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![52
Eye Drops
Cellulose derivatives –
o Hydroxypropyl methylcellulose
o Carboxymethylcellulose [more useful in lipid or
mucous deficiency]
o Appropriate for mild cases.
Polyvinyl alcohol – Better in aqueous deficiency
Povidone
Sodium chloride
Hypromellose
Sodium hyaluronate
Polyethylene and propylene glycol](https://image.slidesharecdn.com/271-dry-eye-241219181131-786ad8fc/75/271-577987666787666666655566dry-eye-pptx-52-2048.jpg)
![54
Other options
Topical cyclosporine [0.05%, 0.1%]
Reduces cell-mediated inflammation of lacrimal
tissue increase in goblet cells, reversal of
squamous metaplasia of conjunctiva.
Oral cholinergic agents (M3) like pilocarpine , cevimeline
Effective in xerostomia & about 40% of KCS patients
also obtain relief
Botulinum toxin injection to orbicularis muscle – controls
blepharospasm in severe dry eye.
Sub-mandibular gland transplantation – for extreme dry eye.](https://image.slidesharecdn.com/271-dry-eye-241219181131-786ad8fc/75/271-577987666787666666655566dry-eye-pptx-54-2048.jpg)
![Dry_Eye_Presentation_Final[1].pptx......](https://cdn.slidesharecdn.com/ss_thumbnails/dryeyepresentationfinal1-250516163834-f963ff70-thumbnail.jpg?width=640&height=640&fit=bounds)
271-577987666787666666655566dry-eye.pptx
- 1. 1 DRY EYE PRESENTER-DR SHEEMAMARIYAM MODERATOR-DR SAI SUSHMA
- 2. 2 DRY EYE Dryeye occurs when there is inadequate tear volume or function, resulting in an unstable tear film and ocular surface disease. It is an extremely common condition, particularly in postmenopausal women and the elderly. Dry eye disease is a multifactorial disease of the ocular surface and tear film accompanied by increased osmolarity of the tear film and inflammation of the ocular surface
- 3. 3 Dry eye isnot a trivial complaint. It can cause significant discomfort and affect quality of life significantly. In 1995 the National Eye Institute defined dry eye disease (DED) as a disorder of the tear film due to tear deficiency or excessive tear evaporation which causes damage to the interpalpebral ocular surface and is associated with symptoms of ocular discomfort.
- 4. 4 In 2007 theInternational Dry Eye Workshop defined it as 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.
- 5. 5 Tear film constituents Thetear film has three layers Lipid layer secreted by the meibomian glands. Aqueous layer secreted by the lacrimal glands. Mucous layer secreted principally by conjunctival goblet cells.
- 6. 6 Lipid layer Theouter lipid layer is composed of a polar phase containing phospholipids adjacent to the aqueous-mucin phase and a non-polar phase containing waxes, cholesterol esters and triglycerides. To prevent evaporation of the aqueous layer and maintain tear film thickness. To act as a surfactant allowing spread of the tear film. Deficiency results in evaporative dry eye.
- 7. 7 Aqueous layer Secretion-The main lacrimal glands produce about 95% of the aqueous component of tears and the accessory lacrimal glands of Krause and Wolfring produce the remainder. To provide atmospheric oxygen to the corneal epithelium. Antibacterial activity due to proteins such as IgA, lysozyme and lactoferrin. To wash away debris and noxious stimuli and facilitate the transport of leukocytes after injury. To optically enhance the corneal surface by abolishing minute irregularities.
- 8. 8 Mucous layer Producedmainly by conjunctival goblet cells but also by the lacrimal glands. To permit wetting by converting the corneal epithelium from a hydrophobic to a hydrophilic surface. Lubrication.
- 9. 9 MECHANISUM The fourcore inter-related mechanisms thought to be responsible for the manifestations of dry eye tear instability tear hyperosmolarity inflammation ocular surface damage.
- 10.
- 11. 11 Sjögren syndrome Autoimmunedisorder characterized by lymphocytic inflammation and destruction of lacrimal and salivary glands and other exocrine organs. The classic clinical triad consists of dry eyes, dry mouth and parotid gland enlargement but other features are common and can affect all organ systems. The condition is classified as primary when it exists in isolation and secondary when associated with another disease, commonly rheumatoid arthritis or systemic lupus erythematosus. Primary SS affects females more frequently than males.
