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DRY EYE
SAMEER BHAILA
MASTER OF OPTOMETRY
TILGANGA INSTITUTE OF OPHTHALMOLOGY
FACILITATOR
DR. YOGITA RAJBHANDARI
Pre-cornealtearfilm
• Superficial thin lipid layer
• Middle bulk aqueous layer
• Innermost mucous layer
Lipidlayer
Lipid layer is secreted by the meibomian glands &
gland of Zeiss
Their function is:
 To reduce the evaporation of the aqueous layer.
 To increase the surface tension & assist in vertical
stability of the tear film
 To act as surfactant and help spread the tear
uniformly
 To lubricate the eyelids.
Aqueouslayer
The middle layer is secreted by lacrimal gland and
accessory glands of Krause and Wolfring & has
following functions:
 To supply atmospheric oxygen to the avascular
corneal epithelium
 Anti –bacterail function
 To reduce the irregularities by enhancing the
anterior corneal surface optically
 To clean away the debris.
Constituents of Aqueous layer
Water
Electrolytes (Na, K, Cl)
Proteins:
1. Epidermal growth factors
2. Immunoglobulins (IgA, IgG, IgM)
Lactoferrin
Lysozyme
Cytokines
Mucinlayer
The inner layer is secreted by the conjunctiva goblet
cells, crypts of Henle & glands of Manz.
It converts the corneal
epithelium from
hydrophobic to
hydrophilic state.
Normaltearfilm
Volume: 7-10 μl
Thickness : 7microns
Production : 1.2 μl/min (0.5-2.2)
Turn over: 16%
Tear evaporation (0.14 μl/min in 30% humidity)
pH : 6.5-7.6
Surface tension : 40.7 dyne/cm
Refractive index : 1.336
Osmolarity : 300-310 mOsm/l
Dry Eye Disease (DED)
 The most frequently encountered ocular
morbidities
 A growing public health problem and
 One of the most common conditions seen by eye
care practitioners
 New concepts illustrates that it is caused by
inflammation mediated by T-cell lymphocytes.
DEFINITION
• Dry eye is a disorder of the tear film due to tear deficiency or
excessive evaporation, which causes damage to the
interpalpebral ocular surface and is associated with
symptoms of ocular discomfort.
(National Eye Institute (NEI)/Industry Dry Eye Workshop: 1995)
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.
(International Dry Eye Workshop, DEWS: 2007)
DEFINITION
• Our understanding of dry eye has evolved from
considering:
Tear volume insufficiency
to
Tear film instability with underlying
inflammation due to altered tear composition
Vicious cycle of ocular surface inflammation
Etiopathogenesis of dry eye disease
CurrentTriggersofDryEyeDisease
Environment
Medications
Contact Lens
Surgery
Rheumatoid Arthritis
SLE
Sjögren’s
Graft vs Host
Post menopause
Meibomian
Gland Disease
Symptoms of Ocular Surface Disease
Inflammation
Tear
Deficiency/
Instability
Irritation
Risk factors
Older age
Female sex
Postmenopausal status
Previous Refractive Surgeries like LASIK, SMILE, etc
Mostsusceptiblegrouptodryeye
 Post menopausal women
 Patient of 50 yrs plus group
 Patient on diuretics , beta blockers, psychotropics &
oral acne medication
 Rheumatoid arthritis patient
 People exposed to heat and dust
 Patient with blepharitis (MGD)
Environmental Stresses
Contact Lens Wear
Wind
Air Pollution
Low Humidity: Heating/Air Cond
 Lack of Sleep
 Use of Computer Terminals
MedicationsThatMayContributetoDryEye
Disease
Systemic
Antihypertensives
Antiandrogens
Anticholinergics
Antidepressants
Cardiac
Antiarrhythmic Drugs
Parkinson’s
Disease Agents
Antihistamines
Topical
Preservatives in tears
Classification of Dry Eye
The 2007 International Dry Eye Workshop (DEWS),
classified dry eye into:
• Aqueous-deficient
• Evaporative
Sjogren Syndrome
Is an autoimmune disorder
Characterized by lymphocytic inflammation and
destruction of lacrimal and salivary gland and other
exocrine glands
Lymphocytic infiltration of the lacrimal gland with
damage to secretory acini
Classic triad
Classic triad consists of:
 Dry eye
 Dry mouth
 Parotid gland enlargement
Sjogren Syndrome
Classified into:
Primary when it exists in isolation
Secondary when associated with other diseases like
