ty
Inflam
mation
of
ocular Increase
surface d
osmolarit
y of tear
film
Evaporative Dry eye
Meibomian gland dysfunction (MGD)
Altered lipid metabolism
Pathogenesis:
Transition from unsaturated to saturated fats
Obstructing the
Glands
Tear-film instability, evaporation,
Hyper osmolarity
Pathogenesis
Tear hyperosmolarity
Stresses the surface epithelium Release of inflammatory mediators
Junction between superficial epithelial cell is disrupted
T cell accumulation
Produce cytokines(TNF & IL 1)
Pathogenesis (contd…)
Causes accelerated detachment of epithelial cell
Apoptosis
Further barrier disruption and influx of cell
Vicious cycle going on
Core Inflammatory cycle
Tear
stresses surface hyperosmolarity
epithelium
influx of inflammatory release inflammatory
cells mediators
further barrier Disrupt epithelial
disruption intercellular junctions
Detachment of
T cells infiltrate
Epithelial cells and
epithelium
apoptosis
produce cytokines
(TNF, IL-1)
Pathological alterations
Ocular surface inflammation
Altered compositions
Increases
Cytokine production Altered protein
T cell activation Altered lipid
Metrix metalloprotease Aqueous
Prostaglandin And mucin distribution
Take Home Message
Dry Eye is a challenging problem now a days world wide.
Every ophthalmologist should know the etiopathogenesis
of dry eye to diagnose as well as treatment of dry eye
patients.
THANK YOU
