Exposure Keratopathy

Exposure keratopathy is damage to the clear front surface of the eye (the cornea) that happens when the eye is not fully protected or wetted by the eyelids and tears. When the eyelids do not close properly, the cornea is left exposed to air. This causes the tear film to evaporate too fast, the surface to dry out, and the fragile corneal epithelial cells to break down. Left untreated, this can progress from mild dryness to serious problems like corneal ulcers, infections, scarring, and even permanent vision loss. EyeWikiScienceDirectScienceDirect

Exposure keratopathy is damage to the front surface of the eye (the cornea) caused when the eyelids do not fully close or blink properly. Because the cornea stays exposed to air, it dries out, loses its protective tear film, and the delicate surface cells begin to break down. This can cause irritation, redness, pain, and in more severe or prolonged cases, persistent corneal defects, infection, scarring, or vision loss. The problem is often mechanical (like when the eyelids cannot close fully due to facial nerve palsy), anatomical (proptosis from thyroid eye disease), or functional (reduced blink from sedation or neurological injury). Exposure keratopathy is a clinical diagnosis made by history and eye examination, and early recognition is critical to preventing serious complications. EyeWikiAmerican Academy of OphthalmologyVagelos CollegeNCBI

The underlying process is a mixture of increased exposure plus reduced natural protection or healing. Normally blinking spreads tears and the eyelids physically shield the cornea; when either of those defenses fails—because of lid position, nerve problems, sedation, or other reasons—the balance is lost, and the cornea becomes damaged. EyeWikiPMC

Pathophysiology

The cornea needs to stay moist and protected. Blinking spreads tears with nutrients and antimicrobial factors, while the eyelids keep dust and drying air away. If blinking is reduced, closure is incomplete, or the tear film breaks up too quickly, the surface dries. Dryness causes tiny breaks in the outermost corneal cells, which invite inflammation and sometimes infection. Without a healthy surface, even normal bacteria can invade, forming ulcers. If the damage goes deep, scar tissue forms and vision can get permanently blurred. WikipediaSemantic ScholarNCBI

When eyelid closure fails (lagophthalmos) or the eye sticks out (proptosis), more of the cornea is exposed to air, making tear evaporation faster. If the nerves to the cornea are damaged (e.g., trigeminal nerve), the eye does not feel the early warning symptoms, so damage accumulates unnoticed. ScienceDirectResearchGate

In critically ill or sedated patients, muscle tone drops, reflex blinking is reduced, and protective eye closures during sleep or sedation are lost. This makes exposure and evaporation worse and is why ICU patients have very high rates of early-stage exposure keratopathy unless proactively protected. accjournal.orgPMC

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Types / Classification of Exposure Keratopathy

Exposure keratopathy is not a single uniform disease; clinicians group it based on the cause and severity. Major types include:

1. Neurogenic exposure keratopathy – when nerve dysfunction leads to poor eyelid movement or reduced corneal sensation. Examples include facial nerve (VII) palsy causing lagophthalmos, or trigeminal nerve damage reducing corneal sensation, sometimes overlapping with neurotrophic keratitis. NCBIScienceDirectResearchGate

2. Mechanical exposure keratopathy – due to eyelid malposition such as eyelid retraction, scarring from burns or cicatricial diseases, postoperative changes (e.g., after blepharoplasty or ptosis surgery), or ectropion that prevent proper lid closure. ScienceDirectAcademic Medicine and Pharmacy

3. Proptosis/exophthalmos-related – forward bulging of the eye (as in thyroid eye disease or orbital tumors) increases corneal exposure, especially if the lids cannot fully cover the globe. WebEyeJournalAgent

4. Lagophthalmos (including nocturnal) – inability to completely close the eyelids, either during wakefulness or sleep (nocturnal lagophthalmos). This alone is a direct risk and may be idiopathic or physiologic. NCBIResearchGate

5. Reduced blink or eyelid closure reflex – from movement disorders (e.g., Parkinson’s disease), sedation, neurological impairment, or lowered consciousness (such as ICU patients with low Glasgow Coma Scale), leading to inadequate surface renewal and protection. PMCaccjournal.org