Rheumatoid Arthritis, Systemic Lupus
Erythematosus, Wegener’s granulomatosis and
other autoimmune disorders
Clinical Features Dry Eye
Common symptoms
 Ocular discomfort
 Irritation such as scratchiness, grittiness, foreign
body sensation, burning, blurring, and itching
Clinical Signs
 Posterior blepharitis and meibomian gland
dysfunction may be present
 Conjunctiva may show mild keratinization and redness
 Tear film
• The lipid-contaminated mucin accumulates in the tear
film as particles and debris that move with each blink
• The marginal tear meniscus becomes thin (< 1 mm) in
height or absent
Cornea
• Punctate epithelial erosions that stain with fluorescein
• Filaments consist of mucus strands lined with
epithelium attached at one end to the corneal surface
which stain well with rose bengal
• Mucous plaques consist of semi-transparent, white-to-
grey, slightly elevated lesions of various sizes
Complications
Occurs in very severe cases which include:
Peripheral superficial corneal neovascularization
Epithelial breakdown
Melting of corneal
Perforation of cornea and
Bacterial keratitis
Severity Grades of DED
 Dry eye is classified according to the clinical
severity into three grades
Grade 1 or mild:
 Patients have symptoms of dryness in normal
environmental conditions
But no signs on slit-lamp examination
Electrophysiological or invasive tests, such as
hyperosmolarity, hypolysozyme or inflammatory
cytokines, may be positive.
Grade 2 or moderate:
 In addition to symptoms, patient has reversible
slitlamp signs such as
 Epithelial erosion
 Punctate keratopathy
 Filamentary keratitis
 Short tear breakup time (TBUT), etc.
Grade 3 or severe:
The patient has, besides the symptoms of ocular
dryness, signs that have evolved to permanent
sequelae such as
 Corneal ulcer
 Corneal opacity
 Corneal neovascularization or
 Squamous epithelial metaplasia
These signs are commonly seen in untreated
patients.
Investigation
The test measure the following parameters:
Tear Film
Stability
• Tear Film Break-up Time (TBUT)
Tear
Production
• Schirmer
• Fluorescein Clearance
• Tear osmolarity
Ocular
Surface Dz
• Corneal Stains
• Impression Cytology
Tear Film Break-up Time
 Abnormal in aqueous tear deficiency and MGDs
Fluorescein 2% or an impregnated strip moistened
with saline is instilled in lower fornix
Patient is asked to blink several times
Tear film is examined under cobalt blue filter
BUT is the interval between the last blink and
appearance of first randomly distributed dark dry
spot
TBUT
 Values of < 10s are considered abnormal
 Values of < 5s are clearly indicative of severe
dry eye
Noninvasive breakup time (NIBUT)
 Is a test of tear stability that does not involve the
instillation of fluorescein dye
 Measurements are performed with a xeroscope
Schirmer Test
Useful in assessment of aqueous tear production
The Schirmer strip is placed over the lateral third of
the lower lid
If using an anesthetic , adequate time should be
given after the drop to minimize reflex tearing
from the burning sensation due to drop
Schirmer I (without anesthesia ) : basic and
reflex secretion
Schirmer II (with anesthesia ): basic secretion
<5mm wetting in 5 min is sign of clinical dry eye
5-10mm wetting suggests borderline dry eye
>10mm wetting represents normal secretion
Ocular Surface Staining
The installation of dyes is a common method to
detect ocular surface epithelial pathology
associated by dry eye
• Fluorescein sodium
• Rose Bengal
• Lissamine green
Fluorescein is the most commonly used :
stains the corneal and conjunctival epithelium
where there is sufficient damage to allow dye
to enter tissue
Stains cornea more readily than conjunctiva
significantly greater amount of staining in
Sjogren’s aqueous tear deficiency
Fluorescein Stain
Rose Bengal unlike fluorescein which stains tissue by
penetrating into intercellular spaces stains:
 Devitalized epithelial cell
 Healthy epithelial cells when they are not
protected by a healthy layer of mucin.
