Khawaja Muhammad Ammar Ali Javed1,2
1 Academic Unit of Ophthalmology, Department of Inflammation and Ageing, School of Infection, Inflammation and Immunology, College of Medicine and Health, University of Birmingham, UK.
2 Birmingham and Midland Eye Centre, City Health Campus Sandwell and West Birmingham NHS Trust, Birmingham, UK.
Introduction
Dry eye disease (DED) is among the most frequently encountered conditions in ophthalmic practice, yet its assessment is often more challenging than its name suggests. Patients may describe persistent irritation, fluctuating vision or excessive watering, sometimes despite using multiple ocular lubricants. Others demonstrate significant ocular surface abnormalities with comparatively modest symptoms. This variability reflects the complex and multifactorial nature of the disease, highlighting why effective assessment requires more than identifying ocular dryness.
The recently published Tear Film and Ocular Surface Society Dry Eye Workshop III (TFOS DEWS III) defines dry eye as a multifactorial, symptomatic disease characterised by loss of tear film and/or ocular surface homeostasis, involving tear film instability, hyperosmolarity, inflammation, tissue damage and neurosensory abnormalities (1).
For clinicians, the challenge is therefore twofold: establishing whether a patient has dry eye disease and identifying the underlying mechanisms responsible for their symptoms. A systematic approach to history-taking, clinical examination and targeted investigations can help achieve both.
The importance of a focused clinical history
A thorough history remains central to the assessment of dry eye disease. Common symptoms include burning, grittiness, foreign body sensation, intermittent blurring and ocular fatigue. Paradoxically, excessive tearing may also occur as a reflex response to ocular surface irritation.
The pattern of symptoms can be particularly informative. Worsening discomfort during prolonged screen use, reading or exposure to air conditioning may suggest tear film instability, while persistent symptoms throughout the day may indicate more significant ocular surface dysfunction.
Relevant risk factors include contact lens wear, previous ocular surgery, topical medications, particularly preserved eye drops, and systemic conditions such as Sjögren’s disease. Medication history should also explore systemic agents that may influence lacrimal secretion or ocular surface function.
Validated questionnaires provide a standardised assessment of symptom burden. The Ocular Surface Disease Index (OSDI) is widely used and incorporates ocular discomfort, visual function and environmental triggers (2). More recently, TFOS DEWS III recommended the shorter OSDI-6 questionnaire for diagnostic screening, using a threshold score of 4 or greater (1).
Importantly, questionnaires quantify the patient’s experience but do not independently establish the diagnosis. Their greatest value lies in providing a reproducible measure that can be interpreted alongside objective clinical findings.
Examining the tear film and ocular surface
Slit-lamp examination provides essential information about tear film stability, epithelial integrity and eyelid function. A structured examination should begin with relatively non-invasive observations before progressing to tests that may alter the tear film (1, 3).
Tear film stability is a fundamental component of assessment. Non-invasive tear breakup time (NIBUT) measures the interval between a blink and the first disruption of the tear film without fluorescein instillation. A NIBUT of less than 10 seconds supports tear film instability under the TFOS DEWS III diagnostic framework (1).
Where non-invasive measurement is unavailable, fluorescein tear breakup time remains a practical alternative. A small quantity of fluorescein is instilled, and the tear film is observed under cobalt blue illumination. An interval of less than 5 seconds is considered abnormal under the updated framework, although results are influenced by fluorescein volume and examination technique (1).
Ocular surface staining provides complementary information about epithelial damage. Fluorescein highlights corneal epithelial disruption, while lissamine green facilitates assessment of conjunctival and lid margin abnormalities.
The distribution of staining is as important as its extent. Inferior corneal staining may suggest exposure-related disease, whereas interpalpebral staining is frequently encountered in dry eye. More extensive or atypical patterns should prompt consideration of alternative ocular surface pathology.
Standardised grading systems, including the Oxford staining scheme, improve the consistency of documentation and allow longitudinal assessment of disease progression or treatment response (4).
The eyelids: an essential part of dry eye assessment
Examination of the eyelids and meibomian glands is frequently overlooked, despite their importance in maintaining a stable tear film.
Meibomian gland dysfunction (MGD) is a major contributor to evaporative dry eye. Dysfunctional glands may produce altered or insufficient meibum, compromising the tear film lipid layer and increasing evaporative loss (5).
Clinical examination should include assessment of lid margin telangiectasia, gland orifice plugging, irregularity of the posterior lid margin and the quality of expressed meibum. Gentle digital pressure can reveal whether secretions are clear and readily expressed or thickened and obstructed.
Where available, meibography provides additional information regarding meibomian gland morphology and dropout. However, structural abnormalities should always be interpreted alongside symptoms and functional findings, rather than treated as diagnostic in isolation.
Blink dynamics also deserve attention. Incomplete blinking, particularly during prolonged visual tasks, can contribute to tear film instability and ocular surface exposure.
When are additional investigations necessary?
Not every patient requires an extensive battery of investigations. The purpose of additional testing is to clarify disease mechanisms, evaluate severity and identify patients who may benefit from further specialist assessment.