6. Combination / mixed forms – patients often have more than one contributing type, e.g., a patient with thyroid eye disease (proptosis) who also has lagophthalmos and decreased blink reflex from fatigue. ScienceDirectaccjournal.org

Severity is often described from mild (punctate epithelial erosions and surface dryness) to moderate (persistent epithelial defects) to severe (ulceration, melting, perforation, infection). Semantic Scholar

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 Causes of Exposure Keratopathy

Below are 20 distinct and common causes, each explained:

1. Facial nerve (VII) palsy – Weakness of the orbicularis oculi muscle means the eyelids cannot close fully (lagophthalmos), exposing the cornea. Causes include Bell’s palsy, stroke, trauma, tumors, and surgical injury. NCBI

2. Lagophthalmos after eyelid surgery – Procedures like blepharoplasty, ptosis repair, or aggressive eyelid tightening can disrupt normal lid closure or Bell’s phenomenon, leading to exposure. ScienceDirectAmerican Academy of Ophthalmology

3. Nocturnal lagophthalmos – The eyelids do not close fully during sleep even without nerve disease; this can cause nightly surface drying and cumulative damage. ResearchGate

4. Thyroid eye disease / Graves’ orbitopathy – Swelling, lid retraction, and proptosis push the eye forward and hold the eyelids open, increasing exposure. WebEyeJournalAgent

5. Proptosis from orbital tumors or inflammation – Any process pushing the globe forward (e.g., tumors, cellulitis) reduces lid coverage. WebEyeJournalAgent

6. Eyelid retraction – Seen in thyroid eye disease or scarring, the lid is pulled away, preventing full coverage. ScienceDirect

7. Ectropion or eyelid laxity – The eyelid is turned outward or loose, causing poor tightness against the globe and ineffective blink-driven tear spread. ScienceDirect

8. Mechanical scarring (burns, cicatricial diseases) – Chemical or thermal burns, ocular cicatricial pemphigoid, or symblepharon can distort eyelid anatomy, impairing closure. ScienceDirect

9. Sedation / neuromuscular blockade in ICU – Drugs used for ventilation reduce protective blinking and eyelid tone, creating passive exposure. PMCaccjournal.org

10. Low consciousness / coma (reduced blink reflex) – Patients with decreased alertness lose spontaneous blinking and protective closures, especially during sleep-like states. accjournal.org

11. Parkinson’s disease or other movement disorders – Reduced spontaneous blink rate means less tear distribution and higher risk of surface drying. PMC

12. Neurotrophic corneal disease (trigeminal nerve damage) – The cornea becomes numb, so early irritation is not felt, and the healing response is impaired, making even minor exposure harmful. ResearchGateNCBI

13. Ocular surgery affecting orbicularis function – Nearby procedures or trauma that weaken eyelid muscles reduce eyelid closure strength. ScienceDirect

14. Orbital radiation or inflammatory damage – Tissue changes around the orbit can alter eyelid mechanics and cause lid lag or incomplete closure. Academic Medicine and Pharmacy

15. Congenital eyelid malformations (e.g., blepharophimosis) – Structural anomalies from birth can prevent full lid coverage or normal blinking. ResearchGate

16. Bell’s phenomenon weakness – Normally the eye rolls upward when the eyelids close; if this is weak, the cornea remains more exposed during partial closures, worsening surface stress. American Academy of Ophthalmology

17. Sleep-related eyelid dysfunction – Poor eyelid closure patterns during sleep beyond classic nocturnal lagophthalmos, such as incomplete micro-closures, contribute to cumulative dryness. ResearchGate

18. Chronic inflammatory eyelid conditions (blepharitis leading to secondary surface instability) – Though not classic exposure, eyelid inflammation impairs tear film and can coexist with mild exposure worsening epithelial breakdown.

