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DRY EYE SYNDROME
PRESENTER – DR.BEMNET T.
MODERATOR – DR.YARED A.(MD ,MPH,
ASSOCIATE PROFESSOR OF OPHTHALMOLOGY,
SUBSPECIALTY IN ANTERIOR SEGMENT AND CORNEAL
DISEASE)
Out line
Introduction
Definition
Classification
Pathophysiology
Presentation
Diagnosis
Treatment
INTRODUCTION
• Dry eye syndrome is a highly prevalent and multifactorial disease of the
tear film and ocular surface
• Can cause problems ranging from mildly irritating to impaired vision
• And also can affect the outcome of corneal, cataract and refractive
surgeries
• Mostly symptoms of dry eye improves with treatment but usually its not
curable
DEFINITION
• The definition of dry eye syndrome is still under continues revision
• According to 2017 TFOS DEWS II Dry eye is:
“A multifactorial disease of the ocular surface characterized by a loss
of homeostasis of the tear film and accompanied by ocular symptoms,
in which tear film instability and hyperosmolarity, ocular surface
inflammation and damage, and neuro sensory abnormalities play
etiological roles. ”
CLASSIFICATION
In 2007/2017 international dry eye workshop (DEWS),classify dry eye into:
 Aqueous-deficient – is due to lacrimal gland dysfunction
Sjögren syndrome dry eye (primary or secondary).
Non- Sjögren syndrome dry eye.
 Evaporative
Intrinsic
Extrinsic
Cont.…
Aqueous deficient dry eye
Sjögren syndrome dry eye
 Is an autoimmune disorder characterized by lymphocytic
inflammation
 Mainly involving lacrimal and parotid gland but it also can affect any
exocrine gland.
 Inflammation block release of neurotransmitters or impact the
cellular response to neuromediators.
12/31/2020 7
Cont..
 The classic clinical triad consists of dry eyes, dry mouth and parotid
gland enlargement
 It can present as:
 Primary – when it present in isolation
 Secondary – when it present with another autoimmune disorder.
Cont..
Non - Sjögren syndrome dry eye
It can be due to:
 Lacrimal deficiency:
 Primary (e.g. Age-related dry eye , congenital alacrima , familial
dysautonomia ) or
 Secondary (e.g. Inflammatory and neoplastic lacrimal gland
infiltration, acquired immunodeficiency syndrome (AIDS), graft-
versus-host disease, lacrimal gland or nerve ablation).
12/31/2020 9
Cont..
Lacrimal gland duct obstruction
E.g. Trachoma, cicatrical pemphigoid, chemical injury, Stevens–johnson
syndrome.
Reflex hypo secretion: sensory
E.g. Contact lens wear, diabetes, refractive surgery, neurotropic keratitis
or motor block (e.g. Seventh cranial nerve damage, systemic drugs).
12/31/2020 10
Cont.…
Evaporative
Intrinsic
 Meibomian gland deficiency,
E.G. Posterior blepharitis , rosacea.
 Disorders of lid aperture,
E.G. Excessive scleral show, lid retraction, proptosis , facial nerve palsy.
 Low blink rate
E.G. Parkinson disease, prolonged computer monitor use, reading, watching television.
 Drug action,
E.G. Antihistamines, beta-blockers, antispasmodics, diuretics.
12/31/2020 11
Cont..
Extrinsic
○ Vitamin A deficiency.
○ Topical drugs including the effect of preservatives.
○ Contact lens wear.
○ Ocular surface disease such as allergic conjunctivitis
12/31/2020 12
Pathophysiology
• The well accepted theory is based on the concept of LFU
• The LFU Consist :
Ocular surface – cornea , conjunctiva and meibomian gland
Main and accessory lacrimal gland
Eye lid
Neural network – CN V AND VII
• OSM
Cont.…
Over all function of the LFU are:
Tear-film integrity
Ocular surface health
The quality of the image projected onto the retina
Any disturbance in the LFU will result in dry eye
The core mechanisms of dry eye are believed to be driven by
Tear hyperosmolarity
Tear-film instability, and
Inflammation.
