dry eyes
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Dry Eye Disease
DR SARANSH JAIN 24/06/2015
Outline of presentation
INTRODUCTION
LACRIMAL FUNCTION UNIT PATHOPHYSIOLOGY
EPIDEMIOLOGY
CLASSIFICATION/GRADING
CLINICAL FEATURES AND EVALUATION
MANAGEMENT
INTRODUCTION
• Dry eye is a multifactorial disease of the tears and the ocular surface that results in symptoms of discomfort, visual disturbance, and tear film instability with potential damage to then ocular surface.
• accompanied by increased osmolarity of the tear film and inflammation of the ocular surface
*2007 Report of the Dry Eye Work Shop (Ocul Surf 2007;5[2]:65-204)
• Ocular surface- entire sheet of epithelium which extends from grey line back over the lid margin onto the back of eyelids, inferior fornix up over the globe and onto cornea
Dry eye is a disturbance of Lacrimal Function Unit (LFU)
•Tearing apparatus
–Production- lacrimal gland
–Clearance- lacrimal passages
•Ocular surface–Conjunctiva –Cornea
•Eyelids•Sensory and motor nerves
Tear and the Tear Film
• Function :Maintain a smooth corneal surface
Moistens cornea and conjunctiva
Lubrication of pre-ocular surface and lids
Transfer of oxygen to cornea from ambient air
Prevents infection
NORMAL TEAR FIM
BIOCHEMISTRY
PHYSICALPROPERTIES
CHEMICAL COMPOSITION
PH- 7.2-7.7
OSMOLARITY -305
REFRACTIVE INDEX – 1.357
TEAR VOLUME- 5-10µl
LIPIDS
PROTEINS
METABOLITES
ELECTROLYTES
ENZYMES
98.2% WATER
Meibomian gland
Lacrimal gland
Ocular Surface Epithelium
Lid Blinking
Lid Closure
Lipid Layer
Aqueous Layer
Mucin Layer
Tear Spread
Evaporation
Tear Clearance
Normal tear film and ocular surface
HEALTHY TEARS TEARS IN CHRONIC INFLAMATION
Solomon et al. Invest Ophthalmol Vis Sci. 2001.Zhao et al. Cornea. 2001.Ogasawara et al. Graefes Arch Clin Exp Ophthalmol. 1996.
Image adapted from: Dry Eye and Ocular Surface Disorders. 2004.
*2007 Report of the Dry Eye Work Shop (Ocul Surf 2007;5[2]:65-204)
PREDISPOSING FACTORS
DRY EYE
Ageing
Allergy
Environmental
Medications
Ocular Surgery
Menopause
HEALTHY EYE FUNCTIONING
Stern et al, Cornea. 1998:17:584
NORMAL TEARINGDEPENDS ON A
NEURONAL FEEDBACK LOOP
Secretomotor Nerve
Impulses
Tears Support and Maintain
Ocular SurfaceLacrimal
GlandsOcular SurfaceNeural
Stimulation
IN DED:IMMUNE MECHANISMINFLAMMATION
DISRUPTSNORMAL NEURONAL
CONTROL OF TEARING.
Lacrimal Glands:
• Neurogenic Inflammation
• T-cell Activation
• Cytokine Secretion into Tears
Interrupted Secretomotor
Nerve Impulses
Tears Inflame Ocular Surface
Cytokines Disrupt Neural
Arc
Stern et al, Cornea. 1998:17:584
Major etiological causes
Dry eye-keratoconjunctivitis sicca
Tear deficiency
Sjögren’s syndrome
Non-Sjögren tear deficiency
Rheumatoid arthritis Systemic lupus erythematosusWegener’somatosis Systemic sclerosis Primary biliary cirrhosis Other autoimmune diseases
Lacrimal disease
Lacrimal obstruction
Reflex
Congenital alacrimaAccquired primary lacrimal gland disease
Trachoma, cicatricial pemphigoidErythema multiformeBurns
Neuro-paralyptic keratitisContact lensVIIth nerve palsySarcoid HIV
Graft vs host Xerophthalmia Other diseasees
Dry eye-keratoconjunctivitis sicca
Evaporative
Oil Deficient
Lid related
Contact Lens
Surface change
Absent glands Distichiasis
Posterior blepharitisObstructive meibomionGland disease
Anterior blepharitis
Blink abnormalities
Lid surface incongruity
Apertureabnormalities
Xerophthalmia
SYMPTOMS
AAO GUIDELINES FOR PATIENTS OCULAR HISTORY
• Contact lens use, lens material, solutions, wearing schedule, lens care.