19. Orbital apex or cranial base tumors affecting nerve control – Tumors compressing facial or trigeminal nerves disrupt eyelid motion or corneal sensation, combining exposure and neurotrophic injury. ScienceDirect

20. Prolonged oxygen therapy / chemosis from fluid overload – Swelling of the eyelids or conjunctiva (chemosis) can mechanically prevent good lid apposition and evoke lagophthalmos-like exposure. PMC

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Symptoms of Exposure Keratopathy

1. Dryness of the eye – A basic early symptom, caused by tear film evaporation. Wikipedia

2. Foreign body sensation – Feeling like something is in the eye, from surface epithelial disruption. American Academy of Ophthalmology

3. Redness (conjunctival injection) – Inflammation from surface stress and potential secondary irritation. ScienceDirect

4. Burning or stinging – Due to exposed nerve endings and tear instability. Semantic Scholar

5. Photophobia (light sensitivity) – Surface irregularity makes bright light uncomfortable. American Academy of Ophthalmology

6. Blurred vision – Irregular tear film and epithelial defects scatter light. ScienceDirect

7. Tearing (reflex epiphora) – Eye produces tears in response to irritation, paradoxically seen with dryness. Wikipedia

8. Decreased vision (if ulcer or scarring develops) – Advanced surface damage reduces visual clarity. Semantic Scholar

9. Grittiness or scratchiness – Mechanical feeling from epithelial loss. Wikipedia

10. Mucous discharge – Chronic irritation causes mucous accumulation. Academic Medicine and Pharmacy

11. Eyelid swelling or chemosis – Secondary inflammation or exposure-related surface irritation. PMC

12. Recurrent corneal epithelial pits/defects – Seen on staining as punctate epithelial erosions.

13. Corneal ulceration (painful, sometimes with discharge) – Progression of surface breakdown into deeper tissue. Semantic Scholar

14. Sensitivity to wind or air movement – Air quickly strips the tear film from an exposed surface. ScienceDirect

15. Nighttime worsening (due to lagophthalmos during sleep) – Symptoms may accumulate overnight if eyelids don’t close. ResearchGate

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Diagnostic Tests

A. Physical Examination (Direct observation and basic clinical tests)

1. Visual acuity testing – Measure how well the patient sees; helps assess if exposure is affecting vision. NCBI

2. External eyelid and closure exam – Look for lagophthalmos, eyelid retraction, ectropion, and eyelid laxity by asking the patient to close their eyes and observing completeness. NCBIScienceDirect

3. Slit-lamp examination with fluorescein staining – Vital to visualize epithelial defects, punctate erosions, and ulcerations (green staining shows damage).

4. Assessment of Bell’s phenomenon – Observe upward movement of the eye during forced eyelid closure; its weakness can worsen exposure consequences. American Academy of Ophthalmology

5. Blink rate observation – Count spontaneous blinks per minute; low blink rate increases risk. PMC

B. Manual / Functional Tests

6. Corneal sensitivity testing (esthesiometry) – Using Cochet-Bonnet or other aesthesiometers to measure sensation; reduced sensitivity signals neurotrophic risk and blunts protective responses. EyeWikiResearchGate

7. Tear breakup time (TBUT) – Place fluorescein and measure how long it takes for dry spots to appear; a short time means unstable tear film and contributes to exposure damage. ScienceDirect

8. Eyelid closure measurement (interpalpebral fissure) – Quantify how open the eye is at rest or during attempted closure; wider fissures mean more exposure. ScienceDirect

9. Manual corneal surface inspection (e.g., using a cotton tip light touch to assess defense reflex) – Quick clinical check for blink reflex and corneal awareness. ResearchGate

C. Laboratory / Pathological Tests

10. Corneal cultures and sensitivity – If infection is suspected (e.g., ulcer or discharge), scrape the epithelium to grow organisms. Semantic Scholar

11. PCR testing for viral agents (HSV, VZV) – When ulceration has atypical features, molecular testing rules in/out viral keratitis overlapping with exposure damage. Academic Medicine and Pharmacy

12. Tear osmolarity – High osmolarity indicates tear film instability and dry eye component worsening exposure injury. NCBI

13. Tear inflammatory marker assay (e.g., MMP-9) – Elevated markers reflect surface inflammation and stress. NCBI

14. Impression cytology – Sampling surface epithelial cells to evaluate chronic damage or goblet cell loss in prolonged exposure/dryness. NCBI

D. Electrodiagnostic Tests

15. Facial nerve conduction studies – Assess the function of the facial nerve controlling eyelid closure; helps determine cause of lagophthalmos. ResearchGate