Cont.…
Tear hyperosmolarity
Is a condition featured by dehydration resulting in increased osmotic
concentration
It can be caused due to:
Tear secretory dysfunction – afferent , efferent , glandular or inflammation of OS
or gland
Increased evaporation – both intrinsic and extrinsic factors
Age, hormones and environmental conditions
Tear film instability
Could be secondary to hyperosmolarity or prime to it
Is caused by;
• Reduced tear production
• Delayed tear clearance
• Reduced quantity and quality of lipid
• OS Irregularity and inflammation
Cont.…
Inflammation
The osmotic stress on ocular surface will result in the release of : IL-1B ,TNF-a ,IL-
8, MMP
This cytokines will result in localized autoimmunity
They also obstruct tearing reflex
• By stimulating release of opioids
• By directly binding to receptors
Once inflammation occur it will result ocular surface damage
Ocular surface microenvironment change in dry eye
Cornea
Corneal scaring, opacification and degeneration
Corneal thinning
Epithelial microvilli reduction
Central endothelial density reduction
NV, pannus formation and ulcers
Conjunctiva
• Squamous metaplasia
• Goblet cell reduction
• Conjunctivochalasis
Lacrimal gland
• Loss of secretory acinar cells
• Fibrosis and gland atrophy
Meibomian gland
• MGD
Eyelids
• Keratinization, thickening and neovascularization
• Blepharitis
• Recurrent Chalazion
Tear film
• Tear Hyperosmolarity
• Tear film instability
• Delayed tear clearance
• Increased tear film evaporation
Immune cells
• CD4 T cells are common
• Th1 and Th17
Nerve supply to ocular surface
DED corneas are characterized by reduced nerve density and altered
morphology
Reduced neuronal stimuli transmission to secretory component
Excessive cytokines inhibit release of Ach
Autoantibodies block receptors
Vascular system
Lymphangiogenesis- is due to chronic inflammation that will result macrophages
• Infiltrate cornea and transdifferentiate to endothelial lymphatics or
• Stimulate VEGF
Heamangiogenesis
Clinical presentation
Aqueous tear deficiency
• Burning, a dry sensation, photophobia, and blurred vision.
• Symptoms tend to be worse :
• Toward the end of the day,
• With prolonged use of the eyes or
• With exposure to environmental extremes
Evaporative Dry Eye
• Burning
• Foreign-body sensation,
• Redness of the eyelids and conjunctiva, and
• Filmy vision that is worse in the morning.
DIAGNOSIS
The diagnosis of DED needs a proper hx, examination and different testes.
History
Symptoms and signs
Exacerbation condition
Duration
Ocular hx must include
Medication(topical or systemic)
Contact lens wear
Allergic conjunctivitis
Previous ocular surface disease – HSV,SJS,GVHD
Previous ocular surgery
Punctal surgery
Bells palsy
Medical hx
Smoking
Dermatologic conditions
Menopause
Atopy
Systemic inflammatory conditions
Trauma
Radiation of orbit
Neurologic condition
Dry mouth, dental cavity and ulcers
EXAMINATION
External examination
Skin – scleroderma, rosacea
Eyelid – position, blink rate ,discharge, inflammation , Entropion, Ectropion
Adnexa – lacrimal gland enlargement, parotid gland enlargement
Proptosis
CN examination
Hand
SLE
Tear film - Height of meniscus, any debris,
mucus strands and foam
Eyelash
Eyelid - Abnormality of meibomian gland,
vascularization, keratinization and scaring
Punctum
Conjunctiva
Inferior fornix and tarsal conj. – mucus
thread, scaring erythema follicles and
papillary rxn
Bulbar conj. – keratinization, localized
dryness, chemosis , chalasis and
Cornea
Interpalpebral drying
Punctate staining
Thinning
Infiltrates
Mucus plaque
Filaments
Keratinization
Pannus formation, scaring,
ulceration and NV
DIAGNOSTIC TESTES
Testes for patients with underlying systemic condition
Tear Break-Up Time – is an indication tear film stability
 Can be measured:
 Invasively - with the instillation of fluorescein
 Best observed with use of a blue exciter and yellow barrier filter
 Appearance of a dry spot in less than or equal to 7 seconds is considered
abnormal
 Noninvasively using a keratometer or xeroscope
