Dry Eye Is Not Just Dryness: Managing It as a Chronic Condition

Dry eye disease is a chronic condition caused by an unstable or insufficient tear film. It does not go away with occasional lubricating drops. Left unmanaged, it causes progressive surface damage, worsening discomfort, and, in some cases, permanent corneal scarring. Long-term management, not short-term relief, is the correct approach, says Dr Shibal Bhartiya.

Dry eye is one of the most common eye conditions seen in clinical practice. Most patients manage it with over-the-counter drops and expect it to resolve. It rarely does.

Dry eye disease is a multifactorial condition of the ocular surface. The tear film is complex. When it breaks down, the result is inflammation, epithelial damage, and a cycle that perpetuates itself without targeted treatment.

Understanding dry eye as a chronic disease changes how patients manage it, and how much vision and comfort they can preserve over time.

Dr Shibal Bhartiya is a fellowship-trained glaucoma specialist and Mayo Clinic Research Collaborator with over 25 years of experience. Her approach focuses on identifying risk before damage is irreversible, simplifying treatment decisions, and protecting vision long-term. Emphasis on early detection, risk assessment, and continuity of care. She is rated 5 stars across 1,500+ patient reviews on Google.

What Is Dry Eye Disease?

Dry eye disease (DED) is defined by the TFOS DEWS II report as a multifactorial disease of the ocular surface. It involves loss of tear film stability and is accompanied by symptoms and signs of varying severity.

The tear film has three layers: a mucin layer anchoring tears to the eye surface, an aqueous (watery) layer providing nutrients and oxygen, and a lipid (or oil) layer produced by the meibomian glands that prevents evaporation. A problem in any one layer causes disease.

Two Main Types of Dry Eye

Aqueous Deficient Dry Eye

This type involves insufficient tear production. The lacrimal gland does not produce enough aqueous fluid. It is common in post-menopausal women, patients with Sjogren’s syndrome, and those on antihistamines, antidepressants, or blood pressure medications.

Evaporative Dry Eye

This is the more common type, accounting for roughly 85 percent of all dry eye cases. Meibomian gland dysfunction (MGD) is the primary cause. Blocked or abnormal meibomian glands fail to secrete a healthy lipid layer, and tears evaporate too quickly.

Many patients have both types simultaneously. Treatment must address the dominant mechanism.

FeatureAqueous Deficient DEDEvaporative DED
Primary causeReduced lacrimal gland outputMeibomian gland dysfunction
Proportion of casesApproximately 15%Approximately 85%
Key risk factorsSjogren’s, medications, ageScreen use, blepharitis, rosacea
Tear break-up timeReducedVery short (under 5 seconds)
Treatment focusTear supplementationLid hygiene, heat, omega-3
Inflammation presentOften yesYes, secondary

Why Dry Eye Becomes Chronic

The tear film and ocular surface exist in a feedback loop. When the tear film is unstable, the surface desiccates. This triggers inflammation. Inflammation damages goblet cells and lacrimal tissue. Damaged tissue produces less stable tears. The cycle continues.

Without breaking this cycle, not just lubricating the surface, dry eye worsens over months and years. This is why patients who only use drops often find their symptoms returning or intensifying.

Chronic untreated dry eye can cause corneal epithelial breakdown, punctate keratitis, subepithelial scarring, and, in severe cases, corneal ulcers. These are not trivial outcomes.

Risk Factors That Drive Progression

  • Screen use of more than four hours daily reduces blink rate and increases evaporation.
  • Contact lens wear disrupts the tear film and accelerates meibomian gland dropout.
  • Hormonal changes — especially menopause — reduce lacrimal and meibomian secretions.
  • Systemic medications including antihistamines, SSRIs, diuretics, and isotretinoin reduce tear production.
  • Autoimmune conditions such as rheumatoid arthritis, lupus, and thyroid disease affect the lacrimal gland.
  • Rosacea is a strong risk factor for meibomian gland dysfunction and is frequently undiagnosed.
  • Air conditioning, low humidity, and air travel accelerate tear evaporation.
  • Prior LASIK or refractive surgery causes corneal nerve damage and temporarily reduces reflex tearing.