16. Electromyography (EMG) of orbicularis oculi – Evaluates muscle activation for eyelid closure; distinguishes neuropathic versus myopathic causes. ResearchGate

17. Blink reflex testing (electrophysiology) – Measures the neural pathway of the blink, useful in assessing associated neurotrophic issues or reflex integrity. ResearchGate

E. Imaging and Objective Surface Evaluation

18. Anterior segment optical coherence tomography (AS-OCT) – Noninvasive imaging of the corneal layers to document epithelial defects, thickness changes, and healing progress. PubMed

19. Ocular surface topography / tear film imaging – Helps visualize tear film stability and surface irregularities that accompany exposure-related damage. ScienceDirect

20. Orbital imaging (CT or MRI) – Evaluates proptosis, orbital tumors, inflammation, or structural causes that increase exposure risk. WebEyeJournalAgent

Non-Pharmacological Treatments

1. Eyelid Taping: Gently taping the eyelids closed, especially during sleep or when the patient is unable to blink or close fully, keeps the cornea covered, reducing exposure and evaporation. It is a simple temporary measure used while more definitive treatments are arranged. American Academy of Ophthalmology

2. Moisture Chambers / Goggles: Transparent goggles or chamber devices trap humidity around the eye, preventing tear evaporation and allowing the corneal surface to stay hydrated. They are particularly useful in critically ill or sedated patients to prevent exposure injuries. ResearchGate

3. Frequent Blinking Exercises: Encouraging conscious blinking (especially during screen use) helps redistribute tear film and reduces localized drying. In partially alert patients, behavioral reinforcement of blinking can lessen early exposure. PMC

4. External Eyelid Weights (Non-surgical temporary): Adhesive or temporary weights placed on the upper eyelid help gravity-assist closure for patients with mild lagophthalmos, improving coverage without immediate surgery. EyeWiki

5. Eyelid Massage and Lid Hygiene: Keeping eyelid margins clean reduces inflammation from blepharitis, which can worsen tear quality and blink function. Regular gentle massage can promote meibomian gland function and more stable tear film. bmrat.biomedpress.org

6. Elevating the Head (Positioning): Especially in hospitalized or critically ill patients, keeping the head elevated (e.g., 30 degrees) reduces orbital and eyelid edema that might interfere with lid closure and predispose to exposure. ResearchGate

7. Environmental Humidification: Adding humidity to ambient air with humidifiers supports tear film retention and slows evaporation, particularly in dry climates or air-conditioned rooms. tearfilm.org

8. Protective Eyewear / Wind Shields: Wearing wraparound glasses or shields outdoors blocks wind and desiccating air, reducing mechanical tear film loss and particulate irritation. Verywell Health

9. Avoiding Sedatives That Decrease Blink: Minimizing or adjusting medications (when medically feasible) that suppress blink reflex or cause incomplete lid closure (e.g., heavy sedatives) can reduce risk. American Academy of Ophthalmology

10. Eyelid Position Monitoring: Regular clinical checks for lagophthalmos in patients with facial palsy, thyroid eye disease, or cranial nerve dysfunction allow early intervention before corneal damage sets in. Vagelos College

11. Use of Eyelid Closure Devices in ICU (Polyethylene/Film Covers): In critically ill patients, using impermeable films or covers over closed eyelids helps maintain moisture and protects the cornea from exposure when blink is absent. ResearchGate

12. Scheduled Eye Exams in At-Risk Patients: Regular ophthalmologic evaluation for patients with known risk (thyroid orbitopathy, facial nerve palsy) ensures early detection of exposure signs. Vagelos College

13. Blink Reminders for Screen Users: Digital or environmental cues to blink during prolonged screen exposure help keep the surface wet; technology fatigue can worsen exposure damage. PMC

14. Limiting Airflow Directly on Eyes (Fans / AC): Redirecting fans or air conditioners away from the face reduces forced evaporation of tears. Verywell Health

15. Cold or Warm Compresses: Depending on underlying eyelid disease, a warm compress can help unblock meibomian glands (improving tear lipid layer), while cool compresses may reduce surface inflammation. PMC

