Dry Eye (Keratoconjunctivitis Sicca, KCS)


The 2017 International Dry Eye Workshop (DEWS II) has provided the following definition: Dry eye is a multifactorial disease of the ocular surface characterised by a loss of homeostasis of the tear film, and accompanied by ocular symptoms, in which tear film instability and hyperosmolarity, ocular surface inflammation and damage, and neurosensory abnormalities play aetiological roles.

Dry eye disease (DED) consists of two predominant categories; aqueous deficient dry eye (ADDE) and evaporative dry eye (EDE). Epidemiological and clinical evidence suggests that the majority of DED is evaporative in nature. Although ADDE can occur without EDE and vice versa, commonly the two categories co-exist.

ADDE and EDE can be sub-classified as follows:

1. Aqueous-deficient Dry Eye (ADDE)

  • Sjögren Syndrome Dry Eye (SSDE) I
  • Non-Sjögren Syndrome Dry Eye (NSDE)

2. Evaporative Dry Eye (EDE)

The core mechanism of DED pathology is tear hyperosmolarity, which damages the ocular surface directly and initiates an inflammatory cascade leading to further ocular surface damage and loss of tear film homeostasis. There is often a poor correlation between clinical signs and symptoms.

Predisposing factors

Wide variation in prevalence estimates worldwide (6.5% to 52.4%) due to clinical and methodological heterogeneity across studies; there is a higher prevalence in post-menopausal women, people of East Asian ethnicity and generally with increasing age.

Prevalence rises with age, between 2.0% and 10.5% per decade

Several medication classes are associated with aqueous tear deficiency e.g., diuretics, antihistamines, and antidepressants

Autoimmune diseases such as Sjögren’s syndrome, ocular cicatricial pemphigoid, rheumatoid arthritis and systemic lupus erythematosus are often linked to DED

Other systemic disease associations e.g. diabetes, thyroid eye disease, Stevens-Johnson syndrome

Corneal and conjunctival surface irregularities

Factors that initiate or aggravate symptoms include:

  • vitamin A deficiency
  • noxious agents (cooking fumes, tobacco smoke)
  • increased evaporation of tears (air conditioning, central heating, low humidity)
  • digital device use (reduced blink frequency and/or blink incompleteness)
  • corneal refractive, and eyelid surgery
  • contact lens wear
  • conjunctivitis medicamentosa (particularly long-term topical therapy)

Symptoms of dry eye

Symptoms in DED can be assessed using several validated tools, including the Dry Eye Questionnaire 5 (DEQ5) and Ocular Surface Disease Index (OSDI).

Symptoms typically variable, bilateral and may include:

  • ocular irritation
  • foreign body, gritty or burning sensation
  • presence of a stringy mucous discharge
  • blurring of vision from epithelial disruption or (transiently) from reflex tearing
  • symptoms exacerbated by smoke, wind, heat or prolonged near activities (e.g. digital device use); may worsen throughout the day
  • symptoms may not be described as a feeling of dryness
  • associated symptoms of dry mouth, systemic disease (e.g. Sjögren’s syndrome, rheumatoid arthritis)

Signs of dry eye

  • reduced tear meniscus at inferior lid margin (following the instillation of fluorescein, normal meniscus is not less than 0.2 mm in height)
  • fluorescein break up time (FBUT) <10 sec
  • raised tear osmolarity (308 mOsm/l is the most sensitive threshold to distinguish normal from mild/moderate DED, while 315 mOsm/l is the most
    specific cut-off)
  • Schirmer test (without anaesthesia) ≤ 5mm in 5 min; may be helpful in the diagnosis of severe ADDE, but of limited value in mild ADDE or EDE
  • punctate epithelial erosions in exposed area of cornea and bulbar conjunctiva (especially in inferior third of palpebral aperture). Stain with vital dye(s) as available. Various grading systems are available (e.g. Oxford staining score)
  • bulbar and limbal conjunctival hyperaemia
  • lid wiper epitheliopathy
  • increased mucus strands and other tear film débris
  • filaments (adherent comma-shaped mucus strands)
  • mucus plaques
  • Dellen
  • Corneal thinning and (very rarely) perforation
  • reduced corneal sensitivity

Differential diagnosis

Anterior blepharitis
Allergic and infective conjunctivitis
Eyelid abnormality or dysfunction leading to exposure (exposure keratopathy)
Nocturnal lagophthalmos (failure to close eyes at night)

Management by optometrist

Practitioners should work within their scope of practice, and where necessary seek further advice or refer the patient elsewhere

GRADE* Level of evidence and strength of recommendation always relates to the statement(s) immediately above

Non pharmacological:

Management of predisposing factors, e.g., MGD (see Blepharitis CMG)