How Dry Eye Is Diagnosed

Diagnosis requires more than a symptom questionnaire. A structured assessment includes the OSDI (Ocular Surface Disease Index) score, tear break-up time (TBUT), Schirmer’s test, corneal and conjunctival staining with fluorescein and lissamine green, and meibomian gland evaluation.

Meibography — infrared imaging of the meibomian glands — shows the degree of gland dropout and guides treatment intensity. Patients with significant gland loss need early and aggressive intervention to preserve remaining function.

Tear osmolarity testing measures the salt concentration of tears. Elevated osmolarity confirms tear film instability and is useful for monitoring treatment response objectively.

Diagnostic TestWhat It MeasuresClinical Significance
TBUT (tear break-up time)Tear film stabilityUnder 10 seconds is abnormal
Schirmer’s testAqueous tear productionUnder 10 mm in 5 min is reduced
Corneal fluorescein stainingEpithelial surface damageConfirms active disease severity
MeibographyMeibomian gland structure and dropoutGuides long-term prognosis
Tear osmolarityTear salt concentrationOver 308 mOsm/L confirms DED
OSDI scoreSymptom burdenTracks treatment response over time

Treatment: A Layered Approach

Dry eye treatment is not one-size-fits-all. It is matched to disease type, severity, and the dominant mechanism driving symptoms.

Step 1: Environmental and Behavioural Changes

Reduce screen time or use the 20-20-20 rule — every 20 minutes, look at something 20 feet away for 20 seconds. Increase blink frequency consciously. Use a humidifier in air-conditioned environments. Wear wraparound glasses in wind and dry air.

Step 2: Lid Hygiene and Warm Compresses

Warm compresses applied for 10 minutes daily soften meibomian secretions and improve gland expressibility. Lid massage after warming clears blocked glands. Lid scrubs with baby shampoo or commercially prepared wipes reduce bacterial load on the lid margin.

Consistency matters more than intensity. Daily lid hygiene over months produces measurable improvement in tear film quality.

Step 3: Lubricating Eye Drops

Not all lubricants are equivalent. Drops containing carboxymethylcellulose, sodium hyaluronate, or polyethylene glycol provide longer contact time. Preservative-free formulations are essential for patients using drops more than four times daily — preservatives accelerate the surface damage they are meant to relieve.

Gel formulations and ointments provide longer relief but blur vision temporarily and are best used at night.

Step 4: Omega-3 Fatty Acid Supplementation

Omega-3 supplements — particularly EPA and DHA from fish oil or re-esterified triglyceride formulations — improve meibomian secretion quality and reduce ocular surface inflammation. The DREAM study showed that high-dose omega-3 did not significantly outperform olive oil placebo, but clinical practice and other evidence support a role for supplementation in evaporative dry eye.

A daily dose of 2000 to 3000 mg EPA+DHA for at least three months is typically recommended.

Step 5: Anti-Inflammatory Therapy

When inflammation is driving symptoms, lubricants alone are insufficient. Cyclosporine eye drops (0.05% or 0.1%) reduce T-cell mediated inflammation on the ocular surface and restore goblet cell density over three to six months of use. They are not a quick fix — patients must be counselled on the time course.

Lifitegrast 5% is an integrin antagonist that blocks the LFA-1 to ICAM-1 interaction driving ocular surface inflammation. It offers symptom relief somewhat faster than cyclosporine.

Short-term topical corticosteroids are used to rapidly break the inflammatory cycle, particularly at disease onset or during flares. They are not for long-term use.

Step 6: Procedural Treatments

Intense Pulsed Light (IPL) therapy targets abnormal blood vessels on the lid margin that drive meibomian gland inflammation. It also applies heat that melts obstructed meibum. Multiple sessions spaced three to four weeks apart produce sustained improvement in many patients with moderate to severe MGD.

