Dry eye

By: Manal Al-Romeih

definition

A condition that occurs when there is:

Inadequate tear volume

Unstable tear film

Ocular surface disease

Keratoconjunctivitis sicca (KCS)

Tear film consists of:

• Lipid layer evaporarive dry eye.

• Aqueous layer

• Mucin layer aqueous deficiencies & evaporative states.

Tears in Chronic Dry Eye↓ water, ↑salts, ↓proteins

↑Electrolyets ↑osomlarity

↓ lipocalins (lipid-binding proteins)

↑ surface tension

↓ lysozyme ↑ inflammation

susceptability

Proteases activated

Cytokines:

Protein protective mechanism

↑ IL-1β (excitatory, initiates the fight,

irritation)

↓ IL-1RA (inhibitory)

↑ TGF ↑ inflammation

Factors affecting resurfacing of tearfilm:

• Normal blink reflex

• Contact between external ocular surface & eyelids

• Normal corneal epithelium

Regulation of tear film component:

Hormonal:

• Androgens lipid production.

• Oestrogen & progesterone receptors in conjunctiva & lacrimal glands normal tissue function.

Neural:

• Adjacent fibers to lacrimal glands & goblet cells aqueous/ mucus secretion.

:Lacrimal gland innervation

12 Cranial nerves:

2nd Optic: vision (II)

3rd Oculomotor: eyelid and eyeball movement (III)

4th Trochlear: motor for vision (turns eye downward & laterally) (IV)

5th Trigeminal: chewing, face and mouth touch and pain

6th Abducens: motor to lateral rectus muscles (VI)

7th Facial: controls most facial expressions , taste, secretion of tears & saliva (VII)

Trigeminal 5th The ophthalmic nerve (V1) carries sensory information from the scalp and forehead, the upper eyelid, the conjunctiva and cornea of the eye, the nose, the nasal mucosa, the frontal sinuses, and parts of the meninges.

Classification

Aqueous layer deficiency

Sjogrensyndrome

Non-Sjogren

evaporative

Meibomianglands disease

exposure

Defective blinking

Contact lens associated

Enviromentalfactors

Causes of Non-Sjogren KCS1. Primary age-related hyposecretion

2. Lacrimal tissue destruction:

• Tumour

• Inflammation

3. Absence/ reduction of lacrimal gland tissue:

• Surgical removal

• Rarely congenital

4. Conjunctival scarring with obstruction of lacrimalgland ductules:

• Chemical burns

• Cicatrical pemphigoid

• Stevens- Johnson syndrome

• Old trachomas

5. Neurological lesions with sensory or motor reflex loss:

• Familial dysautonomia

• Parkinson’s disease

• Reduced sensation after refractive surgery & CL wear

6. Vitamin A deficiency

Causes of evaporative KCS:

1- Meibomian gland dysfunction:

• Posterior blepharitis

• Rosacea

• Atopic keratoconjunctivis

• Congenital meibomian gland absence

2- lagophtalmos:

• Severe proptosis

• Facial nerve palsy

• Eyelid scarring

• Following blepahroplasty

3- miscellaneous:

• CL wear

• Enviromental factors

Symptoms

• Feeling of dryness

• Grittiness & burning that worsen during the day

• Stringy discharge

• Transient blurring of vision

• Redness & crusting of the lids

Signs

1. Posterior blepharitis & meibomian gland dysfunction

2. Conjunctivamild keratinaization & redness

3. Tear film:

• Particles & debris of accumlated lipid-contaminated mucin.

• Thin/ absent tear meniscus

• Forth in tear film or along lid margin//meibomian gland dysfunction.

4. cornea:• Punctuate epithelial erosions (interplabebral &

inferior cornea)• Filaments of mucus strands• Mucus plaques

5. complications:Peripheral superficial corneal neovascularizationEpithelial breakdownMeltingPerforationBacterial keratitis

Diagnosis - parameters• Tear film stability:

break-up time ≥ 10 sec

• Tear production:

- Schirmer 10mm/ 5min c anesthsia,

6mm sc

- fluorescein clearance &tear osmolarity

• Ocular surface disease:

Corneal stains & impression cytology

Break-up time Schirmer test ocular surface staining

The pattern of staining

1- Aqueous tear deficiency interpalpebralstaining of the cornea & conjunctiva.

2- Superior limbic keratoconjunctivitissuperior conjunctival stain.

3- Bleparitis / exposure inferior corneal & conjunctival stain.

Rose Bengal staining inEarly, Moderate and Late KCS

EARLY MODERATE LATE

Treatment

• Not curable

• Control the symptoms & prevent surface damage.

• Choice of treatment depends on severity of the case and source of it.

Blepharitis/ meibomian gland dysfunction management:

Lid hygiene:

Warm compresses.

Lid scrubs.

Antibiotics:

Topical: sodium fusidic acid, bacitracin, chloramphenicol.

Oral: azithromycin, tetracycline.

Weak topical steroids: fluorometholone.

Tear substitutes, Lubricating drops.

Omega 3 supplements.

Patient education:

• Realistic expectation of outcome.

• Emphasis on importance of compliance.

• Avoidance of toxic drugs or enviromentalfactors .

• Discontinuation of toxic topical medication if possible.

• Review of work enviroment.

• Emphasis on importance of blinking wilstreading & using VDU.

• Aids should be provided for patients with a loss of dexterity.

• Caution against laser refractive surgery.

• Discussion of management of CL intolerance.