- 12. 12 The AmericanCollege of Rheumatology (ACR) criteria for diagnosis specify, in patients with a clinical picture suggestive of SS, the following: • Positivity for anti-SSA or anti-SSB antibodies, or positive rheumatoid factor together with significantly positive antinu- clear antibody. • Ocular surface staining • Focal lymphocytic sialadenitis to a specified extent on salivary gland biopsy
- 13. 13 Dry Eye Disease:Predisposing Factors Ageing Menopause - Decreased Androgens Allergy Response Environmental Stresses Contact Lens Wear Wind Air Pollution Ocular Surgery (LASIK, Corneal Transplant) Medications – Low Humidity: Heating/AC – Lack of Sleep – Use of Computer Terminals
- 14. 14 Medications That MayContribute to Dry Eye Disease Systemic Anti-hypertensives Anti-androgens Anti-cholinergics Antidepressants Cardiac Anti-arrhythmic Drugs Parkinson’s Disease Agents Antihistamines Topical – Preservatives in Tears
- 15. 15 Dry Eye Disease: AutoimmuneTriggers Systemic Autoimmunity Rheumatoid Arthritis Lupus Sjögren’s Syndrome Graft vs. Host Disease All can result in immune-mediated inflammation in the eye. Inflammatory mediators secreted into tears. Promote inflammation of ocular surface.
- 16. 16 Environment Medications Contact Lens Surgery Rheumatoid Arthritis Lupus Sjögren’s Graft vsHost Postmenopause Meibomian Gland Disease Symptoms of Ocular Surface Disease Inflammation Tear Deficiency/ Instability Irritation Current Triggers of Dry Eye Disease
- 17.
- 18. 18 Dry Eye DiseaseSymptoms Discomfort Dryness Burning, Stinging Foreign-Body Sensation Gritty Feeling, Stickiness Blurry Vision Photophobia, Itching, Redness
- 19. SIGNS Posterior (seborrhoeic)blepharitis with meibomian gland dysfunction is often present Conjunctiva ○ Redness.Staining with rose Bengal and lissamine green Keratinization. Conjunctivochalasis
- 20. Tear film Inthe normal eye, as the tear film breaks down, the mucin layer becomes contaminated with lipid but is washed away. In the dry eye, the lipid-contaminated mucin accumulates in the tear film as particles and debris that move with each blink The marginal tear meniscus (strip) is a crude measure of the volume of aqueous in the tear film. In the normal eye the meniscus is 0.2–0.4 mm in height, but in dry eye becomes thin (less than 0.25 mm) or absent
- 21. • Cornea Punctateepithelial erosions that stain well with fluorescein Filaments consist of strands of mucus and debris such as shed epithelial cells Conjunctival staining in dry eye. (A) Rose Bengal (B) lissamine green one end to the corneal surface. The filaments stain well with rose Bengal but less so with fluorescein . ○ Mucous plaques with similar constituents may occur in severe dry eye. They consist of semi-transparent, white- to-grey, often slightly elevated lesions of varying size
- 22. Complications canbe vision-threatening and include epithelial breakdown, melting perforation and occasionally bacterial keratitis
- 23. 23 Slit lamp examination Increased debris/mucin strands in tear film Inspection of tear meniscus at lid margin. Normal thickness – 1mm, convex. < 0.5mm – tear deficiency. In severe cases – Marginal tear meniscus is concave, small & absent.
- 24. 24 Bulbar conjunctivalvessels may be dilated Red Eye Corneal surface – irregularity/ dry areas. Blinking – incomplete/infrequent. Meibomian gland dysfunction/ blepharitis.
- 25. 25 Diagnostic Tests Appropriatechoice of test helps the clinician to arrive at an accurate diagnosis as well as for individualization of therapy.
- 26. 26 Stability ofthe tear film as related to its break-up time (BUT). • Tear production (Schirmer, fluorescein clearance and tear osmolarity). • Ocular surface disease (corneal stains and impression cytology). There is no clinical test that allows the diagnosis of evaporative dry eye to be definitively confirmed. It is therefore a presumptive diagnosis based on the presence of associated clinical findings. It is suggested the tests are performed in the following order because the Schirmer strip paper can damage the ocular surface and cause staining.