 Corneal filaments and plaques are stained well by
Rose Bengal
Rose Bengal Stain
 Van Bijsterveld scoring system applied for Rose
Bengal dye
 Intensity of stain is scored in two exposed
conjunctival zones (nasal and temporal) and
cornea.
 Score of 03 is given for each zone
0 is for no stain
+1 for separate spot
+2 for many separate spots
+3 for confluent spots
With a maximum score of 9
Lissamine green B stains in a similar fashion to
Rose Bengal:
Produces much less irritation
Staining pattern to be identical to Rose Bengal
Pattern of Staining
The pattern of staining may aid in diagnosis
Pattern
Interpalpebral staining of cornea is common in
aqueous tear deficiency
Superior conjunctival stai may indicate superior
limbic keratoconjuctivitis
Inferior corneal and conjunctival stain is often
present in blepharitis and exposure keratitis
Other Investigations
Fluorescein clearance test
 The tear function index is assessed by placing 5 μl
of fluorescein on the ocular surface
 Measures the residual dye in a Schirmer strip
placed on the lower lateral lid margin at intervals
of 1, 10, 20 and 30 minutes.
Fluorescein clearance test
 The presence of fluorescein on each strip is
examined under blue light and compared to a
standard scale or measured using
fluorophotometry.
 Normally the value fall to zero after 20 minutes.
 Delayed clearance is observed in all dry eye states.
Lactoferrin
The major protein secreted by the lacrimal gland.
Tear lactoferrin is decreased in Sjögren syndrome
and other lacrimal gland diseases.
Immunoassay kits are available to measure
lactoferrin in body fluids
Phenol red thread test
 Uses a thread impregnated with a pH sensitive dye.
 The end of the thread is placed over the lower lid and
the length wetted (the dye changes from yellow to red
in tears) is measured after 15 seconds.
 A value of 6 mm is abnormal.
 It is comparable to Schirmer test but takes less time.
Tear meniscometry
Technique to quantify the height and thus the volume of
the lower lid meniscus.
Impression cytology
Minimally invasive alternative to ocular surface
biopsy
Superficial layers of the ocular surface epithelium
are collected (e.g. by applying filter paper) and
examined microscopically
Useful for detecting abnormalities such as goblet
cell loss and squamous metaplasia
Treatment
DEWS have produced guidelines based on the level of
severity of disease graded from 1 to 4.
LEVEL 1
1. Education and environmental modification
• Lifestyle review: Importance of blinking while reading,
watching television or using computers, learning to take
breaks while reading, rule of 20-20-20, lowering the
computer monitors to decrease lid aperture
• Environment review: increasing the humidity of the
room or decreasing the temperature of the room
• Caution the patient that laser refractive surgery and
other ocular surface surgeries exacerbate the dry
eye
2. Systemic medication review:
• To exclude contributory effects and eliminate
offending agents
3. Artificial tear substitutes
• Use of preserved artificial tear drops, gels and
ointments
• Are the mainstay of treatment for mild to moderate
aqueous tear deficiency.
• Aqueous solutions containing polymers such as
cellulose derivatives [e.g. hydroxypropyl methyl
cellulose (HPMC), carboxymethyl cellulose], polyvinyl
derivatives (e.g. polyvinyl alcohol), chondroitin sulfate,
and sodium hyluronate.
• Artificial tears containing preservatives, particularly
benzylkonium chloride, are poorly tolerated and
harmful in moderate to severe cases
4. Eyelid therapy
• Warm compression and lid hygiene for blepharitis
and MGDs
• Reparative lid surgeries for entropion, ectropion, lid
laxity and scleral show
LEVEL 2
• Anti-inflammatory agents
Topical steroids like fluometholone
Oral omega fatty acid
Topical cyclosporine A (0.05%) : Is a fungal derived
peptide that prevents Tcell activation and inflammatory
cytokine production
 Oral Tetracyclines (Doxycycline) for mebomianitis,
rosacea
 Punctal plugs
 Secretagogues are cholinergic agonists like pilocarpine
which increases lacrimal secretion
 Moisture chamber spectacles and spectacle side
shields
Level 3
• Serum eye drops:
 Autologous or umbilical cord serum
 Serum and plasma contain many anti-inflammatory
factors which include inhibitors of inflammatory
cytokines and inhibitors of MMPs.