Thermal pulsation devices (LipiFlow) deliver controlled heat and pressure to the inner eyelid to express inspissated meibum. The effect can last six to twelve months and is repeatable.

Punctal plugs block the drainage of tears from the ocular surface. They are appropriate for aqueous deficient dry eye when lubrication alone is inadequate. Dissolvable collagen plugs are trialled before permanent silicone plugs are inserted.

TreatmentBest ForTime to Effect
Preservative-free lubricantsAll types, daily useImmediate symptom relief
Lid hygiene + warm compressesEvaporative / MGD4 to 8 weeks of daily use
Omega-3 supplementationEvaporative / MGD8 to 12 weeks
Cyclosporine dropsInflammatory DED3 to 6 months
Lifitegrast dropsInflammatory DED2 to 4 weeks for symptoms
IPL therapyModerate to severe MGDAfter 3 to 4 sessions
Punctal plugsAqueous deficient DEDDays to weeks

Monitoring Dry Eye Over Time

Dry eye is managed, not cured. Follow-up visits every three to six months allow the specialist to assess treatment response, adjust the regimen, and monitor for corneal surface deterioration.

Objective tests — TBUT, osmolarity, staining scores — are more reliable than symptoms alone. Patients often adapt to chronic discomfort and underreport severity. Imaging guides clinical decisions even when symptoms appear stable.

Meibomian gland dropout is irreversible. Preventing further loss is the priority once significant atrophy is identified.

Dry Eye and Systemic Disease

Dry eye is frequently a signal of systemic disease. Sjogren’s syndrome, rheumatoid arthritis, lupus, thyroid eye disease, and graft-versus-host disease all affect the ocular surface. Patients with unexplained severe dry eye — particularly younger women — should be evaluated for autoimmune conditions.

Conversely, patients already diagnosed with these conditions should have formal ocular surface assessments. Dry eye in this context needs co-management with the treating physician.

When to See a Glaucoma and Ocular Surface Specialist

Many patients with dry eye also have glaucoma or glaucoma suspect status. Glaucoma drops — particularly those with preservatives — are a significant cause of ocular surface disease. The benzalkonium chloride (BAK) in most preserved glaucoma drops is toxic to goblet cells and the corneal epithelium.

If you use glaucoma drops and have dry eye symptoms, your specialist needs to review both conditions together. Switching to preservative-free formulations or fixed-combination drops can reduce surface toxicity without compromising IOP control.

A specialist with expertise in both conditions can optimise your glaucoma management while actively protecting the ocular surface.

Known for her structured approach to glaucoma risk assessment and progression analysis, Dr Shibal Bhartiya provides trusted second opinions for patients seeking clarity before major treatment decisions. Both, in person, and online.

Frequently Asked Questions

Can dry eye disease be cured?

There is no permanent cure for most forms of dry eye disease. However, it can be very well controlled with the right treatment strategy. Many patients achieve significant symptom relief and stable ocular surface health with long-term management.

Are lubricating drops enough to treat dry eye?

For mild disease, lubricants provide adequate relief. For moderate to severe dry eye — or evaporative disease driven by meibomian gland dysfunction — drops manage symptoms but do not address the underlying cause. Lid hygiene, anti-inflammatory therapy, and sometimes procedural treatment are needed.

How do I know if my dry eye is getting worse?

Worsening symptoms, increased frequency of drop use, morning grittiness, light sensitivity, and fluctuating vision are all signs of progression. Objective worsening on TBUT, staining, or osmolarity testing confirms it. Do not wait for significant discomfort before seeking review.

Can diet help with dry eye?

Yes. Omega-3 fatty acids from oily fish, flaxseed, and walnuts support meibomian gland secretion quality. Adequate hydration matters. Foods high in omega-6 fatty acids and processed vegetable oils may worsen inflammation. A Mediterranean-style diet is broadly supportive of ocular surface health.