• Allergic conjunctivitis
• Corneal history (prior keratoplasty, LASIK, photorefractive keratectomy, radial keratotomy, or extracapsular cataract extraction)
• Punctal plugs or surgery
• Eyelid surgery (prior ptosis repair, blepharoplasty, entropion / ectropion repair)
• Chronic ocular surface inflammation (acid or alkaline burns, ocular cicatricial pemphigoid, or Stevens-Johnson syndrome)
AAO GUIDELINES FOR PATIENTS MEDICAL HISTORY
• Smoking, menopause, and atopy
• Dermatological diseases (including seborrhea, eczema, rosacea)
• Trauma (including exposure to chemicals, ultravoilet light, dust, sawdust, fumes)
• Systemic inflammatory diseases (Sjögren’s syndrome, rhematoid arthritis, systemic lupus erythematosus, scleroderma, graft-versus-host disease)
• Chronic viral infections, such as chronic hepatitis C or human immuno deficiency virus.
• Surgery (bone marrow transplant, head and neck surgery)
• Radiation of orbit
• Neurological conditions (including Parkinson’s disease, Bell’s palsy, and Riley-Day syndrome)
• Xerostomia (dry mouth) dental cavities, and oral ulcers
AAO GUIDELINES FOR PATIENTS PHYSICAL EXAMINATION
• Skin (scleroderma, facialchanges indicating rosacea)
• Eyelids (incomplete closure / malposition, erythema of eyelid margins, incomplete / infrequent blinking, abnormal deposits / secretions, entropion, ectropion)
• Adnexa (enlargement of lacrimal glands)
• Proptosis
• Cranial nerve function (including cranial nerve V VII)
• Disorders affecting the hand (joint deformities characteristic of rheumatoid arthritis, gout, or psoriasis)
AAO GUIDELINES FOR PATIENTS SLIT LAMP EXAMINATION
• Tear film (height of meniscus, debris, foam)
• Eyelashes (trichiasis, distichiasis, madrosis, deposits)
• Anterior / posterior eyelid margins and character of meibomian gland secretions
• Vascularisation crossing the mucocutaneous junction, ketatini-zation, and scarring
• Puncta (patency and position)
• Conjunctiva (inferior formix and tarsal conjunctiva and bulbar conjunctiva)
• Cornea (localized interpalpebral drying, punctuate epithelial erosions, filaments, microepitrlial defects, punctate staining with rose bengal or fluorescein dyes, mucous plaques, keratinization, pannusformation, thinning, infiltrates, ulceration, neovascularisation, and scarring)
EVALUATION OF DED• Eye lids:
Lid marginEye lashes InfectionsCrusting/keratinisationLid closure
• Conjunctival sac:Decreased tear meniscus Increased debris in the tear filmMucous discharge
• Bulbar conjunctiva: dry lustreless Muddy Bitot’s spotshyperaemia
• Cornea:
– Dry lustreless, hazy look
– Irregular surface
– Superficial punctuate keratitis (Fluorescein staining may be helpful)
– Filaments
– Ulcers/scars in severe cases
DIAGNOSTIC TESTS
• Aims :
– Tear secretion assessment– Tear volume assessment– Tear clearance assessment– Evaluation of tear film stability– Ocular surface damage assessment
Tear secretion assessment
• Schirmer’s test– Schirmer’s I :
Conjunctival stimulation
– Schirmer’s II : Nasal stimulation
– Schirmer’s III: Retinal stimulation
– Jones’ modification : Basal secretion
(2mts. After LA)
Tear clearance assessment
• Fluorescein clearance test• Basal tear secretion• Reflex tear secretion• Tear clearance
• Fluorophotometry
• Tear function index
Tear volume assessment
• Tear meniscus height
Evaluation of tear film stability
• Tear film break-up time (TBUT)• Fluorescein TBUT• Non-invasive TBUT
• Lipid layer assessment
NIBUT
• Corneal Topography
• Interferometry
• Aberrometry
• Functional visual acuity assessment
• Confocal microscopy
LIPIVIEW INTERFEROMETER TEAR FILM TOPOGRAPHER
WAVEFRONT ABERROMETER
LIPID LAYER ASSESSMENT
a) slit lamp b) Meiboscopy c) Meibography d) Meibometry
Ocular surface damage assessment
• Staining
• Corneal sensitivity
• Impression cytology
• Tear osmolarity
• Tear protein assays
• A vital dye which has no intrinsic toxicity.• Detects epithelial defects & irregularities.• Filter paper strips or 0.25% - 2% solution.• Sodium fluorescein emits green light(520nm) when
excited with with blue light (490nm).
Sodium fluorescein
Rose bengal
• Rose bengal is a vital stain taken up by dead and devitalised epithelial cells.
• Also stains mucous threads, filaments & strands .• Does not diffuse into the epithelial defects or penetrate
corneal stroma like fluorescein.• It is toxic resulting in decreased cell vitality, motility & cell
death.• Causes ocular discomfort –prior anaesthesia is needed.