 Have potential to inhibit mediators of the ocular
surface inflammatory cascade of dry eye
• Contact lens: Low water content SCL or Silicone
hydrogels use or Scleral lenses
• Permanent punctal occlusion
Level 4
• Systemic anti-inflammatory agents
• Surgery:
 Tarsorrhaphy and botulinum toxin induced ptosis
 Salivary gland autotransplantation
 Mucous membrane or amniotic membrane or
limbal stem cell transplantation for corneal
complications
Novel therapeutic agents with anti-inflammatory
properties:
 AntiCD4 monoclonal antibody
 Hydroxychloroquine, when given orally for the
treatment of Sjogren syndrome, has a beneficial
effect on dry eye
Steven-Johnson Syndrome
 also called as Erythema multiforme major / Toxic
epidermal necrolysis (TEN) / Lyell Syndrome
 Involves a cell-mediated delayed hypersensitivity
reaction
Steven-Johnson Syndrome
 Usually related to drug exposure
Antibiotics:
Sulfonamides and trimethoprim
Analgesics:
Paracetamol (acetaminophen), cold remedies and
Anti-convulsants
 Infections due to
Mycoplasma pneumoniae, herpes simplex virus and
some cancers
Ocular Features of SJS
Symptoms:
• Redness
• Mild-severe grittiness
• Photophobia
• Watering and
• Blurring
Signs:
• Acute Signs
• Late Signs
Acute Sign of SJS
Haemorrhagic crusting of lid margins
Papillary conjunctivitis
Cunjunctival membranes and pseudomembranes
Keratopathy: punctate erosions to large epithelial
defects and in severe case perforation as well
Iritis
Late Signs of SJS
Conjunctival cicatrization with forniceal shortening and
symblepharon
Keratinization of conjunctiva and lid margin
Eye lid complications include entropion, ectropion,
triciasis, metaplastic lashes
Keratopathy includes scarring, vascularization and
keratinization
Watering due to fibrosis of lacrimal puncta and severe dry
eye due to fibrosis of lacrimal gland
Late Signs of SJS
Systemic Features of SJS
Symptoms:
• Flu-like symptoms lasting 14 days before
appearance of lesions
• Nasal pain and discharge
• Pain in micturition
• Diarrhoea
• Cough
• Shortness of breath
• Pain on eating and drinking
Systemic Signs of SJS
• Blistering and hemorrhagic crusting of lips, tongue,
oropharynx, nasal mucosa and genitalia
• Small purpuric , vesicular, hemorrhagic or necrotic
skin lesions involving extremities, face and trunk
Systemic Treatment
• Removal of the precipitant drugs having toxic effects
like sulphonamides
• Maintenance of adequate hydration, electrolyte
balance and nutrition
• Intravenous steroids treatment may improve
outcomes
• Immunosuppressant like cyclosporine, azathioprine
can be prescribed
• Systemic antibiotics for prophylaxis having no toxicity
Ocular Treatment
Acute Disease
• Topical preservative free lubricants like
hypromellose (0.3%)
• Topical steroids for iritis and conjunctival
inflammation
• Topical cycloplegia (1% atropine once or twice daily)
Acute Disease
• Lysis of developing symblephara
• Pseudomembrane / membrane peeling
• Prophylactic topical antibiotics for bacterial keratitis
and conjunctivitis
• Conjunctival swab should be considered for
prophylactic culture
Chronic Disease
• Adequate lubrication and punctal occlusion if
required
• Topical transretinoic acid 0.01% or 0.025% may
reverse keratinization
• Bandage contact lens (typically gas permeable scleral
lenses and scleral lenses)
• Mucous membrane grafting (e.g. buccal mucosa
autograft) for forniceal reconstruction.
