Dry Eye Corner Part 8

Assessing the patient’s skin is an essential part of a dry eye consultation

Dry eye disease (DED) is often first encountered as ocular surface findings: reduced tear break-up time (TBUT), corneal fluorescein staining, a thin tear meniscus, or visible meibomian gland obstruction. These signs matter, but they are not the whole story.

The TFOS DEWS III definition describes DED as: “a multifactorial, symptomatic disease characterised by a loss of homeostasis of the tear film and/or ocular surface, in which tear film instability and hyperosmolarity, ocular surface inflammation and damage, and neurosensory abnormalities are etiological factors”¹.

The uncomfortable clinical question, therefore, is whether we sometimes diagnose the stain rather than the patient.

A patient with a short TBUT may indeed have evaporative dry eye, but why is the tear film unstable? Is rosacea driving meibomian gland dysfunction? Is seborrhoeic dermatitis affecting the lid margin? Is the patient taking antihistamines, antidepressants, isotretinoin or multiple preserved eye drops? Are autoimmune disease, thyroid dysfunction, diabetes, menopause, anxiety, poor sleep, digital device use or contact lens wear contributing?^2,3.

A dry eye assessment that stops at fluorescein risks missing the causes that sustain the condition.

Skin assessment

Skin assessment is an essential part of a dry eye consultation. The lid margin is a modified skin surface, and meibomian glands are sebaceous glands. Conditions that affect facial skin and sebaceous function can alter the quality of meibum, promote lid margin inflammation and destabilise the tear film lipid layer^3,4.

Rosacea is a key example. Patients may present with facial flushing, telangiectasia, papules or pustules, but ocular involvement can be disproportionate to skin symptoms. Lid margin erythema, telangiectasia, capped glands, cloudy meibum and recurrent chalazia should prompt the clinician to examine the cheeks, nose, forehead and periocular skin rather than simply recording ‘MGD’ and moving on^3,4.

Seborrhoeic dermatitis is another common clue. Greasy scale around the brows, lashes, scalp or nasolabial folds may accompany blepharitis and contribute to chronic lid margin inflammation.

Atopic dermatitis and eczema can also alter the periocular skin barrier and may coexist with allergic eye disease, rubbing and medication sensitivity³. Demodex infestation is similarly easy to miss unless lashes and lid skin are inspected carefully.

In each case, the ocular findings are part of a wider dermatological pattern.

Health history: DED as a systemic signal

An effective dry eye history should include systemic disease, hormonal status, gut health, pain symptoms and general wellbeing. Autoimmune conditions such as Sjögren’s syndrome, rheumatoid arthritis and systemic lupus erythematosus are particularly important in aqueous-deficient dry eye, especially when symptoms include dry mouth, joint pain, fatigue or recurrent dental problems^4,5.

Thyroid eye disease may increase exposure and tear evaporation through lid retraction, proptosis or incomplete blinking. Diabetes can affect corneal nerves and epithelial healing, while dermatological and inflammatory conditions may drive evaporative disease^3,4.

As covered in the Dry Eye Corner Part 7, hormonal factors also matter. DED is more common in women and prevalence increases with age, but a useful history goes beyond demographic risk. Menopause, endocrine disease and hormonal medication can influence tear production, meibomian gland function and symptom burden^4,5.

Similarly, the TFOS framework recognises neurosensory abnormalities: some patients report severe discomfort despite modest staining, while others show significant staining with fewer symptoms. Asking about chronic pain, migraine, fibromyalgia, anxiety, depression and sleep disturbance can help interpret this sign-symptom mismatch and guide referral or co-management where needed^1,5.

Medication review

Reviewing a patient’s medication should be treated as part of the dry eye examination

Medication review should be treated as part of the dry eye examination, not as background paperwork. The TFOS DEWS II iatrogenic report highlights that topical medications can cause or aggravate DED through allergic, toxic and inflammatory mechanisms, and that preservatives such as benzalkonium chloride may worsen ocular surface compromise². This is particularly relevant in glaucoma, allergy and chronic postoperative care, where patients may use multiple drops for years^2,4.

