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Dry eye ppt

Dry eye ppt






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    Dry eye ppt Dry eye ppt Presentation Transcript

    • 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.
    • TEAR FILM  The presence of precorneal layer of liquid was first demonstrated by Fischer in 1928.  Rollet described it as 6th layer of cornea.  Wolff was the first to describe the structure of tear film.  Tear film is a 3 layered structure-  Lacrimal secretory system has been divided into 2 parts-  a. Basic secretors- goblet cells, accessory lacrimal glands, oil glands  B. reflex secretor- main lacrimal gland
    •  The concept of the 3 layer architecture has been replaced by the concept of an integrated aqueous and mucin gel with a graded concentration of mucins under a dynamic lipid layer.  The outer lipid layer is secreted by the meibomian glands. Lid movement during blinking releases the lipid from the glands. This layer prevents evaporation of the aqueous layer and also acts as a surfactant allowing spread of the tear film. The synthesis and secretion is influenced by hormones. Androgen receptor and receptor proteins are found in the nuclei of the glands.
    •  Middle aqueous layer is secreted by the main and accessory lacrimal glands.  Accessory lacrimal glands of Krause, Wolfring and Manz produce the basal tear secretion. Androgen and Estrogen receptors have been found on these glands, androgen function is more critical.  The main lacrimal gland produces the reflex secretion in response to corneal and conj sensory stimulation, tear break up and ocular inflammation mediated via the 5th cranial nerve. Responsible for 95% of the aqueous component. It is decreased by topical anaesthesia and during sleep. The innervation of the lacrimal gland is by sympathetic, parasympathetic and sensory nerves.
    •  The functions of this layer-  1. to provide oxygen from atmosphere to the cornea  2. anti bacterial function  3. to wash away debris and noxious stimuli and allow passage to leucocytes after injury  4. to provide a smooth optical surface to the cornea. The inner mucin layer is produced by the conjunctival and corneal epithelial cells-goblet cells. Mucins are responsible for the wetting of the corneal surface. Secretory mucins (MUC 5A) are secreted by the goblet cells. The transmembrane mucins ( MUC 1 , MUC 4) form the glycocalyx and are produced by non goblet cell epithelia.
    •  Mucus is produced when the electrolyte composition of the tear film changes from normal or when it becomes hyperosmolar. Also sympathetic and parasympathetic nerves are located adjacent to the conj goblet cells and sensory stimulation of the cornea causes goblet cell mucus discharge.  The potassium concentration of the tear film is about 5 times higher than in aqueous humor or serum. The normal osmolarity is 306 +/- 2 mosm/l. it is lowest in the morning and increases as the day progresses.
    •  Dry eye is recognized as a disturbance of the Lacrimal Functional Unit (LFU), an integrated system comprising -- the lacrimal glands, ocular surface (cornea, conjunctiva and meibomian glands) and lids, and the sensory and motor nerves that connect them.  This functional unit controls the major components of the tear film in a regulated fashion and responds to environmental, endocrinological and cortical influences.
