Keratoconjunctivitis Sicca (KCS) or Dry eye syndrome is mainly caused due to aqueous tear deficiency.
As per Dry Eye Workshop (DEWS) 2007, KCS is defined as ‘a multifactorial disease of the tear film and ocular surface that results in symptoms of discomfort, visual disturbance, and tears film instability with potential damage to the ocular surface. It is accompanied by increased osmolality of tear film and inflammation of the ocular surface’.
Tear film has three components:-
- Outer lipid layer: It is outer oily layer which retards evaporation of aqueous tears. It lubricates eyelids and prevents spillover of tears over lid margin.
- Middle aqueous layer: It supply oxygen to cornea (transparent layer covering front of eye ) and make surface smooth by filling minute irregularities. It prevents bacterial infection and also washes away debris.
- Inner mucin layer: It makes cornea wettable by aqueous in middle layer.
A defect in any component of tear film may lead to dry eye syndrome but primarily it is from aqueous tear deficiency.
Tears have smaller basic (resting) and larger reflex component. Reflex secretion occurs due to corneal sensory stimulation.
Effective spread and resurfacing, in addition to normal tear film, requires:-
- Normal smooth corneal surface.
- Normal rate of blinking.
- Congruent ocular surface and eyelid.
Many patients do not have any symptoms. Some may have noticed deficient or reduced tears on peeling onions or even being emotional.
Common symptoms are:
- Irritation of eyes
- Burning sensations of eyes.
- Foreign body sensation in eyes.
- Mucoid discharge.
- Transient blurring or fluctuation of vision.
- Excessive tearing (due to reflex secretion in response of dry eye).
- Hyperaemia (redness) of eyes.
Less common symptoms may include:
- Tired feeling or heaviness of eyelids.
A. Aqueous layer deficiency :- It can be :
- Pure KCS : Lacrimal gland alone is affected by fibrosis.
- Sjögren’s syndrome : It affects lacrimal glands, salivary glands and other mucous membranes. It is characterised by the presence of antinuclear antibody, rheumatoid arthritis and hypergammaglobulinaemia. It may be primary Sjögren’s syndrome when these changes occur in isolation or secondary Sjögren’s syndrome when associated with other diseases viz. Systemic lupus erythematosus, polymyositis, juvenile chronic arthritis or primary biliary cirrhosis.
- Lacrimal gland destruction by dysthyroid ophthalmopathy, sarcoidosis, tumour or pseudotumour.
- Surgical removal of lacrimal gland.
- Conjunctival scarring blocking excretory ducts of lacrimal gland or causing destruction of mucin secreting glands.
- Congenital absence of lacrimal gland.
- Hyposecretion of tears with increasing age.
- Vitamin A deficiency.
- Neurological lesions with sensory or motor reflex loss.
B. Dry eye due to evaporation of tears :- It can be :
- Defect in lipid layer due to dysfunction of Meibomian glands (lipid secreting glands) or blepharitis ( inflammation of lid margins).
- Defective/ reduced blinking e.g. Parkinson’s disease or extended periods of reading, computer work or driving.
- Exposure keratopathy leading to dry cornea e. g. Bell’s palsy.
- Dry eyes associated with contact lens wear.
- Environmental factors like exposure to heating, air conditioning, increased velocity of air or reduced humidity.
Dry eye should be distinguished from other diseases affecting anterior surface of the eye e.g. conjunctivitis, infectious diseases, corneal abnormalities or keratopathies. Diagnosis depends upon clinical examination of eyes and conduct of certain specialised tests.
Tear film may show :
1. Increase in mucous strands due to accumulation of lipid contaminated mucin in the tear film. Mucous debris move with blinking.
2. Normally marginal tear meniscus is about 1mm high and convex. In dry eye, it is concave or absent altogether.
3. Froth in the tear film or along the lid margin.
Corneal examination may show :
1. Punctate lesions on cornea.
2. Mucous plaque formation. These are slightly elevated lesions on cornea.
3. Corneal filaments with one end attached to cornea and are very painful.
Tear film break-up time (BUT) :
This is the interval between last blink and the appearance of first dry spot.
Fluorescein dye is instilled in the eye and patient blinks to spread it and then stops blinking. Eye is examined under cobalt blue filter. After an interval, appearance of black spots or lines indicate formation of dry areas. Formation of dry area at same spot shows local corneal abnormality and is ignored. A BUT of less than 10 seconds suggests dry eye.
Rose Bengal test :
Rose Bengal dye stains mucus, dead and devitalised cells on cornea, being produced by dry eye. Use a small drop only since it causes ocular irritation, but local anaesthesia should not be instilled to avoid false positive results.
Lissamine green test :
Lissamine green dye stains both, healthy cells not covered by mucin as well as devitalised or dead cells. It does not cause irritation and stinging sensation like Rose Bengal dye but staining is more transient.