 noninvasive break-up time (NIBUT) – is the time from opening the eyes to the
first sign of image distortion is measured in seconds
 normal range for the NIBUT is 40 to 60 seconds
N.B- TBUT decrease in KCS, mucin deficiency and MGD
Ocular surface staining
Fluorescein sodium
• Common stain in ophthalmology
• Stain areas where corneal or conjunctival surface
epithelial cells are loose or desquamated
• Fluorescein uptake graded after the cornea is
divided into 5 areas
• Each area is graded for punctate staining on a
scale of 0 to 3 (the van Bjisterveld grading system)
• Scores > 3 indicates unstable tear film
Rose Bengal
• Is more sensitive for conjunctival staining
• Less tolerated than fluorescein
• Stain devitalized epithelial cells
• In ATD interpalpebral area is the common staining area
Lissamine green
Have similar staining characteristic of Rose Bengal
Much better tolerated than Rose Bengal
In summery
Testes for tear secretion
SCHIRMER I
 Used to evaluate aqueous-deficient dry eye
 This is done by measuring reflex tear secretion in response to conjunctival
stimulation
 The test is performed without anesthesia
Steps in doing the test
A. Place whatman #41 paper at the junction of the middle and lateral thirds of the lower
eyelid of each eye
B. Ask the patient to look forward and blink normally while the strip is held in place for 5
minutes
C. Record amount of wetting in millimeter
Interpretation of results:
Anything less than 10 mm is considered diagnostic of aqueous tear deficiency
Drawback - sensory and psychological stimuli
12/31/2020 35
12/31/2020 36
CONT..
SCHIRMER II
 Measures reflex tear secretion in response to nasal stimulation
 Done like schirmer I test but with nasal stimulation by a cotton-tipped applicator
Interpretation of results:
Wetting of less than 15 mm after 5 minutes is associated with a defect in reflex
secretion
Drawback with test is patient discomfort
12/31/2020 37
12/31/2020 38
CONT..
Phenol red thread test
 Phenol red is a ph sensitive dye
 Indicate tear volume by a schirmer-like test
 Measured over a period of 15 seconds
Interpretation of results:
 <6 mm is diagnostic
Meniscometry
 Is a noninvasive way to assess tear volume indirectly
 This is done by measuring the tear meniscus radius
 Dry eye patients have significantly smaller menisci than normal 12/31/2020 39
Meniscometry
• Is a noninvasive way to assess tear volume indirectly
• This is done by measuring the tear meniscus radius
• Dry eye patients have significantly smaller menisci than normal
MMP-9
The normal level is 3- 40ng/mL
Is done using inflammDry test
Tear Film Osmolarity
1. Tear Film Osmolarity
- effective & sensitive for diagnosing dry eye
- requires expensive equipment & skilled person
- doesn’t differentiate b/n tear deficient & evaporative dry eye
2. Tear Ferning
- depends on the ratio of Na+ & K+ to Ca2+ Mg2+
- diffences in electrolyte concentration related to different ferning patterns
- dry eye patients show less ferning
Management
Is dependent on severity of DED
Mild DED
Education – cessation of smoking, regular breaks and increase blinking during reading
Environmental modification like using humidifier
Revise both topical and systemic medication
If the severity increase
Aqueous enhancement using artificial tear, gel or ointment
Treat contributing factor
Correction of lid abnormality
Tear substitutes
Preservative-free tear substitutes are recommended
In mild cases we can use them with preservative
If installation of drops is frequent its better to use preservative free in mild cases
Emulsions ,gels and ointments can be used
Treat contributing factors like blepharitis and meibomianitis
Correct eye lid abnormality
Moderate DED
Mild DED Management plus
1.Anti- inflammatory medications
Cyclosporine a
• Inhibits the T cell activation and act as immunosuppression
• Inhibits apoptosis of lacrimal and conjunctival epithelial cells
• Dose is 0.005%
• Therapy is often initiated in combination with a short course of topical steroids
Tacrolimus – is macrolide and have an immunosuppressive effect