    • CLASSIFICATION OF DRY EYE  1. AQUEOUS TEAR DEFICIENT DRY EYE– lacrimal tear deficiency  a. Sjogren syndrome- primary/ secondary  b. Non sjogren syndrome- ---lacrimal gland deficiencies ---lacrimal gland duct obstruction ---reflex block ---systemic drugs  2. EVAPORATIVE DRY EYE- A. Intrinsic- meibomian gland dysfunction -- disorders of lid aperture --low blink rate --drug action b. Extrinsic- - Vit A deficiency - Topical drugs- preservatives - Contact lens wear - Ocular surface disease- Allergy
    •  Conditions associated with non-Sjogren syndrome dry eye Primary lacrimal gland deficiencies Age-related dry eye Congenital alacrima Familial dysautonomia Secondary lacrimal gland deficiencies Lacrimal gland infiltration -Sarcoidosis -Lymphoma -AIDS Graft vs host disease Lacrimal gland ablation Lacrimal gland denervation
    • Obstruction of the lacrimal gland ducts Trachoma Cicatricial pemphigoid and mucous membrane pemphigoid Erythema multiforme Chemical and thermal burns Reflex hyposecretion Reflex sensory block Contact lens wear Diabetes Neurotrophic keratitis Reflex motor block VII cranial nerve damage Multiple neuromatosis
    • Age related dry eye With increasing age, there is an increase in ductal pathology that could promote lacrimal gland dysfunction by its obstructive effect. These alterations include periductal fibrosis, interacinar fibrosis, paraductal blood vessel loss and acinar cell Atrophy.  lymphocytic glandular infiltrates were found in 70% of lacrimal glands studied and considered to be the basis of the fibrosis.  Appearances were likened to the less severe grades of Sjogren syndrome. It has been suggested that the low-grade dacryoadenitis could be caused by systemic infection or conjunctivitis or, alternatively, that subclinical conjunctivitis might be responsible for stenosis of the excretory ducts.
    •  Congenital alacrimia- Triple A syndrome ( Allgrove syndrome) – AC, alacrimia, addison‟s disease  Familial Dysautonomia- Riley day syndrome: generalized insensitivity to pain accompanied by a marked lack of both emotional and reflex tearing, within a multisystem disorder. There is a developmental and progressive neuronal abnormality of the cervical sympathetic and parasympathetic innervations of the lacrimal gland and a defective sensory innervation of the ocular surface, which affects both small myelinated (Aδ) and unmyelinated (C) trigeminal neurons.
    •  Obstruction of the lacrimal ducts- can occur following any condition causing cicatricing conjunctivitis. ( trachoma, ocp, erythema multiforme, sjs, chemical and thermal burns)  Mechanisms: -Obstruction of the ducts of the main palpebral and accessory lacrimal glands leads to aqueous-deficient dry eye. -Obstructive MGD. -Lid deformity influences tear film spreading by affecting lid apposition and dynamics.
    • Reflex hyposecretion  1. reflex sensory block- in conditions of ocular sensory loss : decreases reflex induced lacrimal secretion and reduces the blink rate. In addition there is loss of trophic support to the ocular surface due to deficient release of sub P / nerve growth factors. CAUSES: a. Infective Herpes simplex keratitis Herpes zoster ophthalmicus b. Corneal surgery Limbal incision (extra-capsular cataract extraction) Keratoplasty Refractive surgery PRK LASIK RK
    • c. Neurotrophic Keratitis d. Topical anaesthesia – decreases blink rate by about 30% and tear secretion by 60-75% e. Systemic medications Beta blockers Atropine-like drugs f. Other causes Chronic contact lens wear – hard and extended wear Diabetes mellitus – (sensory or autonomic neuropathy or due to microvascular changes in the lacrimal gland) Aging
    • Evaporative dry eye Intrinsic causes Extrinsic causes  1. meibomian gland dysfunction ( posterior blepharitis)- mc  Causes include- acne rosacea, seborrheic dermatitis, atopic dermatitis, treatment of acne with isotretinoin.  Simple/ Cicatricial  Shine and McCulley have shown that constitutional differences in meibomian lipid composition exist in different individuals. 1. ocular surface diseases- imperfect surface wetting, early tear film breakup, tear hyperosmolarity, and dry eye. a. vit A deficiency- Vit A is essential for development of goblet cells and expression of mucins. Its deficiency can also lead to lacrimal acinar damage. b. topical drugs and preservatives ( BAC)- causes expression of inflammatory cell markers leading to epithelial cell damage, apoptosis and goblet cell
    •  In subjects with high levels of cholesterol esters , esterases and lipases produced by normal lid commensals release ffa‟s and glycerides into the tear film which act as source of iritation or soap formation-“meibomian foam”. Therefore there is loss of the normal tear film phospholipids and chol esters which leads to evaporation. In blepharitis these commensals are increased in no.  2. disorders of lid aperture and lid/ globe congruity- ectropion, entropion, lagophthalmos, 2. Contact lens wear – 50% correlation between hydration of CL and dry eye symptoms is controversial.  3. Allergic conjunctivitis- include seasonal allergic conjunctivitis, vernal keratoconjunctivitis, and atopic keratoconjunctivitis - release of inflammatory cytokines lead to loss of cell surface mucins. - surface irregularities on the cornea and conjunctiva lead to tear film instability . - In chronic disease, MGD occurs.