16. Facial Nerve Physical Therapy: For patients with partial facial nerve palsy, therapy to strengthen orbicularis oculi function may improve eyelid closure over time. Vagelos College

17. Patient Education: Teaching patients and caregivers about signs of early exposure (dryness, foreign body sensation, redness) encourages prompt self-reporting and care. American Academy of Ophthalmology

18. Temporary Botulinum-Induced Ptosis: Inducing a mild droop of the upper eyelid temporarily (via botulinum toxin) can protect the cornea in patients with severe exposure when surgery is being planned. American Academy of Ophthalmology

19. Partial Eyelid Closure (Conservative “Manual” Closure): In awake patients, manually helping the eyelids close during rest or sleep (e.g., with a gentle finger) can reduce exposure until more lasting therapy is applied. American Academy of Ophthalmology

20. Therapeutic Contact Lenses (Bandage Lenses): Soft therapeutic lenses act as a protective covering over the cornea, maintaining hydration and shielding the surface while healing occurs. (Note: used with caution due to infection risk and typically under ophthalmologist supervision.) ScienceDirect

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Drug Treatments (Evidence-Based)

1. Preservative-Free Artificial Tears (Lubricants): These are the frontline medications. They add moisture, improve tear film stability, and dilute inflammatory mediators on the surface. Frequent use (every 1–2 hours or as needed) is safe and helps prevent epithelial breakdown. Preservative-free formulations avoid toxicity from preservatives during chronic use. American Academy of OphthalmologyPMC

2. Topical Cyclosporine A (e.g., Restasis, Cequa): This immunomodulator reduces ocular surface inflammation, improves tear production over weeks to months, and helps restore the health of the ocular surface in chronic exposure-related dry inflammation. Dose is commonly twice daily; it may take 2–3 months to see substantive improvement. Side effects include burning or stinging on instillation. PMCScienceDirectFrontiers

3. Lifitegrast (Xiidra): An integrin antagonist that blocks inflammatory cell adhesion signaling, providing quicker symptom relief in dry/inflammatory exposure-related surface disease. Typically dosed twice daily. Side effects may include transient eye irritation or taste disturbance. LongdomVerywell Health

4. Topical Low-Potency Corticosteroids (e.g., Loteprednol): Used short-term to reduce surface inflammation and facilitate healing in moderate cases. Because of intraocular pressure and cataract risks, they are limited-duration, under supervision. American Academy of Ophthalmology

5. Topical Antibiotic Drops (e.g., Moxifloxacin, Polytrim): In patients with epithelial defects or risk of secondary infection (especially when protective barriers are compromised), prophylactic or therapeutic broad-spectrum topical antibiotics are used to prevent corneal ulcers. Use is guided by clinical severity; prolonged or unsupervised use risks resistance. American Academy of Ophthalmology

6. Topical NSAID Drops (with caution): These may be used for surface inflammation or postoperative pain but must be used cautiously because they can delay epithelial healing in exposed/defective corneas. Not first-line in severe epithelial defects. PMC

7. Lubricating Ointments (e.g., Petrolatum-based) at Night: Thick formulations applied before sleep keep the ocular surface lubricated during periods of reduced blinking, particularly in lagophthalmos. They can blur vision temporarily and are mainly for nighttime use. American Academy of Ophthalmology

8. Oral Tetracyclines (e.g., Doxycycline for Meibomian Dysfunction): In cases where meibomian gland dysfunction worsens tear quality and exposure, low-dose doxycycline reduces lid inflammation and improves lipid quality, indirectly supporting tear film and ocular surface health. PMC

9. Topical Secretagogues (e.g., Diquafosol – in countries where available): These promote mucin and aqueous secretion from conjunctival cells, aiding surface lubrication. (More common in Asia; mechanism is via P2Y2 receptor stimulation.) Wikipedia

10. Adjunctive Topical Antioxidants (as formulations or in compounded drops): Emerging use of agents that reduce oxidative stress may support healing, though these are usually in experimental or adjunctive use. tearfilm.org

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Dietary Molecular Supplements