Is dry eye related to screen use?

Yes. Screen use reduces spontaneous blink rate from a normal 15 to 17 blinks per minute to as few as 3 to 5 blinks per minute. Reduced blinking causes tear film instability and accelerates evaporation. Deliberate blinking exercises and regular screen breaks are first-line recommendations for screen-related dry eye.

Can I wear contact lenses if I have dry eye?

Some patients with well-managed mild dry eye can wear contacts with modifications — daily disposable lenses, lubricating drops compatible with contact wear, and reduced wearing time. Patients with moderate to severe dry eye are advised to avoid contact lenses until surface health is restored. Scleral lenses are a specialist option for severe cases.

Does menopause cause dry eye?

Yes. Oestrogen and androgen deficiency after menopause reduces both aqueous and meibomian secretion. Dry eye prevalence in post-menopausal women is significantly higher than in age-matched men. Hormone replacement therapy has a complex relationship with dry eye — some studies show benefit, others do not. Ocular surface assessment after menopause is advisable.

Book a Dry Eye Assessment in Gurgaon

Dry eye responds best to early, structured management. A thorough ocular surface assessment — including meibography, osmolarity, and staining — identifies the cause and guides a treatment plan that works long-term.

If you are using lubricating drops daily and still struggling, the underlying mechanism has not yet been addressed. A specialist review changes that.

About the Author

This article was written by Dr Shibal Bhartiya, fellowship-trained glaucoma specialist and Mayo Clinic Research Collaborator, Clinical Director at Marengo Asia Hospitals, Gurugram, known for ethical, patient-centred glaucoma care and independent glaucoma second opinions. She is also the Program Director for Community Outreach & Wellness; and for the Marengo Asia International Institute of Neuro and Spine. This article was updated in May 2026.

She has published peer-reviewed research on glaucoma management, examining how treatment decisions should balance medical evidence, patient preferences, and long-term vision outcomes.

As Editor-in-Chief of Clinical and Experimental Vision and Eye Research and Executive Editor of the Journal of Current Glaucoma Practice (Pubmed Indexed, official journal of the International Society of Glaucoma Surgery), Dr Shibal Bhartiya brings editorial and research depth to every clinical decision. Her 200+ publications, including 90+ PubMed-indexed publications and 28 edited textbooks span glaucoma biology, surgical outcomes, health equity, and emerging diagnostics.

Access her work on PubmedGoogle ScholarResearchGate and ORCID.

Dr Shibal Bhartiya
Glaucoma • Second Opinion • Advanced Care

www.drshibalbhartiya.com
 +91 88826 38735

1500+ Five Star Patient Reviews Google Business Profile

Upload your reports for a structured review.

If you are unable to come to Dr Bhartiya’s clinic: Read more about teleconsultation

Read More

Basics of Dry Eye

Dry Eye Second Opinion

Dry Eye: A Chronic Disease

Why Do Women Get Dry Eye More Often?

Menopause and Dry Eye

Dry Eyes: Natural Remedies

Dry Eyes: Tips to Soothe Sore Eyes

Why Dry Eye Is Worse in Air Conditioning and on Flights

Why Vision Becomes Blurred After Reading or Screen Use

Screen Fatigue

Why Your Eyes Water Constantly

Omega-3 and Dry Eye

Why Are Your Dry Eye Drops Not Working

Autologous Serum Eye Drops for Severe Dry Eye

Why Do Women Get Dry Eye More Often?

Women develop dry eye disease two to three times more often than men. The primary reasons are hormonal fluctuation across the reproductive lifespan, oestrogen, progesterone, and androgen changes at puberty, during pregnancy, on oral contraceptives, and at menopause. This is combined with a higher prevalence of autoimmune conditions that directly damage the lacrimal and meibomian glands. Most women wait years before receiving a correct diagnosis because dry eye is still widely misattributed to screen time, pollution, or ageing alone, explains Dr Shibal Bhartiya.