Schirmer’s test :
This test measures wetting of special filter paper ( Whatmann No.41) ,which is 35 mm long and 5 mm wide, when placed at the junction of middle and outer third of the lower eye lid. Eye is dried gently and patient keep eyes open and blinks as necessary. It measures basic and reflex secretion(Schirmer’s test 1). But when this test is done under topical anaesthesia(Schirmer’s test 2), it measures basic secretion mainly, since it reduces reflex secretion but does not abolish it completely.
Wetting is measured after 5 minutes. Less than 10 mm of wetting without anaesthesia and less than 6 mm of wetting after anaesthesia is considered abnormal.
InflammaDry test (Rapid Pathogen Screening Inc), 2013 :
InflammaDry test is a recent, FDA approved, rapid in-office test taking less than 2 minutes. It measures inflammatory marker matrix metalloproteinase-9 levels in tears. Matrix metalloproteinase-9 level is elevated in the tears of patients with dry eye disease.
Impression cytology :
Impression cytology determines population of mucin secreting goblet cells. It helps to monitor progression of ocular surface changes leading to dry eye.
Quantitative measurement of tear components :
Measurement of tear film osmolarity or analysis of tear proteins aids in diagnosis of dry eye.
Other tests that may be used are :
a. Tear stability analysis system.
b. Tear ferning test.
c. Tear function index.
Sjögren syndrome as a cause of KCS may be excluded by appropriate immunological blood tests and biopsy of labial salivary glands.
Aim is to provide symptomatic relief to patient. A smooth corneal surface prevents its further damage and aggravation of symptoms.
Various modalities may be :
- Avoiding high room temperature to decrease evaporation of existing tears.
- Use of room humidifiers or moist chamber spectacles to reduce evaporation.
- Contact lenses may be used to protect eyes. These may be of silicone rubber or gas permeable scleral bearing hard contact lenses with or without fenestration or highly gas permeable for overnight wear.
- Lubricating supplements are the medications most commonly used. Artificial tears are used for mild to moderate KCS. These have short duration of action and therefore requires frequent instillation.Artificial tears may be of following types :
- Cellulose derivatives.
- Polyvinyl alcohol .
Other tear substitutes :
- Povidone and sodium chloride.
- Sodium hyaluronate to promote epithelial healing.
Mineral oil ointment may be used at night time before sleep.
- Mucolytic drops e.g. acetylcysteine may be used for corneal filaments and mucous plaques.
- Anti-inflammatory agents like topical corticosteroids, topical cyclosporine or topical or systemic omega-3 fatty acids (omega-3 fatty acids inhibit the synthesis of lipid mediators) may be used.
- Use of topical or systemic tetracycline.
- Use of autologous or umbilical cord serum. Serum eye drops are used in cases of severe KCS with punctate epithelial defects and corneal damage to promote reepithelisation.
- Use of systemic immunosuppressants.
- Patients with lagophthalmos (incomplete lid closure) may be benefitted with small lateral tarsorrhahy (stitching together of upper and lower lid) to preserve tears.
- Occlusion of punctum (punctum is a small hole in lids for drainage of tears from eyes to nose) is useful in severe KCS and also in those showing drug toxicity.Occlusion of punctum may be :
- Temporary: Punctum may be blocked with plug, silicone rods or even with 2/0 catgut suture. Plugs may be absorbable,nonabsorbable,hydrogel or thermoplastic. Initially, all four puncta are blocked. This is to assess whether blockage leads to tearing or not. Based on the results, permanent occlusion may be planned
- Permanent: This is undertaken for severe KCS with Schirmer’s test value consistently being 2mm or less. It is done with gentle heating of proximal canaliculus ( small passage connecting punctum to the lacrimal sac) with cautery at black heat or by Argon laser. Permanent occlusion should be avoided in young patients due to fluctuating tear amount.
- Conjunctival flap may be pulled over to prevent dryness and its complications.
- Mucous membrane grafting.
- Amniotic membrane transplantation may be done.
- Salivary gland duct transposition for lubrication.
- Descemetocele (thin and bulging cornea), impending or frank perforation may be covered with tissue adhesive cyanoacrylate, corneal or corneoscleral patch.
Complications are usually not there or are minimal in mild to moderate KCS.
Severe cases may show :
b. Breakdown of epithelial layer covering front of eye.
c. Superficial peripheral vascularisation of cornea.
d. Secondary bacterial infection of cornea.
e. Descemetocele formation.
f. Melting of cornea.
g. Corneal perforation and its sequlae.
- 2007 Report of the international Dry Eye WorkShop. Ocul Surf. 2007; 5(2):65-204
- Kanski, Jack J; Bowling, Brad. Synopsis of Clinical Ophthalmology. Third Edition. Saunders Ltd., 2012.