• Can be used in patients with GVHD,SJS and intolerance to cyclosporine
• Is prepared as 0.03%
Corticosteroids
Are highly effective in suppressing OS inflammation
Have to be used in low dose and infrequently for short duration(2 -3 wk)
Doxycycline and azithromycin
Dietary supplementation
Omega-3 fatty acids has been shown to increase average tear production and
tear volume
It also block the proinflammatory eicosanoids and cytokines
2.Punctal plugs
• Use to retain lubricants and
inhibit the natural tear
drainage
• Are effective in patient with
ATD
• Can be temporary, reversible
prolonged and permanent
3. Use of eyeglass side shields
This is to decrease tear film evaporation
Moisture retaining goggles, swimming goggles and gas permeable scleral
lenses could be used
Sever DED
In addition of the above treatments for mild and moderate DED we have to add
Secretagogues
Topical
Aqueous Secretagogues – Diquafosol tetrasodium 3%,lacritin
Mucin Secretagogues – rebamipide suspension increase MUC1,4 and
16experession
Lipid stimulation – IGF -1, androgen
Oral medication –to improve tear secretion by stimulation of lacrimal gland by inducing
cholinergic signaling pathway
Pilocarpine
-5mg po QID
Cevimeline - Is also a muscarinic agent acting as agonist on M1 and M3
• Autologous serum drop
• Can induce proliferation, migration and restore tight junction of OS epithelia
• Can be prepared from 3 to 4 red toped blood drown tubes
• Topical EGF - is also being tried to stimulate integrity of epithelium and
improve tear stability
• Human amniotic membrane
• Anti MMP-9
• Mucolytic - acetylcysteine 10% qid is used in filamentary keratopathy
• Permanent Punctal occlusion
• Limited tarsoraphy
Prognosis and Follow up
Most patient who keep up with their regimen could function either symptom free
or with minimal difficulty
Frequency and extent of follow up depend on
Severity
Therapeutic approach and
Response
On follow up evaluation we have to monitor for any OS damage
REFERENCE
• BCSC ,Section 8
• KANSKI 8TH EDITION
• PRACTICAL OPHTHALMOLOGY FOR BEGINNERS
• DRY EYE SYNDROME PPP BY AAO
• INTERNATIONAL JOURNAL OF MOLECULAR SCIENCE
• eyewiki.com
Thank u

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Dry eye syndrome

  • 1. DRY EYE SYNDROME PRESENTER – DR.BEMNET T. MODERATOR – DR.YARED A.(MD ,MPH, ASSOCIATE PROFESSOR OF OPHTHALMOLOGY, SUBSPECIALTY IN ANTERIOR SEGMENT AND CORNEAL DISEASE)
  • 3. INTRODUCTION • Dry eye syndrome is a highly prevalent and multifactorial disease of the tear film and ocular surface • Can cause problems ranging from mildly irritating to impaired vision • And also can affect the outcome of corneal, cataract and refractive surgeries • Mostly symptoms of dry eye improves with treatment but usually its not curable
  • 4. DEFINITION • The definition of dry eye syndrome is still under continues revision • According to 2017 TFOS DEWS II Dry eye is: “A multifactorial disease of the ocular surface characterized by a loss of homeostasis of the tear film and accompanied by ocular symptoms, in which tear film instability and hyperosmolarity, ocular surface inflammation and damage, and neuro sensory abnormalities play etiological roles. ”
  • 5. CLASSIFICATION In 2007/2017 international dry eye workshop (DEWS),classify dry eye into:  Aqueous-deficient – is due to lacrimal gland dysfunction Sjögren syndrome dry eye (primary or secondary). Non- Sjögren syndrome dry eye.  Evaporative Intrinsic Extrinsic
  • 6.
  • 7. Cont.… Aqueous deficient dry eye Sjögren syndrome dry eye  Is an autoimmune disorder characterized by lymphocytic inflammation  Mainly involving lacrimal and parotid gland but it also can affect any exocrine gland.  Inflammation block release of neurotransmitters or impact the cellular response to neuromediators. 12/31/2020 7
  • 8. Cont..  The classic clinical triad consists of dry eyes, dry mouth and parotid gland enlargement  It can present as:  Primary – when it present in isolation  Secondary – when it present with another autoimmune disorder.