Schirmer testing assesses aqueous tear production and is particularly relevant when aqueous deficiency is suspected. Reduced tear production may occur in association with lacrimal gland dysfunction or systemic autoimmune disease. However, results can vary with testing conditions, reflex tearing and the use of topical anaesthesia, limiting their value as an isolated diagnostic measure (3).
Tear osmolarity provides an objective measure of tear film homeostasis. TFOS DEWS III identifies an osmolarity of at least 308 mOsm/L in either eye, or an interocular difference exceeding 8 mOsm/L, as supportive diagnostic criteria when measured using the validated system described in the report (1).
Meibography and automated non-invasive tear film analysis can further characterise glandular structure and tear film behaviour. These investigations are particularly valuable in complex presentations, although access varies considerably between clinical settings.
Ultimately, sophisticated investigations should supplement rather than replace careful clinical examination. Recent UK expert consensus guidance similarly emphasises pragmatic, accessible assessment pathways and appropriate escalation according to disease severity (6).
Understanding the underlying mechanism
Traditionally, dry eye disease has been divided into aqueous-deficient and evaporative subtypes. Although clinically useful, this classification does not fully capture the overlapping mechanisms contributing to ocular surface dysfunction.
TFOS DEWS III proposes a broader framework incorporating deficiencies of tear film components, eyelid abnormalities and ocular surface disturbances, including neural dysfunction and inflammation (1).
This distinction matters because patients with apparently similar symptoms may have substantially different underlying disease processes.
A patient with reduced tear production and significant staining requires a different clinical approach from someone with meibomian gland obstruction and rapid tear film breakup. In many patients, several mechanisms coexist.
Identifying the dominant contributors therefore provides a more meaningful basis for management than assigning a diagnosis of dry eye alone.
When dry eye is not the whole story
Perhaps one of the most important aspects of assessment is recognising when symptoms and clinical findings do not correspond.
Severe ocular discomfort in the presence of minimal staining may reflect neurosensory abnormalities, including neuropathic ocular pain. Conversely, patients with reduced corneal sensation may demonstrate significant epithelial disease without proportionate discomfort.
Such discrepancies should encourage further clinical evaluation rather than automatic escalation of lubricating treatment.
The differential diagnosis also includes allergic conjunctivitis, blepharitis, exposure keratopathy, medication-related ocular surface toxicity and other inflammatory or cicatrising disorders.
Particular attention should be given to persistent unilateral symptoms, marked photophobia, unexplained visual reduction, corneal infiltrates, epithelial defects or progressive conjunctival scarring. These findings are not typical of uncomplicated dry eye and warrant further investigation or specialist assessment.
Bringing the findings together
The final stage of assessment is to integrate symptoms, examination findings and investigations into a coherent clinical picture.
An effective evaluation should establish whether objective evidence supports the diagnosis, identify the principal mechanisms contributing to ocular surface dysfunction and determine whether features of more complex disease are present.
The same clinical measures should then be documented consistently during follow-up. Symptom questionnaires, tear breakup time, staining scores and relevant eyelid findings provide useful reference points when evaluating progression or response to treatment.
This structured approach reduces reliance on empirical treatment and helps ensure that management is directed towards the underlying pathology.
Conclusion
Dry eye disease is considerably more complex than a simple deficiency of tears. Its assessment requires an understanding of tear film physiology, ocular surface integrity, eyelid function and the relationship between symptoms and clinical signs. For clinicians beginning their ophthalmology careers, developing a systematic approach to dry eye assessment provides a valuable foundation for managing one of the specialty’s most prevalent conditions. The central principle is straightforward: the objective is not merely to diagnose dry eye, but to understand why the ocular surface is failing to maintain homeostasis. Once that distinction is recognised, assessment becomes more informative, management more targeted and the care of patients with persistent ocular surface symptoms more effective.
References
1. Wolffsohn JS, Benítez-Del-Castillo JM, Loya-Garcia D, Inomata T, Iyer G, Liang L, et al. TFOS DEWS III: Diagnostic Methodology. Am J Ophthalmol. 2025;279:387-450.
2. Schiffman RM, Christianson MD, Jacobsen G, Hirsch JD, Reis BL. Reliability and validity of the Ocular Surface Disease Index. Arch Ophthalmol. 2000;118(5):615-21.
3. Wolffsohn JS, Arita R, Chalmers R, Djalilian A, Dogru M, Dumbleton K, et al. TFOS DEWS II Diagnostic Methodology report. Ocul Surf. 2017;15(3):539-74.
4. Bron AJ, Evans VE, Smith JA. Grading of corneal and conjunctival staining in the context of other dry eye tests. Cornea. 2003;22(7):640-50.
5. Nichols KK, Foulks GN, Bron AJ, Glasgow BJ, Dogru M, Tsubota K, et al. The international workshop on meibomian gland dysfunction: executive summary. Invest Ophthalmol Vis Sci. 2011;52(4):1922-9.
6. Manzouri B, Ahmad S, Harper S, Kolli S, Lockington D, O’Gallagher M, et al. Assessment and management of dry eye disease in the UK: standardising reality-based best practice. Eye (Lond). 2026;40(8):1185-95.