1. Omega-3 Fatty Acids (EPA/DHA): Commonly taken as fish oil capsules (e.g., 1000–3000 mg/day of combined EPA/DHA), they modulate inflammation in the tear film, improve meibomian gland function, and enhance tear stability. They shift the lipid mediator balance toward anti-inflammatory profiles. Evidence is mixed but often beneficial in chronic ocular surface dryness. PMCMDPI

2. Vitamin A: Critical for corneal epithelial health and mucin production. Dietary sources (carrots, leafy greens) or supplementation in deficiency (dosage tailored clinically) support surface regeneration. Vitamin A prevents keratinization and maintains a healthy epithelium. EyeWiki

3. Vitamin D: Low serum vitamin D is associated with dry eye signs. Supplementation (e.g., 1000–2000 IU daily or per deficiency correction guidelines) may reduce inflammation and improve tear production indirectly. EyeWikiFrontiers

4. Curcumin: A natural anti-inflammatory from turmeric, curcumin downregulates inflammatory cytokines that can exacerbate ocular surface stress. Studies combining it with lutein/zeaxanthin and vitamin D show protective effects in dry eye models. Typical supplemental doses vary; bioavailability-enhanced formulations are preferred. Frontiers

5. Lutein and Zeaxanthin: Carotenoids with antioxidant properties; they protect ocular surface cells from oxidative stress and may help reduce inflammatory signaling. Often included in combination supplements for eye health. Frontiers

6. Vitamin C: Supports collagen synthesis and acts as an antioxidant on the ocular surface; helps neutralize reactive oxygen species generated during chronic inflammation. Dietary intake from citrus and supplementation can support healing. EyeWiki

7. Vitamin E: Lipid-soluble antioxidant that protects cell membranes in corneal epithelium from oxidative damage; often paired with other vitamins in ocular supplements. EyeWiki

8. Zinc: Trace element important for wound healing and immune modulation. Adequate zinc supports corneal epithelial turnover and resilience. Foods include oysters, meat, and seeds; supplementation should avoid excess. EyeWiki

9. N-acetylcysteine (NAC): Acts as a mucolytic and antioxidant; in ocular surface disease it may improve tear film quality and reduce surface inflammation by replenishing glutathione. Typical oral dosages are 600 mg twice daily in other contexts, but ocular-specific use should be guided by practitioner. MDPI

10. Gamma-Linolenic Acid (GLA): Found in evening primrose or borage oil, GLA can modulate inflammatory pathways and has been studied for ocular surface dryness, helping stabilize tear film in select patients. MDPI

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Regenerative / “Hard Immunity” / Biologic / Stem Cell–Related Therapies

1. Cenegermin (Recombinant Human Nerve Growth Factor): An FDA-approved topical biologic for neurotrophic keratitis, typically dosed as one drop six times a day for eight weeks. It promotes corneal nerve healing, restores epithelial integrity, and improves sensation. It acts by binding to TrkA receptors, stimulating nerve growth and epithelial recovery. Side effects are generally mild; cost and access can be limiting factors. PubMedMDPIFrontiers

2. Autologous Serum Eye Drops: Made from the patient’s own blood, these drops contain growth factors, vitamins, and proteins similar to natural tears, promoting epithelial healing in persistent defects. Concentrations (often 20–100%) and dosing vary, usually instilled multiple times daily. They are especially useful in refractory exposure-related epithelial breakdown or combined neurotrophic states. PMCPMCNature

3. Platelet-Rich Plasma (PRP) Eye Drops: Prepared from patient’s blood, PRP delivers high concentrations of growth factors (like PDGF, TGF-β) to the ocular surface, accelerating healing and reducing inflammation. Clinical studies show symptom improvement and epithelialization in surface disease. Dosing protocols vary, typically several times daily for weeks. PMCBMJ OphthalmologyResearchGate

4. Topical Insulin: Emerging data support topical insulin’s role in healing persistent epithelial defects, especially in neurotrophic or combined exposure situations. It promotes cellular metabolism and regeneration via insulin receptor pathways. Early-use regimens vary (case reports describe multiple daily applications), and larger studies are ongoing. Modern OptometryMDPI