  • 9. Cont.. Non - Sjögren syndrome dry eye It can be due to:  Lacrimal deficiency:  Primary (e.g. Age-related dry eye , congenital alacrima , familial dysautonomia ) or  Secondary (e.g. Inflammatory and neoplastic lacrimal gland infiltration, acquired immunodeficiency syndrome (AIDS), graft- versus-host disease, lacrimal gland or nerve ablation). 12/31/2020 9
  • 10. Cont.. Lacrimal gland duct obstruction E.g. Trachoma, cicatrical pemphigoid, chemical injury, Stevens–johnson syndrome. Reflex hypo secretion: sensory E.g. Contact lens wear, diabetes, refractive surgery, neurotropic keratitis or motor block (e.g. Seventh cranial nerve damage, systemic drugs). 12/31/2020 10
  • 11. Cont.… Evaporative Intrinsic  Meibomian gland deficiency, E.G. Posterior blepharitis , rosacea.  Disorders of lid aperture, E.G. Excessive scleral show, lid retraction, proptosis , facial nerve palsy.  Low blink rate E.G. Parkinson disease, prolonged computer monitor use, reading, watching television.  Drug action, E.G. Antihistamines, beta-blockers, antispasmodics, diuretics. 12/31/2020 11
  • 12. Cont.. Extrinsic ○ Vitamin A deficiency. ○ Topical drugs including the effect of preservatives. ○ Contact lens wear. ○ Ocular surface disease such as allergic conjunctivitis 12/31/2020 12
  • 13. Pathophysiology • The well accepted theory is based on the concept of LFU • The LFU Consist : Ocular surface – cornea , conjunctiva and meibomian gland Main and accessory lacrimal gland Eye lid Neural network – CN V AND VII • OSM
  • 14. Cont.… Over all function of the LFU are: Tear-film integrity Ocular surface health The quality of the image projected onto the retina Any disturbance in the LFU will result in dry eye The core mechanisms of dry eye are believed to be driven by Tear hyperosmolarity Tear-film instability, and Inflammation.
  • 15. Cont.… Tear hyperosmolarity Is a condition featured by dehydration resulting in increased osmotic concentration It can be caused due to: Tear secretory dysfunction – afferent , efferent , glandular or inflammation of OS or gland Increased evaporation – both intrinsic and extrinsic factors Age, hormones and environmental conditions
  • 16. Tear film instability Could be secondary to hyperosmolarity or prime to it Is caused by; • Reduced tear production • Delayed tear clearance • Reduced quantity and quality of lipid • OS Irregularity and inflammation
  • 17. Cont.… Inflammation The osmotic stress on ocular surface will result in the release of : IL-1B ,TNF-a ,IL- 8, MMP This cytokines will result in localized autoimmunity They also obstruct tearing reflex • By stimulating release of opioids • By directly binding to receptors Once inflammation occur it will result ocular surface damage
  • 18.
  • 19. Ocular surface microenvironment change in dry eye Cornea Corneal scaring, opacification and degeneration Corneal thinning Epithelial microvilli reduction Central endothelial density reduction NV, pannus formation and ulcers
  • 20. Conjunctiva • Squamous metaplasia • Goblet cell reduction • Conjunctivochalasis Lacrimal gland • Loss of secretory acinar cells • Fibrosis and gland atrophy
  • 21. Meibomian gland • MGD Eyelids • Keratinization, thickening and neovascularization • Blepharitis • Recurrent Chalazion
  • 22. Tear film • Tear Hyperosmolarity • Tear film instability • Delayed tear clearance • Increased tear film evaporation Immune cells • CD4 T cells are common • Th1 and Th17
  • 23. Nerve supply to ocular surface DED corneas are characterized by reduced nerve density and altered morphology Reduced neuronal stimuli transmission to secretory component Excessive cytokines inhibit release of Ach Autoantibodies block receptors Vascular system Lymphangiogenesis- is due to chronic inflammation that will result macrophages • Infiltrate cornea and transdifferentiate to endothelial lymphatics or • Stimulate VEGF Heamangiogenesis
  • 24. Clinical presentation Aqueous tear deficiency • Burning, a dry sensation, photophobia, and blurred vision. • Symptoms tend to be worse : • Toward the end of the day, • With prolonged use of the eyes or • With exposure to environmental extremes Evaporative Dry Eye • Burning • Foreign-body sensation, • Redness of the eyelids and conjunctiva, and • Filmy vision that is worse in the morning.