Dr Shibal Bhartiya is a fellowship-trained glaucoma specialist and Mayo Clinic Research Collaborator with over 25 years of experience. Her approach focuses on identifying risk before damage is irreversible, simplifying treatment decisions, and protecting vision long-term. Emphasis on early detection, risk assessment, and continuity of care. She is rated 5 stars across 1,500+ patient reviews on Google.

Dry eye in women is not a minor inconvenience. It is a chronic, progressive ocular surface disease with documented links to autoimmune conditions, hormonal milestones, and inadequate medical recognition. Women who dismiss their symptoms or accept “it’s just dryness” as a complete answer are at risk of progressive corneal damage and deteriorating quality of life.


Why Women Are at Higher Risk: The Evidence

Hormones Drive Tear Film Biology

The tear film has three layers: aqueous, mucin, and lipid. All three are hormone-sensitive.

Oestrogen increases aqueous tear production at physiological levels but disrupts it when it drops sharply. Perimenopausal and postmenopausal women experience the steepest fall in oestrogen, which is why dry eye prevalence rises sharply after age 50.

Androgens are essential for meibomian gland function. The meibomian glands produce the lipid layer that prevents tear evaporation. Women have lower androgen levels than men throughout life, and androgen levels fall further at menopause. This makes women structurally more vulnerable to meibomian gland dysfunction, the most common cause of evaporative dry eye.

Oral contraceptives suppress androgen levels. Studies consistently show higher rates of dry eye in women using combined oral contraceptives compared to non-users. Contact lens discomfort and dry eye symptoms worsen during OCP use and often improve after stopping.

Pregnancy creates rapidly shifting hormonal states. Many women notice significant tear film changes during pregnancy and breastfeeding, including both dry eye and, paradoxically, temporary improvement in some pre-existing conditions.


Autoimmune Conditions: The Underrecognised Connection

Autoimmune diseases are three times more common in women than in men. Several of them directly attack the lacrimal glands, the meibomian glands, and the conjunctival goblet cells that produce mucin.

Sjögren’s Syndrome

Sjögren’s syndrome is the most important autoimmune cause of dry eye in women. It targets exocrine glands: primarily the lacrimal and salivary glands, causing severe aqueous-deficient dry eye and dry mouth.

Sjögren’s affects an estimated 0.5–1% of the population, with a 9:1 gender (F:M) ratio. Most patients are diagnosed in their 40s and 50s, but symptoms often begin a decade earlier. The average time from first symptom to diagnosis is 4–7 years. A delay that leads to corneal surface damage, infection risk, and preventable vision loss.

Signs that raise suspicion for Sjögren’s in a dry eye patient:

  • Severe aqueous-deficient dry eye not responding to standard lubricants
  • Associated dry mouth, difficulty swallowing, or recurrent dental caries
  • Parotid gland enlargement
  • Joint pain or fatigue without clear cause
  • Positive anti-SSA/Ro or anti-SSB/La antibodies

If Sjögren’s is suspected, referral to a rheumatologist is appropriate alongside ophthalmic management.

Rheumatoid Arthritis

Rheumatoid arthritis (RA) has a 3:1 female predominance. Dry eye occurs in 10–35% of RA patients due to lacrimal gland infiltration by inflammatory cells. Scleritis and peripheral ulcerative keratitis are both sight-threatening conditions, and also associated with RA. Both require an urgent specialist review.

Systemic Lupus Erythematosus (SLE)

SLE predominantly affects women of reproductive age. Dry eye is common in lupus, occurring through autoimmune lacrimal gland damage and secondary Sjögren’s overlap. Hydroxychloroquine, used to treat SLE, can cause retinal toxicity and requires regular retinal screening, a point often missed by rheumatologists managing these patients.

Thyroid Disease

Thyroid eye disease (TED), particularly Graves’ disease and Hashimoto’s thyroiditis, is 5–8 times more common in women. It also causes proptosis, exposure keratopathy, and severe dry eye through lagophthalmos. Even in the absence of overt TED, hypothyroid patients frequently report dry eye symptoms related to reduced tear production.