- 27. 27 Tear film break-uptime The tear film BUT is abnormal in aqueous tear deficiency and meibomian gland disorders. Fluorescein 2% or an impregnated fluorescein strip moistened with non-preserved saline is instilled into the lower fornix. The patient is asked to blink several times. The tear film is examined at the slit lamp with a broad beam using the cobalt blue filter. After an interval, black spots or lines appear in the fluorescein-stained film indicating the formation of dry areas. The BUT is the interval between the last blink and the appearance of the first randomly distributed dry spot. A BUT of less than 10 seconds is suspicious. The development of dry spots always in the same location may indicate a local corneal surface abnormality (e.g. epithelial base- ment membrane disease) rather than an intrinsic instability of the tear film.
- 28.
- 29. 29 Schirmer test TheSchirmer test is a useful assessment of aqueous tear production. The test involves measuring the amount of wetting of a special (no. 41 Whatman) filter paper, 5 mm wide and 35 mm long. The test can be performed with or without topical anaesthesia. In theory, when performed with an anaesthetic (Schirmer 2) basic secretion is measured and without anaesthetic (Schirmer 1) it measures maximum basic plus reflex secretion. topical anaesthesia cannot abolish all sensory and psychological stimuli for reflex secretion.
- 30. 30 Excess tearsare delicately dried. If topical anaesthesia is applied the excess should be removed from the inferior fornix with filter paper. The filter paper is folded 5 mm from one end and inserted at the junction of the middle and outer third of the lower lid, taking care not to touch the cornea or lashes The patient is asked to keep the eyes gently closed. After 5 minutes the filter paper is removed and the amount of wetting from the fold measured. Less than 10 mm of wetting after 5 minutes without anaesthesia or less than 6mm with anaesthesia is considered abnormal. Results can be variable and a single Schirmer test should not be used as the sole criterion for diagnosing dry eye, but repeatedly abnormal tests are highly supportive.
- 31. 31 Normal wetting10-15 mm Dry Eye Mild 9-14 mm Moderate 4-8 mm Severe < 4 mm
- 32. 32 OTHER OCULAR STAINING Rose Bengal is a dye that has an affinity for dead or devitalized epithelial cells that have a lost or altered mucous layer Corneal filaments and plaques are also shown up more clearly by the dye and the use of a red-free filter may help visualization. A 1% solution of rose Bengal or a moistened impregnated strip can be used. The dye may cause intense stinging that can last for up to a particularly in patients with severe KCS. To minimize irritation a very small drop should be used, immediately preceded by a drop of topical anaesthetic and the excess washed out with saline.
- 33. 33 Rose Bengal Staining Positive test – show triangular stipple staining of nasal and temporal bulbar conjunctiva in the interpalpebral area & possible punctate staining of the cornea (esp. lower 2/3rd ).
- 34. 34 Rose Bengal Staining False positive – Chronic conjunctivitis Acute chemical conjunctivitis, secondary to hair spray use and drugs such as tetracaine & cocaine Exposure keratitis Superficial punctate keratitis, secondary to toxic or idiopathic phenomena. Foreign bodies in conjunctiva.
- 35. 35 Fluorescein stainscorneal and conjunctival epithelium where there is sufficient damage to allow the dye to enter the tissues.
- 36. 36 Lissamine greenstains in a similar fashion to rose Bengal but causes less irritation and may be preferred . • The pattern of staining may aid diagnosis: Interpalpebral staining of the cornea and conjunctiva is common in aqueous tear deficiency. Superior conjunctival stain may indicate superior limbic keratoconjunctivitis. Inferior corneal and conjunctival stain is often present in patients with blepharitis or exposure In dry eye syndrome lissamine green solution is preferable to 1% rose Bengal solution as it stains in a similar fashion, but causes less irritation.
- 37. 37 • Fluoresceinclearance test and the tear function index may be assessed by placing 5 μl of fluorescein on the ocular surface and measuring the residual dye in a Schirmer strip placed on the lower lateral lid margin at set intervals. Delayed clearance observed in all dry eye patients
- 38. 38 Tear filmosmolarity measurement techniques are available and are emerging as an accurate means of diagnosis. The threshold value that distinguishes between a healthy eye and an eye with dry eye syndrome varies from 305 mOsm/l and 316 mOsm/l, depending on the degree of tear film instabil- ity. A widely accepted threshold is 308 mOsm/l and a value of 316 mOsm/l appears to discriminate between mild and moderate/severe dry eye. Tear osmolarity may not correlate with ocular symptoms, but it does correlate with effective treatment when evaluated in the long term.