Patient education regarding the chronic nature of the condition

Modification of local environment

  • avoid environmental pollutants
  • avoid overheated and air-conditioned environments
  • consider air humidification
  • digital device use (improve blinking, optimise the work environment and encourage regular breaks)

(GRADE*: Level of evidence=low, Strength of recommendation=strong)

A 2024 Cochrane review examined the effectiveness of the LipiFlow Thermal Pulsation System (LipiFlow) in Meibomian gland disease and DED and found that LipiFlow performs similarly to other commonly used DED treatments 
(GRADE*: Level of evidence=low  Strength of recommendation=weak)

A 2019 Cochrane review concluded that long-chain omega-3 oral supplementation may have a possible role in managing DED, although the evidence is uncertain and inconsistent.
(GRADE*: Level of evidence=low, Strength of recommendation=weak)

Intense-pulse light (IPL) therapy (there is a scarcity of RCT evidence relating to the effectiveness and safety of IPL as a treatment for DED)
(GRADE*: Level of evidence=low  Strength of recommendation=weak)

Tear conservation

  • diminish outflow – punctal plugs. May need to be in place for at least 3 months before achieving a beneficial effect.

(GRADE*: Level of evidence=moderate, Strength of recommendation=weak)

Lid hygiene for meibomian dysfunction (hot compresses, lid hygiene) (see Clinical Management Guideline on Blepharitis)
(GRADE*: Level of evidence=moderate, Strength of recommendation=strong)

Therapeutic contact lenses to treat complications in severe disease e.g. soft, scleral, amniotic membrane contact lenses
(GRADE*: Level of evidence=low, Strength of recommendation=weak)


Tear supplements (preferably unpreserved) for use during the day ± unmedicated ointment for use at bedtime. Selection of lubricant type and frequency of administration can be advised in a stepwise approach according to disease severity.

(A 2016 Cochrane review found no evidence to support the superiority of any particular tear supplement)
(GRADE*: Level of evidence=moderate, Strength of recommendation=strong)

Topical steroids (such as fluorometholone or loteprednol, preferably unpreserved) may be considered for short-term use in some cases. The usual precautionary surveillance is required.
(GRADE*: Level of evidence=moderate, Strength of recommendation=weak)

Topical 0.1% ciclosporin A (CsA) cationic emulsion (Ikervis) is licensed in the UK for patients with severe DED with severe punctate keratopathy, which has not improved despite treatment with tear substitutes. However there is limited evidence of efficacy and safety of CsA preparations.
(GRADE*: Level of evidence=low, Strength of recommendation=weak)

Topical 5% acetylcysteine for associated filamentary keratitis 
(GRADE*: Level of evidence=moderate, Strength of recommendation=strong)

NB Patients on long-term medication may develop sensitivity reactions which may be to active ingredients or to preservative systems (see Clinical Management Guideline on Conjunctivitis Medicamentosa). They should be switched to unpreserved preparations.

Management category

B2: alleviation or palliation; normally no referral.

B1: initial management followed by routine referral if adequate trial of topical treatment or punctal plugs fails to improve symptoms, or for secondary complications (vascularisation, corneal scaring, melt, or infection). If lid anatomy or function is abnormal, refer. If the condition is not idiopathic, for example if Sjögren’s syndrome or an unidentified systemic disease are suspected, refer.

A3: if Stevens-Johnson syndrome or Ocular cicatricial pemphigoid are suspected, refer urgently (within one week).

Possible management in secondary care or local primary/community pathways where available

Additional guidance may be available

  • drug treatment for underlying disease (eg SJS, OCP)
  • correction of lid aperture abnormalities (surgery, botox)

In cases of severe dry eye:

  • autologous serum eye drops
  • permanent (surgical) occlusion of puncta
  • tarsorrhaphy (surgical or botulinum toxin)

Evidence base

*GRADE*: Grading of Recommendations Assessment, Development and Evaluation (www.gradeworkinggroup.org)

Sources of evidence

Akpek EK, Amescua G, Farid M, Garcia-Ferrer FJ, Lin A, Rhee MK, Varu DM, Musch DC, Dunn SP, Mah FS (American Academy of Ophthalmology Preferred Practice Pattern Cornea and External Disease Panel). Dry Eye Syndrome Preferred Practice Pattern. Ophthalmology. 2019;126(1):P286-P334

Bron AJ, de Paiva CS, Chauhan SK, Bonini S, Gabison EE, Jain S, Knop E, Markoulli M, Ogawa Y, Perez V, Uchino Y, Yokoi N, Zoukhri D, Sullivan DA TFOS DEWS II Pathophysiology Report. Ocul Surf. 2017;15(3):438-510. 

Cote S, Zhang AC, Ahmadzai V, Maleken A, Li C, Oppedisano J, Nair K, Busija L, Downie LE. Intense pulsed light (IPL) therapy for the treatment of meibomian gland dysfunction. Cochrane Database Syst Rev. 2020;3(3):CD013559.