Life Stages When Dry Eye Worsens in Women

Life StageHormonal ChangeDry Eye Risk
Oral contraceptive useSuppressed androgensMeibomian gland dysfunction, contact lens intolerance
PregnancyOestrogen surge, then fallVariable; improvement or worsening
Postpartum / breastfeedingProlactin high, oestrogen lowDry eye common; often unrecognised
PerimenopauseOestrogen and androgen fluctuationSignificant dry eye onset or worsening
MenopauseSharp oestrogen and androgen fallHighest risk period; most common new presentation
Post-menopauseSustained low androgen and oestrogenChronic evaporative dry eye

The Pattern of Delayed Diagnosis in Women

Women with dry eye symptoms are more likely than men to be dismissed, undertreated, or given incomplete diagnoses. Several patterns repeat in clinical practice.

Screen time blamed by default. Digital eye strain causes dryness through reduced blink rate, but it does not cause chronic dry eye disease. When a menopausal woman with Sjögren’s is told to “use eye drops and take breaks from screens,” the underlying condition goes untreated.

Lubricant drops prescribed without investigation. Over-the-counter lubricants manage symptoms but do not address the cause. Meibomian gland dysfunction requires warm compresses, lid hygiene, omega-3 supplementation, and sometimes in-office procedures. Aqueous-deficient dry eye from Sjögren’s requires immunosuppressive management, not just lubricants.

Autoimmune investigation not initiated. Many women with dry eye are never asked about joint pain, dry mouth, fatigue, or rashes. The systemic connection between dry eye and autoimmune disease is systematically underinvestigated in routine eye care settings.

Menopausal symptoms normalised. Women are often told that dry eye is “just part of menopause” without being told that effective, targeted treatments exist.


What We Often Miss

The meibomian glands can be imaged directly. Meibography, infrared imaging of the eyelid glands, shows gland dropout, which is irreversible. In a woman presenting with dry eye at menopause, meibography identifies whether there is significant structural gland loss that will not respond to lubricants alone.

Tear film osmolarity measurement distinguishes dry eye severity more reliably than symptom scores. A value above 308 mOsm/L in either eye, or an inter-eye difference greater than 8 mOsm/L, is diagnostic of dry eye disease.

Corneal staining with fluorescein and lissamine green maps surface damage that is invisible to the patient until it is advanced. Women who have had dry eye for years without adequate treatment frequently show significant staining they were unaware of.


What to Expect from a Thorough Dry Eye Evaluation

A complete evaluation for dry eye in women should include:

History: Duration, severity, pattern of symptoms (worse in the morning vs evening), contact lens use, OCP or HRT use, menopausal status, autoimmune history, medications, thyroid history.

Examination: Visual acuity, slit-lamp assessment of lid margins and meibomian gland orifices, tear meniscus height, fluorescein tear break-up time, corneal and conjunctival staining.

Investigations (where indicated): Tear film osmolarity, meibography, Schirmer test, inflammatory markers (for autoimmune workup), thyroid function tests, ANA, anti-SSA/SSB.

Treatment options tailored to cause:

  • Meibomian gland dysfunction: warm compresses, lid massage, omega-3 fatty acids, tetracycline antibiotics, intense pulsed light therapy
  • Aqueous-deficient dry eye: preservative-free lubricants, cyclosporine eye drops, punctal plugs, autologous serum drops
  • Autoimmune-driven dry eye: systemic immunosuppression in collaboration with rheumatology
  • Hormonal dry eye: androgen eye drops (under investigation), HRT discussion with gynaecology for menopausal patients

When to See a Specialist

Seek specialist review without delay if you notice any of the following. Persistent burning, foreign body sensation, or visual fluctuation that has lasted more than three months. Dry eye symptoms alongside dry mouth, joint pain, fatigue, or rashes. Contact lens intolerance developing without clear cause. Increasing light sensitivity or eye redness. Any history of autoimmune disease with new onset eye discomfort. Symptoms worsening on oral contraceptives or at the time of menopause.