  • 25. DIAGNOSIS The diagnosis of DED needs a proper hx, examination and different testes. History Symptoms and signs Exacerbation condition Duration Ocular hx must include Medication(topical or systemic) Contact lens wear Allergic conjunctivitis Previous ocular surface disease – HSV,SJS,GVHD Previous ocular surgery Punctal surgery Bells palsy
  • 26. Medical hx Smoking Dermatologic conditions Menopause Atopy Systemic inflammatory conditions Trauma Radiation of orbit Neurologic condition Dry mouth, dental cavity and ulcers
  • 27. EXAMINATION External examination Skin – scleroderma, rosacea Eyelid – position, blink rate ,discharge, inflammation , Entropion, Ectropion Adnexa – lacrimal gland enlargement, parotid gland enlargement Proptosis CN examination Hand
  • 28. SLE Tear film - Height of meniscus, any debris, mucus strands and foam Eyelash Eyelid - Abnormality of meibomian gland, vascularization, keratinization and scaring Punctum Conjunctiva Inferior fornix and tarsal conj. – mucus thread, scaring erythema follicles and papillary rxn Bulbar conj. – keratinization, localized dryness, chemosis , chalasis and
  • 29. Cornea Interpalpebral drying Punctate staining Thinning Infiltrates Mucus plaque Filaments Keratinization Pannus formation, scaring, ulceration and NV
  • 30. DIAGNOSTIC TESTES Testes for patients with underlying systemic condition
  • 31. Tear Break-Up Time – is an indication tear film stability  Can be measured:  Invasively - with the instillation of fluorescein  Best observed with use of a blue exciter and yellow barrier filter  Appearance of a dry spot in less than or equal to 7 seconds is considered abnormal  Noninvasively using a keratometer or xeroscope  noninvasive break-up time (NIBUT) – is the time from opening the eyes to the first sign of image distortion is measured in seconds  normal range for the NIBUT is 40 to 60 seconds N.B- TBUT decrease in KCS, mucin deficiency and MGD
  • 32. Ocular surface staining Fluorescein sodium • Common stain in ophthalmology • Stain areas where corneal or conjunctival surface epithelial cells are loose or desquamated • Fluorescein uptake graded after the cornea is divided into 5 areas • Each area is graded for punctate staining on a scale of 0 to 3 (the van Bjisterveld grading system) • Scores > 3 indicates unstable tear film
  • 33. Rose Bengal • Is more sensitive for conjunctival staining • Less tolerated than fluorescein • Stain devitalized epithelial cells • In ATD interpalpebral area is the common staining area
  • 34. Lissamine green Have similar staining characteristic of Rose Bengal Much better tolerated than Rose Bengal In summery
  • 35. Testes for tear secretion SCHIRMER I  Used to evaluate aqueous-deficient dry eye  This is done by measuring reflex tear secretion in response to conjunctival stimulation  The test is performed without anesthesia Steps in doing the test A. Place whatman #41 paper at the junction of the middle and lateral thirds of the lower eyelid of each eye B. Ask the patient to look forward and blink normally while the strip is held in place for 5 minutes C. Record amount of wetting in millimeter Interpretation of results: Anything less than 10 mm is considered diagnostic of aqueous tear deficiency Drawback - sensory and psychological stimuli 12/31/2020 35
  • 37. CONT.. SCHIRMER II  Measures reflex tear secretion in response to nasal stimulation  Done like schirmer I test but with nasal stimulation by a cotton-tipped applicator Interpretation of results: Wetting of less than 15 mm after 5 minutes is associated with a defect in reflex secretion Drawback with test is patient discomfort 12/31/2020 37
  • 39. CONT.. Phenol red thread test  Phenol red is a ph sensitive dye  Indicate tear volume by a schirmer-like test  Measured over a period of 15 seconds Interpretation of results:  <6 mm is diagnostic Meniscometry  Is a noninvasive way to assess tear volume indirectly  This is done by measuring the tear meniscus radius  Dry eye patients have significantly smaller menisci than normal 12/31/2020 39
  • 40. Meniscometry • Is a noninvasive way to assess tear volume indirectly • This is done by measuring the tear meniscus radius • Dry eye patients have significantly smaller menisci than normal MMP-9 The normal level is 3- 40ng/mL Is done using inflammDry test
  • 41. Tear Film Osmolarity 1. Tear Film Osmolarity - effective & sensitive for diagnosing dry eye - requires expensive equipment & skilled person - doesn’t differentiate b/n tear deficient & evaporative dry eye 2. Tear Ferning - depends on the ratio of Na+ & K+ to Ca2+ Mg2+ - diffences in electrolyte concentration related to different ferning patterns - dry eye patients show less ferning
  • 42.
