DRY EYEDry 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The concept of the 3 layer architecture has been replaced by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 eyeIntrinsic 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

loss

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,

eyelid coloboma, proptosis

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.

CAUSATIVE MECHANISM OF 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 SCORINGIntensity scored in 2 exposed conjunctival zones and corneaScore 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 GRADINGGrade 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.

FREEMAN SILICON PLUG

HERRICK’S INTRA CANALICULAR PLUG

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

Schirmer score (mm/5 min)

Variable </=10 </= 5 </= 2

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)