    •  3. low blink rate- Physiological / extrapyramidal disorders (parkinson‟s) - Lid swelling can interfere with lid apposition and tear film spreading - Use of antihistaminics also contribute to dry eye.
    •  Reflex tear secretion is the initial compensatory mechanism in response to the ocular irritation but with time the chronic inflammation leads to decrease in corneal sensation which compromises the reflex response and leads to an even greater tear film instability.  Ocular protection index- TFBUT divided by Inter-blink interval (IBI) If the OPI is <1.0, the patient has an exposed ocular surface, putting them at risk for the development of the signs and symptoms of dry eye, whereas if the OPI is ≥1.0, the patient's ocular surface is tear film protected. The OPI has proven to be useful in assessing the factors that may cause or exacerbate dry eye.
    • CLINICAL FEATURES  Symptoms-  Most common symptoms include FB sensation, burning, itching, dryness, soreness, heavy lids, photophobia, ocular fatigue and reflex tearing.  These symptoms characteristically worsen during the day.  Stringy discharge, crusting of lids and transient blurring of vision can also occur.  A history of exacerbation by reading, computer use, or in windy environment is often elicited.  Enquire about contact lens use, ocular allergy, infections, and eyelid, corneal and prior refractive surgery.  Medical history includes presence of any CTD/ autoimmune disease, DM, thyroid eye disease, parkinson‟s, sarcoidosis, Bells‟s palsy, bone marrow transplant, periorbital radiation or cranial tumors.
    •  Signs  External observation of the face for acne rosacea.  Lids and lashes- examined for lagophthalmos, infrequent blinking, floppy eyelids, lid retraction, ectropion, entropion, notching, trichiasis, distichiasis.  Lid margins- observation of meibomian gland architecture and openings, presence of blepharitis, telangiectasia, scurf and position and siza of lacrimal puncta. Enlargement of lacrimal gland is checked.  Function of 5th and 7th cranial nerve has to be checked.  Conjunctiva- may show mild redness and keratinization.  Tear film- marginal tear meniscus, presence of foam or debris suggestive of MGD. In the dry eye, lipid contaminated mucin accumulates in the tear film as particles and debris that move with each blink.
    •  Cornea- a. Punctate epithelial erosions in the interpalpebral and inferior cornea. b. Mucus filaments- stain with rose bengal c. Mucus plaques- composed of mucus, epithelial cells, proteinaceous and lipoidal material.
    • TESTS USED TO DIAGNOSE AND MONITOR DRY EYE DISEASE  The tests measure the following parameters-  A. tear film stability – Break up time  B. tear production – Schirmer test, Fluorescein Clearance, Tear osmolarity  C. Ocular surface disease – corneal / conjunctival stains and impression cytology
    •  TFBUT:  it is the interval between the last complete blink and the appearance of the first randomly distributed dry spot.  Flourescein 2% or a flourescein strip moistened with normal saline is instilled in the lower fornix.  The patient is asked to blink several times.  Tear film is examined with broad beam in cobalt blue filter. The time taken for the appearance of a dark spot is noted.  The established cut off for diagnosing dry eye is < 10 sec. however, few authors have suggested a cut off of < 5 sec when small volume of fluorescein is instilled.  Abnormal in ADDE and MGD  Fluorescein BUT has important limitations. Touching of the filter paper strip to the conjunctiva can stimulate reflex tearing.