5. Amniotic Membrane Transplantation (Biologic Graft): Surgically applied as a biological scaffold (e.g., PROKERA or sutured graft), the amniotic membrane delivers anti-inflammatory cytokines and supports epithelial regrowth in non-healing defects. It modulates fibrosis, reduces inflammation, and provides a substrate for cells to migrate. ScienceDirect

6. Allogeneic Serum / Umbilical Cord–Derived Eye Drops: Similar to autologous serum but from donor sources, these provide growth factors for patients who cannot donate their own blood (e.g., severe anemia). They support healing of epithelial defects when autologous is not feasible. Nature

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Surgeries

1. Tarsorrhaphy: Partial sewing together of eyelids to reduce the exposed corneal surface area. It is done to protect the cornea when closure or blink cannot be restored and to allow healing of persistent defects by mechanically limiting exposure. American Academy of Ophthalmology

2. Upper Eyelid Weight Implantation (Gold or Platinum Weight): Surgically implanted into the upper eyelid (usually in facial nerve palsy) to assist eyelid closure by gravity. It helps prevent exposure when orbicularis oculi function is impaired. EyeWiki

3. Eyelid Repositioning / Lid Tightening (Canthoplasty, Lid Retraction Repair): Corrects structural eyelid malposition (e.g., lid retraction in thyroid eye disease) so that the lid covers the cornea properly, restoring a normal blink and reducing exposure. Vagelos College

4. Botulinum-Induced Ptosis (Temporary Surgical/Injection Procedure): Used as a temporary protective measure by lowering the upper eyelid to cover the cornea, often used while planning permanent surgery. American Academy of Ophthalmology

5. Amniotic Membrane Transplantation (also surgical, as noted): Applied directly to the damaged cornea to promote epithelial healing and reduce inflammation, particularly for persistent epithelial defects unresponsive to conservative therapy. ScienceDirect

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Preventions

1. Early Identification of Risk Factors: Screening patients with facial palsy, thyroid eye disease, or decreased consciousness for eyelid closure problems prevents delayed onset of keratopathy. Vagelos College

2. Routine Lubrication: Scheduled use of artificial tears or ointments before damage begins, especially at night and during dry conditions, keeps the surface protected. American Academy of Ophthalmology

3. Moisture Chamber Use in High-Risk Periods: Applying humidity barriers during sedation, sleep, or in ICUs stops tear evaporation before injury occurs. ResearchGate

4. Manage Underlying Proptosis or Eyelid Retraction Early: Treating thyroid eye disease or correcting lid malposition reduces mechanical exposure. Vagelos College

5. Protect Eyes from Dry Ambient Air (Humidifiers): Maintaining environmental humidity reduces baseline stress on the tear film. tearfilm.org

6. Avoidance of Medications That Worsen Blink When Possible: Reviewing sedating or nerve-affecting medications that reduce eyelid closure or blink reflex. American Academy of Ophthalmology

7. Frequent Eye Checks in Critical Care: Protocolized eye care (checks, lubrication, covers) in sedated or ventilated patients prevents silent exposure. ResearchGate

8. Use of Eyelid Closure Techniques During Surgery or Sedation: Taping or temporary closure during procedures avoids perioperative exposure. American Academy of Ophthalmology

9. Hydration and Systemic Health Optimization: Adequate systemic hydration and addressing systemic inflammation support tear production and surface defense. tearfilm.org

10. Educating Caregivers and Patients: Awareness of warning signs leads to faster intervention before irreversible damage. American Academy of Ophthalmology

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When to See a Doctor

You should see an eye doctor promptly if you experience persistent redness, pain, foreign body sensation not resolving with basic lubrication, blurry or decreased vision, sensitivity to light, a visible white spot on the cornea (possible ulcer), discharge suggesting infection, inability to close the eyelid fully, or if an epithelial defect has not healed in 5–7 days despite conservative care. Also seek care if symptoms occur in someone unable to report them (e.g., hospitalized/comatose) and preventive protocols are failing. American Academy of OphthalmologyLippincott Journals

