Dry eye syndrome

ppt on DED and its mgt

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)

2. Out line Introduction Definition Classification Pathophysiology Presentation Diagnosis Treatment

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. 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. 7/15/2018 7

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 .

8. 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). 7/15/2018 9

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). 7/15/2018 10

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. 7/15/2018 11

11. Cont.. Extrinsic ○ Vitamin A deficiency. ○ Topical drugs including the effect of preservatives. ○ Contact lens wear. ○ Ocular surface disease such as allergic conjunctivitis 7/15/2018 12

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

13. 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.

14. 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

15. 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

16. 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

17. 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

18. Conjunctiva Squamous metaplasia Goblet cell reduction Conjunctivochalasis Lacrimal gland Loss of secretory acinar cells Fibrosis and gland atrophy

19. Meibomian gland MGD Eyelids Keratinization, thickening and neovascularization Blepharitis Recurrent Chalazion

20. Tear film Tear Hyperosmolarity Tear film instability Delayed tear clearance Increased tear film evaporation Immune cells CD4 T cells are common Th1 and Th17

21. 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

22. 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.

23. 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

24. Medical hx Smoking Dermatologic conditions Menopause Atopy Systemic inflammatory conditions Trauma Radiation of orbit Neurologic condition Dry mouth, dental cavity and ulcers

25. 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

26. 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 punctate staining

27. Cornea Interpalpebral drying Punctate staining Thinning Infiltrates Mucus plaque Filaments Keratinization Pannus formation, scaring, ulceration and NV

28. Diagnostic testes Testes for patients with underlying systemic condition

29. 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

30. 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

31. 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

32. Lissamine green Have similar staining characteristic of Rose Bengal Much better tolerated than Rose Bengal In summery

33. 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 Place whatman #41 paper at the junction of the middle and lateral thirds of the lower eyelid of each eye Ask the patient to look forward and blink normally while the strip is held in place for 5 minutes 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 7/15/2018 35

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35. 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 7/15/2018 37

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37. 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 7/15/2018 39

38. 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

39. 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

40. 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

41. 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

42. 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%

43. 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 I t also block the proinflammatory eicosanoids and cytokines

44. 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

45. 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

46. 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

47. 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

48. 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

49. reference Bcsc , Section 8 Kanski 8 th edition Practical ophthalmology for beginners Dry eye syndrome ppp by AAO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCE eyewiki.com Thank u