    •  The Non-Invasive Tear Film Break-up Time Test  They are called Non Invasive because the eye is not touched. Instruments such as a keratometer, hand-held keratoscope or Tearscope are required to measure NIBUT. A prerupture phase that precedes actual break up of the tear film can also be observed with some techniques. This pre-rupture phase is termed Tear Thinning Time (TTT). Measurement is achieved by observing the distortion (TTT) and/or break up (NIBUT) of a keratometer mire (the reflected image of keratometer grid). The clinician focuses and views the crisp mires, and then records the time taken for the mire image to distort (TTT) and/or break up (NIBUT). NIBUT measurements are longer than fluorescein break up time. NIBUT values of less than 15 seconds are consistent with dry eyes. TTT / NIBUT are considered to be more patient- friendly, repeatable and precise.
    •  Schirmer Test-  Assesses the aqueous tear production.  No. 41 Whatmann filter paper is placed in the lower fornix for 5 min and the amount of wetting is seen. The patient is instructed to look forward and to blink normally during the course of the test. A negative test (more than 10 mm wetting of the filter paper in 5 minutes) means normal quantity of tears. Patients with dry eyes have wetting values of less than 5 mm in 5 minutes.  Its main utility is in diagnosing patients with severe dry eyes.  Schirmer 1- is done without anaesthesia so it measures the basal and the reflex secretion.  Schirmer 2- measures the basal secretion- after putting anaesthetic  Abnormal- <10mm without anaesthesia , for diagnosis- <5 mm <6mm with anaesthesia  Sensitivity is poor : 10%- 25%
    •  Many clinicians regard the Schirmer test as unduly invasive and of little value for mild to moderate dry eyes. Other less invasive methods to assess the adequacy of tear production have been developed. The Phenol red thread test is one such test . A cotton thread impregnated with phenol red dye is used. Phenol red is pH sensitive and changes from yellow to red when wetted by tears. The crimped end of a 70mm long thread is placed in the lower conjunctival fornix. After 15 seconds, the length of the color change on the thread - indicating the length of the thread wetted by the tears -is measured in millimeters. Wetting lengths should normally be between 9mm and 20mm. Patients with dry eyes have wetting values of less than 9 mm.
    • Flourescein clearance test  5 microliter of fluorescein is placed on the ocular surface and the residual dye is measured in a schirmer strip placed on the lower lateral margin at intervals of 1, 10, 20, 30 minutes. At the end of the 30 min, i.e., the last test, Schirmer strip is inserted after nasal stimulation.The presence of flourescein on each strip is compared to a standard scale or measured using flourophotometry. In normal eyes the value will have fallen to zero after 20 minutes. Delayed clearance is observed in all dry eye states.  It allows one to determine the basal tear secretion, reflex tear secretion under nasal stimulation, and tear clearance, at the same time.
    • ATD- aq tear deficiency
    • DTC- delayed tear clearnce
    •  Vital staining-  A. Flourescein- synthesised by Baeyer in 1871 the intact corneal epithelium because of its high lipid content resists penetration of water soluble flourescein and so is not stained by it. Any break in the epithelial barrier permits rapid penetration leading to staining of the areas with denuded epithelium.  B. Rose bengal stain- :  1% liquid rose bengal is instilled into the eye. The examiner uses white light to assess the amount of staining.
    • VAN BIIJSTERVELD SCORING Intensity scored in 2 exposed conjunctival zones and cornea Score 0-3 for each zone. 0 for absent, 1 for just present, 2 for moderate staining and 3 for gross staining. Maximum score 9. Score more than 3.5 was considered abnormal. Rose bengal stains the dead or devitalized epithelial layer which have lost or altered mucous layer.
    •  C. Lissamine green- similar to rose bengal but much less irritating.