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What to Eat

Eating foods that support tear film quality, reduce inflammation, and provide essential micronutrients helps overall ocular surface resilience. Recommended foods include fatty fish (salmon, mackerel) for omega-3s; carrots and sweet potatoes for beta-carotene (vitamin A); leafy greens (spinach, kale) for lutein/zeaxanthin; eggs for lutein and zinc; citrus fruits for vitamin C; nuts and seeds for vitamin E and zinc; bell peppers for multiple antioxidants; berries for anti-inflammatory flavonoids; whole grains for stable blood sugar supporting microvascular health; and staying well-hydrated with water to maintain tear volume. PreventionEyeWiki

What to Avoid

Avoid smoking (oxidative stress), excessive screen time without breaks (reduced blink), dehydration (low tear volume), high refined sugar intake (promotes systemic inflammation), excessive omega-6-rich processed oils that can imbalance inflammatory mediators, unprotected exposure to wind or dry air, overuse of contact lenses in compromised surfaces, indiscriminate use of preserved eye drops (can cause surface toxicity), over-the-counter steroid misuse without supervision, and environmental irritants like smoke or chemical fumes. Verywell Healthtearfilm.org

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Frequently Asked Questions (FAQs)

1. What is the earliest sign of exposure keratopathy?
   The earliest signs are dryness, redness, a gritty feeling, or small punctate erosions on the cornea seen with a slit lamp. These often precede more serious damage. American Academy of Ophthalmology

2. Can it heal on its own?
   Mild exposure can improve with protective measures like lubrication and eyelid taping, but persistent or severe cases need targeted treatment to avoid complications. American Academy of Ophthalmology

3. Are artificial tears enough?
   Artificial tears are the foundation, but if the eyelid closure problem persists or defects don’t heal, additional interventions (like tarsorrhaphy or biologics) are needed. American Academy of OphthalmologyPMC

4. What if I have facial nerve palsy?
   Early use of eyelid weights, lubrication, and possibly surgical eyelid procedures can protect the cornea while nerve function recovers. EyeWiki

5. Is surgery always needed?
   Not always. Many cases are managed non-surgically, but surgery becomes necessary when exposure is severe, chronic, or threatens vision (e.g., tarsorrhaphy, weight implants). American Academy of OphthalmologyVagelos College

6. What is the role of nerve growth factor?
   Recombinant nerve growth factor (cenegermin) stimulates corneal nerve healing and epithelial recovery in neurotrophic-related defects, improving both sensation and surface integrity. MDPIFrontiers

7. Are autologous serum drops safe?
   Yes, when prepared properly, they are safe and biologically supportive for chronic epithelial defects, supplying growth factors and vitamins similar to natural tears. PMCPMC

8. Can diet help?
   Yes. Nutrients like omega-3s, vitamins A, D, C, E, lutein, and zinc support surface health and reduce inflammation. A balanced diet with these can complement direct treatments. EyeWikiMDPI

9. What are the risks of untreated exposure keratopathy?
   It can progress to persistent epithelial defects, corneal ulcers, infections, scarring, and vision loss — some of which can be permanent. American Academy of OphthalmologyLippincott Journals

10. How quickly does cenegermin work?
    Most patients with moderate-to-severe disease show healing over the 8-week course, with many achieving complete epithelial closure by the end of therapy. Frontiers

11. Can I use contact lenses?
    Therapeutic (bandage) contact lenses can be used under supervision for protection, but regular contacts should be avoided if the cornea is compromised due to increased infection risk. ScienceDirect

12. Is exposure keratopathy painful?
    It can cause pain, though in neurotrophic variants the sensation may be reduced and patients might not feel severe damage until advanced. ScienceDirectLippincott Journals

13. Do I need antibiotics?
    If there is an epithelial defect with signs of infection or high risk (like prolonged exposure), topical prophylactic antibiotics may be used to prevent ulcers. American Academy of Ophthalmology

14. Can inflammation alone cause exposure-like damage?
    Yes. Chronic surface inflammation (for example from dry eye) can destabilize the tear film, worsening exposure and creating a vicious cycle; treating inflammation is important. PMC

15. Are there any new or experimental treatments?
    Yes—topical insulin and evolving stem cell or exosome-based therapies are being studied to promote healing in refractory cases, showing promise in early reports. MDPIResearchGate

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Last Updated: August 04, 2025.

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