• Corneal rehabilitation
Superficial keratectomy for keratinization
Lamellar corneal grafting for superficial scarring
Amniotic membrane grafting
Limbal stem cell transplantation
Keratoprosthesis implantation in end-stage disease
Thank you!!!

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Dry eye sameer

  • 1. DRY EYE SAMEER BHAILA MASTER OF OPTOMETRY TILGANGA INSTITUTE OF OPHTHALMOLOGY FACILITATOR DR. YOGITA RAJBHANDARI
  • 2.
  • 3. Pre-cornealtearfilm • Superficial thin lipid layer • Middle bulk aqueous layer • Innermost mucous layer
  • 4. Lipidlayer Lipid layer is secreted by the meibomian glands & gland of Zeiss Their function is:  To reduce the evaporation of the aqueous layer.  To increase the surface tension & assist in vertical stability of the tear film  To act as surfactant and help spread the tear uniformly  To lubricate the eyelids.
  • 5. Aqueouslayer The middle layer is secreted by lacrimal gland and accessory glands of Krause and Wolfring & has following functions:  To supply atmospheric oxygen to the avascular corneal epithelium  Anti –bacterail function  To reduce the irregularities by enhancing the anterior corneal surface optically  To clean away the debris.
  • 6. Constituents of Aqueous layer Water Electrolytes (Na, K, Cl) Proteins: 1. Epidermal growth factors 2. Immunoglobulins (IgA, IgG, IgM) Lactoferrin Lysozyme Cytokines
  • 7. Mucinlayer The inner layer is secreted by the conjunctiva goblet cells, crypts of Henle & glands of Manz. It converts the corneal epithelium from hydrophobic to hydrophilic state.
  • 8. Normaltearfilm Volume: 7-10 μl Thickness : 7microns Production : 1.2 μl/min (0.5-2.2) Turn over: 16% Tear evaporation (0.14 μl/min in 30% humidity) pH : 6.5-7.6 Surface tension : 40.7 dyne/cm Refractive index : 1.336 Osmolarity : 300-310 mOsm/l
  • 9. Dry Eye Disease (DED)  The most frequently encountered ocular morbidities  A growing public health problem and  One of the most common conditions seen by eye care practitioners  New concepts illustrates that it is caused by inflammation mediated by T-cell lymphocytes.
  • 10. DEFINITION • Dry eye is a disorder of the tear film due to tear deficiency or excessive evaporation, which causes damage to the interpalpebral ocular surface and is associated with symptoms of ocular discomfort. (National Eye Institute (NEI)/Industry Dry Eye Workshop: 1995)
  • 11. 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. (International Dry Eye Workshop, DEWS: 2007)
  • 12. DEFINITION • Our understanding of dry eye has evolved from considering: Tear volume insufficiency to Tear film instability with underlying inflammation due to altered tear composition
  • 13. Vicious cycle of ocular surface inflammation
  • 14. Etiopathogenesis of dry eye disease
  • 15. CurrentTriggersofDryEyeDisease Environment Medications Contact Lens Surgery Rheumatoid Arthritis SLE Sjögren’s Graft vs Host Post menopause Meibomian Gland Disease Symptoms of Ocular Surface Disease Inflammation Tear Deficiency/ Instability Irritation
  • 16. Risk factors Older age Female sex Postmenopausal status Previous Refractive Surgeries like LASIK, SMILE, etc
  • 17.
  • 18. Mostsusceptiblegrouptodryeye  Post menopausal women  Patient of 50 yrs plus group  Patient on diuretics , beta blockers, psychotropics & oral acne medication  Rheumatoid arthritis patient  People exposed to heat and dust  Patient with blepharitis (MGD)
  • 19. Environmental Stresses Contact Lens Wear Wind Air Pollution Low Humidity: Heating/Air Cond  Lack of Sleep  Use of Computer Terminals
  • 21. Classification of Dry Eye The 2007 International Dry Eye Workshop (DEWS), classified dry eye into: • Aqueous-deficient • Evaporative
  • 22.
  • 23.