Systemic medication is equally important. Antihistamines, antidepressants, anxiolytics, decongestants, diuretics, some antihypertensives and hormonal therapies are commonly associated with dry eye symptoms^2,4. Isotretinoin is especially relevant to skin-focused assessment because it reduces sebaceous gland activity and can adversely affect meibomian gland function. A patient treated for acne or rosacea may therefore carry both the dermatological risk factor and the medication-related risk factor for DED^2,3.

Obviously, it is not for the clinician to alter systemic medication independently, but to recognise modifiable contributors and communicate clearly with the patient’s GP, dermatologist, rheumatologist or pharmacist.

Where a medicine is essential, management may focus on ocular surface protection, preservative-free options, lid disease control and realistic counselling. Where a medicine is elective or one of several options, collaborative discussion may reduce ocular surface burden^2,4.

From test battery to clinical reasoning

TFOS DEWS II diagnostic methodology recommends symptom screening, exclusion of mimicking conditions and a set of objective signs including tear film break-up, osmolarity where available, and ocular surface staining, followed by assessment of meibomian gland dysfunction, lipid layer behaviour and tear volume to subclassify disease⁶.

In day-to-day practice, this means the clinician should move from, ‘Does this patient have dry eye?’ to ‘What pattern of dry eye is present?’; ‘What is driving it?’; and ‘What must be addressed for treatment to work?’^4,6.

A practical consultation might include three additional habits.

1. Observe: facial redness, scaling, lid margin vascularity, lash debris, incomplete blink and skin products around the eye all provide data before any dye reaches the cornea³.
2. Ask targeted systemic questions: dry mouth, autoimmune disease, thyroid disease, diabetes, dermatology treatment, menopause, pain syndromes, sleep and screen behaviour^3,4,5.
3. Review medication and drops: including over-the-counter antihistamines, acne treatments, antidepressants and preserved topical therapy^2,4.

Conclusion

DED is multifactorial in definition, mechanism and management^1,5. Skin clues may uncover rosacea, seborrhoeic disease, eczema or Demodex³. Health history may reveal autoimmune, endocrine, neurological or hormonal influences^4,5. Medication review may identify iatrogenic contributors that explain treatment resistance².

If we accept the TFOS definitions in theory, our assessment must reflect them in practice: dry eye care should be ocular surface medicine, not fluorescein pattern recognition.

References

1. Perez VL, Chen W, Craig JP et al. TFOS DEWS III: Executive Summary. American Journal of Ophthalmology 2026;282:135-145.

2. Gomes JAP, Azar DT, Baudouin C et al. TFOS DEWS II Iatrogenic Dry Eye Report. The Ocular Surface 2017;15(3):516-543.

3. Craig JP, Alves M, Wolffsohn JS et al. TFOS Lifestyle Report Executive Summary: A Lifestyle Epidemic – Ocular Surface Disease. The Ocular Surface 2023;30:240-253.

4. Jones L, Downie LE, Korb D et al. TFOS DEWS II Management and Therapy Report. The Ocular Surface 2017;15(3):575-628.

5. Craig JP, Nichols KK, Akpek EK et al. TFOS DEWS II Definition and Classification Report. The Ocular Surface 2017;15(3):276-283.

6. Wolffsohn JS, Arita R, Chalmers R et al. TFOS DEWS II Diagnostic Methodology Report. The Ocular Surface. 2017;15(3):539-574.

Keith Tempany FBDO CL FBCLA qualified in 1976 and worked in both independent and multiple practice before opening a fee-based contact lens only practice in 2002. He is a fellow and a past president of the British Contact Lens Association (BCLA) and oversaw the development and launch of its Myopia Management Certificate. Keith is the store director of Leightons & Tempany Opticians & Hearing Care in Poole, and works as an independent consultant. He is an experienced author, lecturer and facilitator of contact lens and dry eye education both nationally and internationally.