Courtin R, Pereira B, Naughton G, Chamoux A, Chiambaretta F, Lanhers C, Dutheil F. Prevalence of dry eye disease in visual display terminal workers: a systematic review and meta-analysis. BMJ Open. 2016;6(1):e009675

Craig JP, Nichols KK, Akpek EK, Caffery B, Dua HS, Joo C-K, Liu Z, Nelson JD, Nichols JJ, Tsubota K, Stapleton F. TFOS DEWS II definition and classification report. Ocul Surf. 2017;15:276-83

Demolin L, Es-Safi M, Soyfoo MS, Motulsky E. Intense Pulsed Light Therapy in the Treatment of Dry Eye Diseases: A Systematic Review and Meta-Analysis. J Clin Med. 2023;12(8):3039. 

Downie LE, Ng SM, Lindsley KB, Akpek EK Omega-3 and omega-6 polyunsaturated fatty acids for dry eye disease. Cochrane Database Syst Rev. 2019;12(12):CD011016

Dry Eye Assessment and Management Study Research Group. n-3 Fatty Acid Supplementation for the Treatment of Dry Eye Disease. N Engl J Med. 2018;378(18):1681-90

Ervin A-M, Law A, Pucker AD, Punctal occlusion for dry eye syndrome: summary of a Cochrane systematic review. Br J Ophthalmol. 2019;103:301-6

Jones L, Downie LE, Korb D, Benitez-del-Castillo JM, Dana R, Deng, SX, Dong PN, Geerling G, Yudi Hida R, Liu Y, Yul Seo K, Tauber J, Wakamatsu TH, Xu J, Wolffsohn JS, Craig JP. TFOS DEWS II management and therapy report. Ocul Surf. 2017;15:575-628

Liu SH, Saldanha IJ, Abraham AG, Rittiphairoj T, Hauswirth S, Gregory D, Ifantides C, Li T. Topical corticosteroids for dry eye. Cochrane Database Syst Rev. 2022;10(10):CD015070

McCann P, Kruoch Z, Lopez S, Malli S, Qureshi R, Li T. Interventions for dry eye: An overview of systematic reviews. JAMA Ophthalmol. 2024;142(1):58-74. 

de Paiva CS, Pflugfelder SC, Ng SM, Akpek EK. Topical cyclosporine A therapy for dry eye syndrome.
Cochrane Database Syst Rev. 2019;9:CD010051

Pucker AD, Ng SM, Nichols JJ. Over the counter (OTC) artificial tear drops for dry eye syndrome. Cochrane Database Syst Rev. 2016;2:CD009729

Pucker AD, Yim TW, Rueff E, Ngo W, Tichenor AA, Conto JE. LipiFlow for the treatment of dry eye disease. Cochrane Database Syst Rev. 2024;2(2):CD015448.

Wolffsohn JS, Arita R, Chalmers R, Djalilian A, Dogru M, Dumbleton K, Gupta PK, Karpecki P, Lazreg S, Pult H, Sullivan BD, Tomlinson A, Tong L, Villani E, Yoon KC, Jones L, Craig JP. TFOS DEWS II diagnostic methodology report. Ocul Surf.2017;15:539-74


What is Dry Eye Disease?

Dry Eye Disease is also known by the medical term Keratoconjunctivitis Sicca, which means inflammation of the conjunctiva (the membrane overlying the white of the eye) and the cornea (the clear window of the eye) caused by dryness resulting from a deficiency or disorder of the tear film (the thin layer of tears covering the surface of the eye). It is a common condition affecting many people in the later decades of life. Most cases have no apparent cause but some are related to various inflammatory conditions, surgical treatment or as a side-effect of drug treatment. Some are caused by abnormalities of the eyelids or blinking, or by disorders of the meibomian (oil) glands of the eyelid margin.

Patients complain of irritation of the eyes, a feeling that there is something in the eye, a discharge from the eye, and sometimes blurred vision. They notice that their symptoms are worse in windy or dry conditions or when irritants such as smoke are in the air. When they are examined in the clinic they may be found to have reduced tear production or increased tear evaporation (sometimes due to lack of normal oil gland secretion). There may be damage to the surface of the eye produced by the increased saltiness of the tears.

How is Dry Eye Disease managed?

Tears can be supplemented with various drops and ointments. It is also possible to conserve natural tears by blocking the openings of the tear ducts, either temporarily with tiny plugs or permanently by surgery. Where the problem relates to a disorder of the oil glands, treatment is directed to the eyelids.

Dry eye (Keratoconjunctivitis Sicca) (KCS)
Version 16
Date of search 16.04.24
Date of revision 30.05.24
Date of publication 02.07.24
Date for review 15.04.26
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