  • 43. Management Is dependent on severity of DED Mild DED Education – cessation of smoking, regular breaks and increase blinking during reading Environmental modification like using humidifier Revise both topical and systemic medication If the severity increase Aqueous enhancement using artificial tear, gel or ointment Treat contributing factor Correction of lid abnormality
  • 44. Tear substitutes Preservative-free tear substitutes are recommended In mild cases we can use them with preservative If installation of drops is frequent its better to use preservative free in mild cases Emulsions ,gels and ointments can be used Treat contributing factors like blepharitis and meibomianitis Correct eye lid abnormality
  • 45. Moderate DED Mild DED Management plus 1.Anti- inflammatory medications Cyclosporine a • Inhibits the T cell activation and act as immunosuppression • Inhibits apoptosis of lacrimal and conjunctival epithelial cells • Dose is 0.005% • Therapy is often initiated in combination with a short course of topical steroids Tacrolimus – is macrolide and have an immunosuppressive effect • Can be used in patients with GVHD,SJS and intolerance to cyclosporine • Is prepared as 0.03%
  • 46. Corticosteroids Are highly effective in suppressing OS inflammation Have to be used in low dose and infrequently for short duration(2 -3 wk) Doxycycline and azithromycin Dietary supplementation Omega-3 fatty acids has been shown to increase average tear production and tear volume It also block the proinflammatory eicosanoids and cytokines
  • 47. 2.Punctal plugs • Use to retain lubricants and inhibit the natural tear drainage • Are effective in patient with ATD • Can be temporary, reversible prolonged and permanent
  • 48. 3. Use of eyeglass side shields This is to decrease tear film evaporation Moisture retaining goggles, swimming goggles and gas permeable scleral lenses could be used
  • 49. Sever DED In addition of the above treatments for mild and moderate DED we have to add Secretagogues Topical Aqueous Secretagogues – Diquafosol tetrasodium 3%,lacritin Mucin Secretagogues – rebamipide suspension increase MUC1,4 and 16experession Lipid stimulation – IGF -1, androgen Oral medication –to improve tear secretion by stimulation of lacrimal gland by inducing cholinergic signaling pathway Pilocarpine -5mg po QID Cevimeline - Is also a muscarinic agent acting as agonist on M1 and M3
  • 50. • Autologous serum drop • Can induce proliferation, migration and restore tight junction of OS epithelia • Can be prepared from 3 to 4 red toped blood drown tubes • Topical EGF - is also being tried to stimulate integrity of epithelium and improve tear stability • Human amniotic membrane • Anti MMP-9 • Mucolytic - acetylcysteine 10% qid is used in filamentary keratopathy • Permanent Punctal occlusion • Limited tarsoraphy
  • 51. Prognosis and Follow up Most patient who keep up with their regimen could function either symptom free or with minimal difficulty Frequency and extent of follow up depend on Severity Therapeutic approach and Response On follow up evaluation we have to monitor for any OS damage
  • 52.
  • 53.
  • 54. REFERENCE • BCSC ,Section 8 • KANSKI 8TH EDITION • PRACTICAL OPHTHALMOLOGY FOR BEGINNERS • DRY EYE SYNDROME PPP BY AAO • INTERNATIONAL JOURNAL OF MOLECULAR SCIENCE • eyewiki.com Thank u