- 39. 39 Tear constituentmeasurement. Tear samples can be assayed for the presence of markers known to be elevated (e.g. matrix metalloproteinase-9) or decreased (e.g. lactoferrin) in dry eye. • 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 the Schirmer test but takes less time to perform.
- 40. 40 Tear meniscometryis a technique to quantify the height and thus the volume of the lower lid meniscus. • Impression cytology can determine goblet cell numbers.
- 41. 41 DEWS Dry eyeseverity grading scheme Dry Eye Severity Level 1 2 3 4 Discomfort, severity & frequency Mild and/or episodic; occurs under environmental stress Moderate episodic or chronic, stress or no stress Severe frequent or constant without stress Severe and/or disabling and constant Visual symptoms None or episodic mild fatigue Annoying and/or activity-limiting episodic Annoying, chronic and/or constant, limiting activity Constant and/or possibly disabling Conjunctival injection None to mild None to mild +/- +/++ Conjunctival staining None to mild Variable Moderate to marked Marked Corneal staining severity/ None to mild Variable Marked central Severe punctuate erosions
- 42. 42 Dry Eye Severity Level1 2 3 4 Corneal/tear signs None to mild Mild debris, ↓ meniscus Filamentary keratitis, mucus clumping, increased tear debris Filamentary keratitis, mucus clumping, increased tear debris, ulceration Lid/meibomian glands MGD variably present MGD variably present Frequent Trichiasis, keratinization, symblepharon TBUT (sec) Variable ≤ 10 ≤ 5 Immediate Schirmer score (mm/5 min) Variable ≤ 10 ≤ 5 ≤ 2
- 43. 43 Aims of Treatment Relieve discomfort Provide smooth optical surface Prevent structural ocular surface damage
- 44. 44 Modalities of treatment Preservation of existing tears Reduction of tear drainage Tear substitutes Treat any other associated eye disease which predisposes to dry eye Other options
- 45. 45 Preservation of existingtears Environmental modifications such as humidification, avoidance of wind/dusty or smoky environment, avoid central heating Lifestyle/workplace modifications taking regular breaks from reading or computer use lowering computer monitor below eye level increasing blink/fast blinking exercise discontinuing medications that exacerbate DED A small lateral tarsorrhaphy – useful in incomplete lid closure.
- 46. 46 Reduction of teardrainage Done by punctual occlusion • Preserves natural tears & prolongs effect of artificial tears • Greatest value in severe KCS who have not responded to frequent use of topical treatment. • May be – o Short term occlusion o Permanent occlusion
- 47. 47 Temporary occlusion Collagenplugs are used. Dissolve in 1-2 weeks time. Initially all four puncta are occluded If epiphora occurs, then upper two plugs removed If patient is asymptomatic, then lower puncta are permanently occluded
- 48. 48 Reversible occlusion Reversibleprolonged occlusion with silicone/ long acting collagen plugs (that dissolve in 2-6 wks). Problems – Extrusion Granuloma formation Distal migration.
- 49. 49 Permanent occlusion Donein severe KCS & repeated Schirmer < 2mm Should not be done in – Patients who develop epiphora following temporary occlusion of lower puncta Young patients as their tear production tends to fluctuate Done by cautery
- 50. 50 Tear substitutes ArtificialTear Drops used. Stabilize & thicken pre-corneal tear film . Prolongs tear film B.U.T. Keeps ocular surface wet & lubricated . Helps to repair ocular surface damage Keeps ocular surface smooth
- 51. 51 Tear substitutes Drops- Frequent instillation is required Preservative free drops are better Gels – Consists of carbomers Less frequent instillation required Ointments – Contains petroleum mineral oil & used at bedtime Mucolytic agents – 5 % acetylcysteine drops QID to disperse corneal filaments & mucous plaques.