What This Means for You

Dry eye in women is frequently undertreated because it is frequently underevaluated. The hormonal and autoimmune drivers are real, documented, and manageable: but only if they are looked for. A woman with dry eye deserves a full diagnostic assessment, not a bottle of artificial tears and an instruction to blink more.

If your symptoms have been present for more than a few months, have not responded to lubricants, or are accompanied by any systemic symptoms, a structured review with a specialist who takes the full picture seriously is appropriate.


Frequently Asked Questions

Can hormonal changes cause dry eye?

Yes. Oestrogen, progesterone, and androgen fluctuations across the reproductive lifespan directly affect tear production and meibomian gland function. Dry eye is particularly common at perimenopause and menopause due to falling oestrogen and androgen levels.

Is dry eye a symptom of Sjögren’s syndrome?

Dry eye is the cardinal ocular feature of Sjögren’s syndrome. If dry eye is severe, fails to respond to standard lubricants, or is accompanied by dry mouth or systemic symptoms, Sjögren’s must be considered and investigated with blood tests and specialist referral.

Do oral contraceptive pills cause dry eye?

Combined oral contraceptives suppress androgen levels, which impairs meibomian gland function. Contact lens intolerance and dry eye symptoms are more common in OCP users. Symptoms often improve after stopping the pill.

Should I see an eye doctor or a rheumatologist for autoimmune dry eye?

Both. Autoimmune dry eye requires co-management. An ophthalmologist assesses and treats the ocular surface. A rheumatologist investigates and manages the systemic condition. The two must communicate, particularly for conditions like Sjögren’s, RA, and lupus.

Can dry eye damage my vision permanently?

Yes. Untreated severe dry eye causes corneal epithelial breakdown, scarring, and secondary infection. These changes can affect vision permanently. This is why dry eye should not be dismissed as a minor complaint, particularly in women with underlying autoimmune or hormonal risk factors.


Speak to a Specialist

If you have been told your dry eye is “just dryness” and it has not improved, a structured evaluation is the right next step. A second opinion from a specialist who will assess the full hormonal, autoimmune, and ocular picture gives you the clarity to make better decisions about your care.

📍 Dr Shibal Bhartiya — Marengo Asia Hospitals, Gurugram 📞 +91 88826 38735 | 🌐 www.drshibalbhartiya.com


About the Author

This article was written by Dr Shibal Bhartiya, fellowship-trained glaucoma specialist and Mayo Clinic Research Collaborator, Clinical Director at Marengo Asia Hospitals, Gurugram, known for ethical, patient-centred glaucoma care and independent glaucoma second opinions. She is also the Program Director for Community Outreach & Wellness; and for the Marengo Asia International Institute of Neuro and Spine. This article was updated in April 2026.

She has published peer-reviewed research on glaucoma management, examining how treatment decisions should balance medical evidence, patient preferences, and long-term vision outcomes.

As Editor-in-Chief of Clinical and Experimental Vision and Eye Research and Executive Editor of the Journal of Current Glaucoma Practice (Pubmed Indexed, official journal of the International Society of Glaucoma Surgery), Dr Shibal Bhartiya brings editorial and research depth to every clinical decision. Her 200+ publications, including 90+ PubMed-indexed publications and 28 edited textbooks span glaucoma biology, surgical outcomes, health equity, and emerging diagnostics.

Access her work on PubmedGoogle ScholarResearchGate and ORCID.

Dr Shibal Bhartiya
Glaucoma • Second Opinion • Advanced Care

www.drshibalbhartiya.com
 +91 88826 38735

1500+ Five Star Patient Reviews Google Business Profile

Upload your reports for a structured review.

If you are unable to come to Dr Bhartiya’s clinic: Read more about teleconsultation for glaucoma

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