Tear subtitutes:

1- Drops & gels:

• Mild cases cellulose derevatives.

• Mucin defeciency polyvinyl alcohol (↑persistence of tear film).

• Severe cases autologous serum.

• Carbomers cling to eyelids & are longer lasting.

• Sodium hyaloronate maybe useful in promoting conjunctival & corneal epithelial healing.

• Povidone & sodium chloride.

Tear substitutes:

2- Ointment:

Petrolatum mineral oil.

Used at bed time.

3- Mucolytic agents:

Useful in patients c corneal filaments & mucus plaques

Acetylcysteine 5% drops q.i.d

It may cause irritation

Malodorous

Limited bottle life 2 wks max

Medication

Type of KCSName Formulation

Evaporative lubricants

HYDROXYETHYLCELLULOSE, SODIUM CHLORIDE:MINIMS ARTIFICIAL TEARSSODIUM CARBOXY METHYLCELLULOSE, GLYCERIN:OPTIVE LUBRICANT EYE DROPSCARBOXYMETHYLCELLULOSEREFRESH LIQUIGEL 1% EYE DROPSREFRESH PLUSREFRESH TEARS 0.5% EYE DROPS

Cellulose derevatives

Aqueous deficiencyCARBOMERS (POLYACRYLIC ACID):LACRYVISC EYE GELPOLYACRYLIC ACID:VISCOTEARS OPTH.GEL

Carbomers

Aqueous deficiencyPolyvinyl alcohol, Povidone

Aqueous deficiencySODIUM CHLORIDE:APISAL 0.9% EYE-NOSE DROPSSODIUM CHLORIED, HYPROMELLOSE:OCULAC

Sodium chloride

Aqueous deficiency-SODIUM HYALURONATE, DEXPANTHENOL-HYLO-COMOD 0.1% EYE DROP-HYFRESH 2 MG- ML OPHTHALMIC SOLUTIONHYALURONATE:HYFRESH 2 MG- ML OPHTHALMIC SOLUTION

Sodium hyaluronate

Aqueous deficiencyHYPOTEARS OPHTHALMIC GELVitamin A (retinol), polyacrylic acid,cetramide

Evaporative Lipids & oils

Mucus deficiencyAcetylcysteine (mucolyctic)

Punctal occlusion:

To reduce drainage In moderate to severe cases

Temporary:

Inserting collagen plugs into the canaliculi that dissolve in 1-2 wks.

To ensure non-occurance of epiphoria following permanent occlusion.

Occlusion of inferior puncta review after 2 wks No symptoms permanent occlusion.

In severe KCS

plug of both inferior & superior canaliculi.

Punctal occlusion:

Reversible:

Prolonged occlusion (plugs that dissolve in 2–6 months.

Can cause extrusion, granuloma formation & distal migration.

Permanent:

Only in severe dry eye with schirmer test of 5mm or less.

Positive response to temporary plugs without epiphora.

Not in pt c reversible pathology.

Performed after punctal dilatation.

Lacrimal drainage.

Cannula inserted in lower punctum after dilation. Cannula is swung towards the temporal side before saline is released.

On removing the cannula. The punctum is now wide and open.

Anti-inflammatory agents:

1- Low dose topical steroids:

Supplementary treatment for acute exacerbations.

Balance the risk of long-term ttt against benefit of increased comfort.

2- Tropical ciclosporin:

↓ T-cell mediated lacrimal tissue inflammation ↑ no. of goblet cells.

3- Systemic tetracyclines:

Control associated blepharitis & reduce inflammatory mediators in the tears.

Contact lenses:

Reservoir effect of fluid trapped behind the lens.

Low water (Hema) moderate cases.

Silicone (No water) to protect cornea in extreme cases

Occlusion gas permable scleral CL reservoire of saline over the cornea (extremly dry).

Conservative of existing tears

1. Reduction of room temperature:

Avoiding central heating to minimize tearevaporation.

2. Room humidifiers.

3. Moist chamber goggles.

4. Side shields to glasses.

Other options

1. Tarsorrhapy reducing palbebral aperture.

2. Botulinum toxin injection control blepharospasm.

3. Oral chlinergic agonists Pilocarbine (5mg q.i.d), Sjogren.

4. Zidovudine antiretroviral agent, Sjogren.

5. Submandibular gland transplantationextreme dry, requires surgery, produceunacceptable level of mucus in the tear film.

Dry eye medication in

the Saudi market:Cellulose derivatives:

Carboxymethylcellulose Sodium 0.5%

Aqueous insufficiency & lubricant.

Systane:

Polyethylene Glycol 400 0.4% (lubricant)

Propylene Glycol 0.3% (lubricant)

Hydroxypropyl Guar (GEL FORMING MATRIX)

Polyquaternium-1 as preservative

Enhance the mucus layer.

Tears Naturale Free:

0.3% HPMC (hydroxypropyl methyl cellulose), 0.1% Dextran 70Preservative-Free.

Aqueous deficiency

HYLO-COMOD lubricant eye drops:

sodium hyaluronate (1mg in 1ml), citric buffer and sorbitol

Aqueous deficiency

Hyfresh eye drops:

sodium hyaluronate

Aqueous deficiency

Optifresh eye drops:

Polyvinyl Alcohol : 14.0 mg, Povidone : 6.0 mg,

Chlorobutanol (as preservative), Sodium Chloride, HCI and / or Sodium hydroxide and Water for Injection.

Aqueous deficiency

Viscotears:

Polyacrylic acid

carbomer

Aqueous deficiency

Thank you!