  • 24. Sjogren Syndrome Is an autoimmune disorder Characterized by lymphocytic inflammation and destruction of lacrimal and salivary gland and other exocrine glands Lymphocytic infiltration of the lacrimal gland with damage to secretory acini
  • 25. Classic triad Classic triad consists of:  Dry eye  Dry mouth  Parotid gland enlargement
  • 26. Sjogren Syndrome Classified into: Primary when it exists in isolation Secondary when associated with other diseases like Rheumatoid Arthritis, Systemic Lupus Erythematosus, Wegener’s granulomatosis and other autoimmune disorders
  • 27. Clinical Features Dry Eye Common symptoms  Ocular discomfort  Irritation such as scratchiness, grittiness, foreign body sensation, burning, blurring, and itching
  • 28. Clinical Signs  Posterior blepharitis and meibomian gland dysfunction may be present  Conjunctiva may show mild keratinization and redness  Tear film • The lipid-contaminated mucin accumulates in the tear film as particles and debris that move with each blink • The marginal tear meniscus becomes thin (< 1 mm) in height or absent
  • 29. Cornea • Punctate epithelial erosions that stain with fluorescein • Filaments consist of mucus strands lined with epithelium attached at one end to the corneal surface which stain well with rose bengal • Mucous plaques consist of semi-transparent, white-to- grey, slightly elevated lesions of various sizes
  • 30. Complications Occurs in very severe cases which include: Peripheral superficial corneal neovascularization Epithelial breakdown Melting of corneal Perforation of cornea and Bacterial keratitis
  • 31. Severity Grades of DED  Dry eye is classified according to the clinical severity into three grades Grade 1 or mild:  Patients have symptoms of dryness in normal environmental conditions But no signs on slit-lamp examination Electrophysiological or invasive tests, such as hyperosmolarity, hypolysozyme or inflammatory cytokines, may be positive.
  • 32. Grade 2 or moderate:  In addition to symptoms, patient has reversible slitlamp signs such as  Epithelial erosion  Punctate keratopathy  Filamentary keratitis  Short tear breakup time (TBUT), etc.
  • 33. Grade 3 or severe: The patient has, besides the symptoms of ocular dryness, signs that have evolved to permanent sequelae such as  Corneal ulcer  Corneal opacity  Corneal neovascularization or  Squamous epithelial metaplasia These signs are commonly seen in untreated patients.
  • 34. Investigation The test measure the following parameters: Tear Film Stability • Tear Film Break-up Time (TBUT) Tear Production • Schirmer • Fluorescein Clearance • Tear osmolarity Ocular Surface Dz • Corneal Stains • Impression Cytology
  • 35. Tear Film Break-up Time  Abnormal in aqueous tear deficiency and MGDs Fluorescein 2% or an impregnated strip moistened with saline is instilled in lower fornix Patient is asked to blink several times Tear film is examined under cobalt blue filter BUT is the interval between the last blink and appearance of first randomly distributed dark dry spot
  • 36. TBUT  Values of < 10s are considered abnormal  Values of < 5s are clearly indicative of severe dry eye
  • 37. Noninvasive breakup time (NIBUT)  Is a test of tear stability that does not involve the instillation of fluorescein dye  Measurements are performed with a xeroscope
  • 38. Schirmer Test Useful in assessment of aqueous tear production The Schirmer strip is placed over the lateral third of the lower lid If using an anesthetic , adequate time should be given after the drop to minimize reflex tearing from the burning sensation due to drop
  • 39. Schirmer I (without anesthesia ) : basic and reflex secretion Schirmer II (with anesthesia ): basic secretion <5mm wetting in 5 min is sign of clinical dry eye 5-10mm wetting suggests borderline dry eye >10mm wetting represents normal secretion
  • 40.