    •  Tear lysozyme levels- lysozyme is produced by the main and accessory lacrimal gland. It represents 20% of the protein content in tears. Its levels are decreased in early stages of dry eye.  Tear lactoferrin levels- it is also secreted by the lacrimal gland. Levels are decresed in dry eye. Immunoassay kits are available to measure its levels. Like „LACTOPLATE‟ It is a plate containing gel loaded with rabbit anti-human- lactoferrin antiserum. Tear-moistened filter paper discs containing lactoferrin were placed on the gel. The lactoferrin concentration could be determined by measuring the concentric ring of precipitate after 72 hours incubation at room temperature.
    •  Tear film osmolarity- the recommended cut off value is 316 mosm/ l (overall predictive accuracy of 89% for the diagnosis). In the past it has been offered as a gold standard in dry eye diagnosis, but its general utility is hindered because it needs expert technical support, available in only a small no of specialized laboratories.
    • Impression cytology It is a non invasive technique of collection of the most superficial layers of the ocular surface by applying different collecting device (usually nitrocellulose filter papers) so that cells adherent to that surface are subsequently removed from the tissue and further processed. It was first introduced in 1977 by Egbert et al. 1. A piece of filter paper is applied to the conjunctival surface for approximately 2-5 seconds. 2. The filter paper is removed from the conjunctiva in a peeling motion to ensure maximal collection of surface cells. 3. The cells are fixed using fixatives like formaldehyde , glutaraldehyde, ethanol and methanol.
    • 4. The cells that are adherent to the filter paper are stained to enhance the visibility of the goblet cells with counter staining of the epithelial cells to increase the contrast of the goblet cells. 5. The specimen is examined under a light microscope and various analyses of the visible cells are conducted.
    • NELSON‟S GRADING Grade 0: small round epithelial cells with a eosinophilic staining cytoplasm, large basophilic nuclei with an n/c ratio of 1:2, abundant goblet cells( >5oo cells/mm2) Grade 1: Slightly larger and more polygonal cells , smaller nuclei,with n/c ratio of 1:3 , goblet cells are reduced in number (350-500 cells/mm2), preserved plump , with an intensely oval shape PAS positive cytoplasm. Grade 2: even larger& polygonal epithelial cells, occasionally multinucleated with variable staining cytoplasm, small nuclei with n/c ratio 1:4- 1:5, goblet cells markedly decreased in number (100-150 cells mm2) , smaller and less intensely PAS positive. Grade 3: large &polygonal with basophilic staining cytoplasm small pyknotic nuclei ,occasionly completely absent,n/c ratio >1:6, very few goblet cells(100 cells/mm2).
    •  Squamous metaplasia involves 3 major steps- loss of goblet cells, increase in cellular stratification and keratinization  Stages- Stage0- normal cellular structure Stage 1 – partial loss of goblet cell, no keratinization Stage 2- total loss of goblet cells, increase in sixe of epithelial cells Stage 3- early and mild keratinization Stage 4 – moderate keratinization Stage 5- advanced keratinization
    • TREATMENT  A. tear supplementation- Lubricants  B. tear retention- 1. punctal occlusion 2. moisture chamber spectacles 3. Bandage Contact lenses  C. Tear stimulation- Secretagogues  D. biological tear substitutes- 1. serum 2. Salivary gland autotransplantation  E. Anti- inflammatory therapy- 1. cyclosporine 2. Corticosteroids 3. tetracyclines  F. essential fatty acids  G. environmental strategies
    • The foremost objectives in caring for patients with dry eye disease are to improve the patient‟s ocular comfort and quality of life, and to return the ocular surface and tear film to the normal homeostatic state. Although symptoms can rarely be eliminated, they can often be improved, leading to an improvement in the quality of life.
    • lubricants  The term artificial tears is a misnomer as they do not mimic the composition of human tears. Most of them function only as lubricants. Few recent ones mimic the electrolyte composition of tears.  The ideal artificial lubricant should be preservative-free, contain potassium, bicarbonate, and other electrolytes and have a polymeric system to increase its retention time.  The main variables in the formulation of ocular lubricants regard the concentration of and choice of electrolytes, the osmolarity and the type of viscosity/polymeric system, the presence or absence of preservative, and, if present, the type of preservative.