- 52. 52 Eye Drops Cellulosederivatives – o Hydroxypropyl methylcellulose o Carboxymethylcellulose [more useful in lipid or mucous deficiency] o Appropriate for mild cases. Polyvinyl alcohol – Better in aqueous deficiency Povidone Sodium chloride Hypromellose Sodium hyaluronate Polyethylene and propylene glycol
- 53. 53 Treatment of associated diseases Meibomian gland disease/ Blepharitis – Lid hygiene – warm compresses, lid massage Lid scrubs Systemic Doxycycline/ Azithromycin/ Roxitromycin Correction of eyelid abnormalities – blepharoptosis, lagophthalmos
- 54. 54 Other options Topicalcyclosporine [0.05%, 0.1%] Reduces cell-mediated inflammation of lacrimal tissue increase in goblet cells, reversal of squamous metaplasia of conjunctiva. Oral cholinergic agents (M3) like pilocarpine , cevimeline Effective in xerostomia & about 40% of KCS patients also obtain relief Botulinum toxin injection to orbicularis muscle – controls blepharospasm in severe dry eye. Sub-mandibular gland transplantation – for extreme dry eye.
- 55. 55 Level 1: Education andcounselling Environmental management Elimination of offending systemic medications Preserved tear substitutes, allergy eye drops Level 2: If Level 1 treatments are inadequate, add: Unpreserved tears, gels, ointments Steroids Cyclosporine A Secretagogues Nutritional supplements The DEWS treatment recommendations were based on the modified severity grading (based on severity level)
- 56. 56 Level 3: If Level2 treatments are inadequate, add: Tetracyclines Autologous serum tears Punctal plugs (after control of inflammation) Level 4: If Level 3 treatments are inadequate, add: Topical vitamin A Contact lenses Acetylcysteine Moisture goggles Surgery-Amniotic Membrane Transplanatation Limbal stem cell graft Keratoplasty
- 57.
Editor's Notes
- #11 Now that we understand the continuum of dry eye, how can we use this information to understand who is at risk and how best to diagnose dry eye?
- #13 Some of the predisposing factors for development of dry eye disease can be understood in view of the new disease paradigm. Aging and menopause are associated with drops in hormone (androgen) levels that lead to loss of the protective anti-inflammatory environment of the lacrimal glands. Environmental factors cause the chronic ocular surface irritation that can initiate dry eye disease when the anti-inflammatory environment is compromised. These include environmental conditions such as low humidity, wind, and high altitudes. Indoor air conditioning, heating, and air travel all produce drying environments. Surgery such as LASIK can cause sensory denervation of the cornea. Some medications that exacerbate dry eye disease are listed on the next slide.
- #15 Dry eye disease can be triggered by autoimmune syndromes. Rheumatoid arthritis and lupus patients are more susceptible to dry eye disease. Sjögren’s syndrome, characterized by altered lacrimal and salivary function, is a leading cause of dry eye disease. Lymphocytic infiltration of lacrimal glands results in secretion of inflammatory mediators (cytokines) into tears, promoting inflammation of the ocular surface. Graft vs host disease directly results in inflammation of the ocular surface.
- #16 The new dry eye disease paradigm. The underlying disease involves: Inflammation Of lacrimal glands and ocular surface Resulting in tear deficiency And tear instability due to altered composition And ocular surface irritation One disease - many triggers: Environmental insults, side effects of medications, contact lens wear have more profound effects on an ocular surface already compromised by tear insufficiency or altered tear composition LASIK cuts corneal nerves: can exacerbate pre-existing mild tear insufficiency Autoimmune syndromes cause inflammation in lacrimal glands (rheumatoid arthritis, lupus, or Sjögren’s) or on the ocular surface (graft vs host) Result: mediators of inflammation in tears, propagates to other tissues Decreased androgens in postmenopausal women Decreases/alters lacrimal production, can lead to surface inflammation Meibomian gland disease Compromises lipid layer of tear film, increased evaporation
- #18 Symptomatology of Chronic Dry Eye Disease Patients describe a variety of symptoms Typically include discomfort, blurriness, stickiness, burning, stinging, foreign-body sensation, grittiness, dryness, photophobia, itching, and redness (Lemp, 1995)
- #23 Convex concave tear meniscus
- #42 M ust have signs & symptoms. T B U T : fluroscein tear break-u p time. M G D: meibomian gland disease
- #51 Acetyl cysteine…can b used only for 2 weeks…and foul smelling.
- #54 Botulinum toxin is injected at the median canthus ---reduces tear drainage, presumably blocking lid movement.
- #56 How to make autologous serum , percentage.