Score 0 - absent Score 1-just present Score 2-moderate staining Score 3-gross staining
• Dark green, water soluble
• Degenerated cells, mucus, dead cells
• Less irritating
Lissamine green
Deficient values
Parameters Normal Values
Mild Medium Severe
Lysozyme 1.75 g/l <1.5 <1 <0.5
Lactoferrin 1.75 g/l <1.5 <1 <0.5
IgA 240 mg/l <120 <120 <120
Osmolarity 300-310 mOsm/l
320 330 340
DRY EYE : SEVERITY GRADING SCHEME
The ocular surface April 2007; vol 15 no 2 :
MANAGEMENT
• Goals of management:– Establish the diagnosis.– Differentiate from other causes of
similar symptoms.– Establish presence/absence of limbal
cell deficiency.– Decide appropriate therapy.
• To relieve symptoms• To prevent complications
– Educate patient / relatives about nature of disease and its management.
TREATMENT
Psychological control of surrounding
medical surgical
APPROACH TO TREATMENT
• Elimination/avoidance of exacerbating factors which
• Decrease tear production• Increase tear evaporation
– Humidification of rooms– Avoidance of dusty/smoky rooms– Breaks between prolonged computer use– Lowering the computer monitor below eye level– Low water content contact lenses for Shorter duration at
a time.– Blinking exercises*
• *Wolkoff P et al. Occup Environ Med 2005;62:4-12
Eyelid hygiene
– Hot fomentation– Topical/systemic antibiotics– Topical steroids/CyclosporineA– Artificial tear substitutes
1.Tear supplementation
• Be preservative free
• Contain K+, HCO3- and other electrolytes
• Have a polymeric system to increase its viscosity, hence retention time
• Have neutral to slightly alkaline Ph
• Have osmolarity- 181-354 mOsm/L
• Gels (carbomers) require less frequent application than drops.
• Ointments using petrolatum, lanolin and mineral oil base, dissolve at the temperature of ocular tissue, retained in the cul-de-sac for long - used mainly at night time.
Anti-inflammatory therapy
• Topical cyclosporine(0.05%-0.1% - two to four times a day)• Only pharmacological agent approved by FDA for treatment of dry eye• Reduces conjunctival IL-6 levels, activated lymphocytes, inflammatory
and apoptotic markers• Increases conjunctival goblet cell number
• Corticosteroids• Recommended only for short-term use
• Systemic medications• Oral tetracyclines (used for anti-inflammatory action)
– Decrease matrix metalloproteinase activity and production of cytokines such as IL-1 and TNF-ɑ
A stagnant and unstable tear film who continue to have symptoms that are not relieved by artificial tears AND/OR corneal epithelial disease.
Newer treatment modalities
• Ocular inserts6-
• Cylindrical rod containing 5mg Hydroxypropyl methyl cellulose (HPMC) placed in the lower cul-de-sac.
• Imbibes fluid and swells
• Lasts for 12 -24 hrs
• Secretagogues
• Stimulate endogenous tear production
• Oral pilocarpine (Salagen) 5mg four times a day7 – cholinergic side effects.
• Cevilemine – Fewer side effects
Newer treatment modalities
• Mucolytic agents as acetylcysteine 5% drops used in patients with corneal filaments and mucous plaques.
• Autologous serum drops [diluted 1:3 with saline] have reported to reduce ocular irritation and conjuntival and corneal dye staining in Sjogren’s syndrome associated aqueous tear deficiency.
• Tear retention–Punctal occlusion: Temporary
and Permanent.• Absorbable
– collagen or polymers– Duration- 1 week- 6 months
• Nonabsorbable– Silicone or acrylic
–Moisture chamber spectacles–Contact lenses
• Severe dry eye– Retain tear film– Promote ocular surface healing
–Tarsorrhaphy
Surgical options
• Reserved for severe-very severe dry eyes
• Tarsorrhaphy
• Mucous membrane grafting
• Salivary gland transposition
• Amniotic membrane transplantation
NEWER DRUGS ON THE BLOCK
– Tear stimulation: secretogogues• Diquafosol (P2y2 receptor agonist)• Ecabet sodium (mucous secretion
stimulant)• Rebamipide• Gefarnate
– N-acetyl-cystine eye drops.– Chloroquine Phosphate eye drops
(0.3mg/ml). – Lacriserts, collagen shields.– Androgen ointment.
SUMMARY
• Eliminating the etiological factors
• Tears replacement therapy
• Maintain moisture in the eyes
• Increasing the tear secretion
• Immune inhibition therapy
• Re-establish the tear film
• Other supporting treatment
CARRY HOME MESSAGE…
• Methodical approach to diagnosis.
• Do not miss subtle clinical signs.
• Carefully plan the line of treatment.
• Irrespective of cause of dry eye- immunomodulation + tear replacement.
• Educate the patient and family members about the dilemmas in management.
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