  • 41. Ocular Surface Staining The installation of dyes is a common method to detect ocular surface epithelial pathology associated by dry eye • Fluorescein sodium • Rose Bengal • Lissamine green
  • 42. Fluorescein is the most commonly used : stains the corneal and conjunctival epithelium where there is sufficient damage to allow dye to enter tissue Stains cornea more readily than conjunctiva significantly greater amount of staining in Sjogren’s aqueous tear deficiency
  • 44. Rose Bengal unlike fluorescein which stains tissue by penetrating into intercellular spaces stains:  Devitalized epithelial cell  Healthy epithelial cells when they are not protected by a healthy layer of mucin.  Corneal filaments and plaques are stained well by Rose Bengal
  • 45. Rose Bengal Stain  Van Bijsterveld scoring system applied for Rose Bengal dye  Intensity of stain is scored in two exposed conjunctival zones (nasal and temporal) and cornea.  Score of 03 is given for each zone 0 is for no stain +1 for separate spot +2 for many separate spots +3 for confluent spots With a maximum score of 9
  • 46. Lissamine green B stains in a similar fashion to Rose Bengal: Produces much less irritation Staining pattern to be identical to Rose Bengal
  • 47. Pattern of Staining The pattern of staining may aid in diagnosis Pattern Interpalpebral staining of cornea is common in aqueous tear deficiency Superior conjunctival stai may indicate superior limbic keratoconjuctivitis Inferior corneal and conjunctival stain is often present in blepharitis and exposure keratitis
  • 48. Other Investigations Fluorescein clearance test  The tear function index is assessed by placing 5 μl of fluorescein on the ocular surface  Measures the residual dye in a Schirmer strip placed on the lower lateral lid margin at intervals of 1, 10, 20 and 30 minutes.
  • 49. Fluorescein clearance test  The presence of fluorescein on each strip is examined under blue light and compared to a standard scale or measured using fluorophotometry.  Normally the value fall to zero after 20 minutes.  Delayed clearance is observed in all dry eye states.
  • 50. Lactoferrin The major protein secreted by the lacrimal gland. Tear lactoferrin is decreased in Sjögren syndrome and other lacrimal gland diseases. Immunoassay kits are available to measure lactoferrin in body fluids
  • 51. Phenol red thread test  Uses a thread impregnated with a pH sensitive dye.  The end of the thread is placed over the lower lid and the length wetted (the dye changes from yellow to red in tears) is measured after 15 seconds.  A value of 6 mm is abnormal.  It is comparable to Schirmer test but takes less time. Tear meniscometry Technique to quantify the height and thus the volume of the lower lid meniscus.
  • 52. Impression cytology Minimally invasive alternative to ocular surface biopsy Superficial layers of the ocular surface epithelium are collected (e.g. by applying filter paper) and examined microscopically Useful for detecting abnormalities such as goblet cell loss and squamous metaplasia
  • 53. Treatment DEWS have produced guidelines based on the level of severity of disease graded from 1 to 4. LEVEL 1 1. Education and environmental modification • Lifestyle review: Importance of blinking while reading, watching television or using computers, learning to take breaks while reading, rule of 20-20-20, lowering the computer monitors to decrease lid aperture
  • 54. • Environment review: increasing the humidity of the room or decreasing the temperature of the room • Caution the patient that laser refractive surgery and other ocular surface surgeries exacerbate the dry eye 2. Systemic medication review: • To exclude contributory effects and eliminate offending agents
  • 55. 3. Artificial tear substitutes • Use of preserved artificial tear drops, gels and ointments • Are the mainstay of treatment for mild to moderate aqueous tear deficiency. • Aqueous solutions containing polymers such as cellulose derivatives [e.g. hydroxypropyl methyl cellulose (HPMC), carboxymethyl cellulose], polyvinyl derivatives (e.g. polyvinyl alcohol), chondroitin sulfate, and sodium hyluronate. • Artificial tears containing preservatives, particularly benzylkonium chloride, are poorly tolerated and harmful in moderate to severe cases
  • 56. 4. Eyelid therapy • Warm compression and lid hygiene for blepharitis and MGDs • Reparative lid surgeries for entropion, ectropion, lid laxity and scleral show