    •  A. Electrolyte composition- solutions containing electrolytes/ ions have been shown to be beneficial in treating ocular surface damage due to dry eye. Potassium and bicarbonate are most critical. Potassium is important to maintain corneal thickness, and bicarbonate promotes recovery of the epithelial barrier function and helps in maintaining the normal epithelial ultrastructure. ( hypotears , genteel eye drops)  B. Osmolarity- since the tear film in patients with dry eye is hyperosmolar, these lubricants should be hypo-osmolar but with a high colloidal osmolality. so compatible solutes like glycerin, erythritol and levocarnitine.
    •  C. Viscosity agents- macromolecule complexes added to lubricants act as viscosity agents. They increase the residence time, incresing the duration of action and penetration of the drug. Viscous agents also protect the ocular surface epithelium. Eg. CMC (mc), HPMC, HMC, polyvinyl alcohol, PEG, glycol 400, propylene glycol. Highly viscous agents have the disadvantage that they cause blurring of vision and caking and drying on eyelashes. Lower molecular wt viscous agents help to minimize these problems. ( Systane contains HP- Guar which is a gelling agent containing glycol 400 and propylene glycol.) Hyaluronic acid has also been tried as a viscosity agent.
    •  D. Preservatives- particularly BAK and disodium EDTA. Most commonly used preservative in eye drops is BAK. It has been found that its excessive use excites the inflammatory cell markers like HLA-DR and ICAM 1 and causes epithelial cell damage, apoptosis and decrease in goblet cell density. Therefore leading to decrease in mucin- MUC 5A. The toxicity is related to its concentration, frequency of dosing and the severity of dry eye. In mild dry eye it can be well tolerated even if used 4- 6 times a day but in mod- sev dry eye potential for toxicity is high due to decreased tear secretion and decreased turnover.
    •  Less toxic preservatives are now used more frequently. Like polyquad, Na chlorite( purite), Na perborate. These are „vanishing‟ preservatives. < Na chlorite - Na and Cl on exposure to UV light, Na perborate- water and oxygen on contact with tear film. >  Ointments and gels have a longer retention time as compared to artificial tears.
    • Punctal occlusion  It is of greatest value in patients with mod- sev KCS who have not responded to topical treatment. Introduced by Beetham in 1935, he used electrocautery.  1. temporary occlusion- by inserting collagen plugs into the canaliculi that dissolve in 1-2 wks. If patient is asymptomatic after 1-2 weeks permanent occlusion can be done.  2. reversible occlusion- by inserting silicon or long lasting collagen plugs that dissolve in 2-6 months. They include – FREEMAN silicon plug which is dumbbell shaped and a HERRICK plug which is shaped like a golf tee.  3. permanent occlusion- is done in patients with severe dry with repeated schirmer‟s test value less than 5 mm. it is done by coagulating the proximal canaliculus with cautery, either thermal coagulation or diode laser cautery.
    •  Beneficial outcome has been reported in 74-86% patients treated with punctal plugs.  Contraindications- 1. allergy to the materials used 2. punctal ectropion 3. pre existing NLD block 4. patients with clinical ocular surface inflammation 5. infection of lacrimal canaliculus or sac  Complications- 1. spontaneous extrusion – mc , particularly with freeman style (50%) 2. internal migration of the plug 3. biofilm formation and infection and pyogenic granuloma
    • Moisture chamber spectacles  Tsubota et al reported an increase in periocular humidity in subjects wearing these spectacles.
    • Bandage Contact lenses  They help to protect and hydrate the corneal surface in severe dry eye conditions. Silicone rubber lenses and gas permeable scleral bearing hard contact lenses can be used.
    • Tear stimulation- secretagogues  They increase the aqueous secretion or mucin production or both.  These agents are currently under investigation  They include- diquafosol, rebamipide, gefarnate, ecabet sodium, 15- HETE.  Cholinergic agonists- pilocarpine ( 5 mg qid) , cevimeline
    • Biological tear substitutes  Include serum or saliva.  They maintain the morphology and support the proliferation of primary corneal epithelial cells better than tear substitues.  Serum has been used in the concentration ranging from 20% to 100%. The efficacy is dose dependant. It is not FDA approved as yet.  Salivary gland autotransplantation can be done. But since saliva is hypo osmolar as compared to tears it can lead to microcystic corneal edema. Therefore this is indicated only in end stage dry eye disease, with schirmer test value </=1 mm, conjunctivalized surface epithelium and persistent severe pain despite punctal occlusion and hourly application of unpreserved lubricating drops.
    • Anti inflammatory therapy  Hyperosmolarity of tear film is pro -inflammatory. Inflammation leads to ocular surface disease. So, anti inflammatory agents have been evaluated for use in dry eye. These include- a. cyclosporin b. corticosteroids c. tetracycline Cyclosporin is used in the concentration of 0.1% or 0.05%. Treated eyes had approximately 200% increase in conjunctival goblet cell density. It is used in moderate to severe aqueous deficiency. Most common side effect includes burning on instillation. Other is conjunctival hyperemia. Therapeutic benefit is achieved in about a month.
    •  Corticosteroids have been reported to decrease ocular irritation, decrease corneal fluorescein staining and improve filamentary keratitis. Low dose steroid therapy can be used for short term (2 weeks) to suppress discomfort and epithelial disease secondary to inflammation. It is usually used along with or before starting cyclosporin therapy.
    •  TETRACYCLINES- they are attributed to have anti- bacterial properties ( therefore decreasing the bacteria producing lipases) , anti- inflammatory properties( by decreasing wbc chemotaxis and phagocytosis and also decreasing the activity of collagenase, phospholipase , MMP‟s and decreasing the production of IL-1 and TNF alpha) and anti- angiogenic properties.  They are therefore indicated in-  Acne rosacea  Posterior blepharitis – 100 mg doxycycline is given BD for the first week and then OD for 6-12 weeks. Some studies have suggested equal improvement with even 20 mg BD for 1-2 months.
    • Essential fatty acids  Omega 6 fatty acids are precursors of arachidonic acid and certain pro-inflammatory lipid mediators ( PGE2, LTB4), whereas omega 3 fatty acids found in fish oil ( also in walnuts, flax seeds, soyabean, tofu) inhibit the synthesis f these lipid mediators and block the production of IL 1 and TNF alpha. So they have been found to decrease the incidence of dry eye.
    • DRY EYE SEVERITY 1 2 3 4 DISCOMFORT Mild or episodic Under env stress Moderate episodic or chronic Severe frequent or constant Severe, disabling Visual symptoms None or episodic Annoying episodic Chronic / constant Constant, disabling Conj. injection None- mild None-mild +/- +/++ Conj. staining None-mild variable Moderate- marked marked Corneal staining None-mild variable Marked central Severe punctate erosions Corneal/ tear signs None- mild Mild debris, decrease meniscus Filamentary keratitis, mucus clumping, inc tear debris Fil. Keratitis, mucus clumping, inc tear debris, ulcer Lid/ meibomian glands MGD +/- +/- frequent Trichiasis, keratinizn, symblepharon TFBUT (sec) Variable </=10 </= 5 immediate
    • Treatment recommendations according to severity level Level 1: Education and environmental/dietary modifications Elimination of offending systemic medications Artificial tear substitutes, gels/ointments Eye lid therapy Level 2: If Level 1 treatments are inadequate, add: Anti-inflammatories Tetracyclines (for meibomianitis, rosacea) Punctal plugs Secretogogues Moisture chamber spectacles
    • Level 3: If Level 2 treatments are inadequate, add: Serum Contact lenses Permanent punctal occlusion Level 4: If Level 3 treatments are inadequate, add: Systemic anti-inflammatory agents Surgery (lid surgery, tarsorrhaphy; mucus membrane, salivary gland, amniotic membrane transplantation)