  • 57. LEVEL 2 • Anti-inflammatory agents Topical steroids like fluometholone Oral omega fatty acid Topical cyclosporine A (0.05%) : Is a fungal derived peptide that prevents Tcell activation and inflammatory cytokine production  Oral Tetracyclines (Doxycycline) for mebomianitis, rosacea  Punctal plugs  Secretagogues are cholinergic agonists like pilocarpine which increases lacrimal secretion  Moisture chamber spectacles and spectacle side shields
  • 58. Level 3 • Serum eye drops:  Autologous or umbilical cord serum  Serum and plasma contain many anti-inflammatory factors which include inhibitors of inflammatory cytokines and inhibitors of MMPs.  Have potential to inhibit mediators of the ocular surface inflammatory cascade of dry eye • Contact lens: Low water content SCL or Silicone hydrogels use or Scleral lenses • Permanent punctal occlusion
  • 59. Level 4 • Systemic anti-inflammatory agents • Surgery:  Tarsorrhaphy and botulinum toxin induced ptosis  Salivary gland autotransplantation  Mucous membrane or amniotic membrane or limbal stem cell transplantation for corneal complications
  • 60. Novel therapeutic agents with anti-inflammatory properties:  AntiCD4 monoclonal antibody  Hydroxychloroquine, when given orally for the treatment of Sjogren syndrome, has a beneficial effect on dry eye
  • 61. Steven-Johnson Syndrome  also called as Erythema multiforme major / Toxic epidermal necrolysis (TEN) / Lyell Syndrome  Involves a cell-mediated delayed hypersensitivity reaction
  • 62. Steven-Johnson Syndrome  Usually related to drug exposure Antibiotics: Sulfonamides and trimethoprim Analgesics: Paracetamol (acetaminophen), cold remedies and Anti-convulsants  Infections due to Mycoplasma pneumoniae, herpes simplex virus and some cancers
  • 63. Ocular Features of SJS Symptoms: • Redness • Mild-severe grittiness • Photophobia • Watering and • Blurring Signs: • Acute Signs • Late Signs
  • 64. Acute Sign of SJS Haemorrhagic crusting of lid margins Papillary conjunctivitis Cunjunctival membranes and pseudomembranes Keratopathy: punctate erosions to large epithelial defects and in severe case perforation as well Iritis
  • 65. Late Signs of SJS Conjunctival cicatrization with forniceal shortening and symblepharon Keratinization of conjunctiva and lid margin Eye lid complications include entropion, ectropion, triciasis, metaplastic lashes Keratopathy includes scarring, vascularization and keratinization Watering due to fibrosis of lacrimal puncta and severe dry eye due to fibrosis of lacrimal gland
  • 67. Systemic Features of SJS Symptoms: • Flu-like symptoms lasting 14 days before appearance of lesions • Nasal pain and discharge • Pain in micturition • Diarrhoea • Cough • Shortness of breath • Pain on eating and drinking
  • 68. Systemic Signs of SJS • Blistering and hemorrhagic crusting of lips, tongue, oropharynx, nasal mucosa and genitalia • Small purpuric , vesicular, hemorrhagic or necrotic skin lesions involving extremities, face and trunk
  • 69. Systemic Treatment • Removal of the precipitant drugs having toxic effects like sulphonamides • Maintenance of adequate hydration, electrolyte balance and nutrition • Intravenous steroids treatment may improve outcomes • Immunosuppressant like cyclosporine, azathioprine can be prescribed • Systemic antibiotics for prophylaxis having no toxicity
  • 70. Ocular Treatment Acute Disease • Topical preservative free lubricants like hypromellose (0.3%) • Topical steroids for iritis and conjunctival inflammation • Topical cycloplegia (1% atropine once or twice daily)
  • 71. Acute Disease • Lysis of developing symblephara • Pseudomembrane / membrane peeling • Prophylactic topical antibiotics for bacterial keratitis and conjunctivitis • Conjunctival swab should be considered for prophylactic culture
  • 72. Chronic Disease • Adequate lubrication and punctal occlusion if required • Topical transretinoic acid 0.01% or 0.025% may reverse keratinization • Bandage contact lens (typically gas permeable scleral lenses and scleral lenses) • Mucous membrane grafting (e.g. buccal mucosa autograft) for forniceal reconstruction.
  • 73. • Corneal rehabilitation Superficial keratectomy for keratinization Lamellar corneal grafting for superficial scarring Amniotic membrane grafting Limbal stem cell transplantation Keratoprosthesis implantation in end-stage disease