ICU-Associated Exposure Keratopathy and Preventable Corneal Blindness: A Clinical Review

Abstract

Exposure keratopathy is an ocular surface injury caused by prolonged corneal exposure, most often from incomplete eyelid closure. Critical illness can intensify exposure through reduced blinking, chemosis, impaired corneal reflexes, sedation, mechanical ventilation, and tear film instability. This narrative clinical review synthesizes contemporary evidence on epidemiology, mechanisms, risk factors, bedside assessment, prevention, protocol implementation, and care in resource-constrained intensive care units (ICUs). PubMed/MEDLINE was searched for English language literature from January 2000 through 15 September 2026, supplemented by reference list and guideline searches. Systematic reviews, randomized trials, cohort studies, quality improvement reports, and relevant guidance were prioritized. Pooled evidence indicates that exposure keratopathy is common among critically ill patients, and recent trials support scheduled lubrication, eyelid closure support, and moisture chamber approaches, particularly when the cornea remains exposed. Fluorescein assessment and clear ophthalmology referral criteria improve detection of epithelial injury and complications that threaten vision. The review distinguishes evidence from randomized and observational studies and proposes a pragmatic bedside risk framework without presenting it as a validated score. Its principal contribution is the integration of prevention, nursing workflow, clinical escalation, and resource appropriate implementation into a single ophthalmic patient safety framework. The intended audience is ophthalmologists, intensivists, ICU nurses, optometrists, and quality improvement teams. Early structured eye care may reduce avoidable corneal morbidity while supporting consistent practice across settings with different resources.

Introduction

Vision preservation is commonly discussed in relation to cataract, glaucoma, diabetic retinopathy, refractive error, and retinal disease. Avoidable corneal injury during hospital care is also an important source of visual morbidity. The World Health Organization has emphasized integrated people‑centred eye care and reduction of avoidable vision impairment across health systems.¹ Patient safety frameworks similarly prioritize harm that can be reduced through reliable clinical processes, staff training, and better implementation.² Exposure keratopathy in the ICU lies at the intersection of these priorities because it is an ophthalmic complication, a quality of care problem, and a potential pathway to severe corneal morbidity.

Exposure keratopathy is an ocular surface injury caused by prolonged corneal exposure, usually because eyelid closure is incomplete or absent. Reduced blinking, tear film instability, lagophthalmos, chemosis, sedation, mechanical ventilation, and impaired consciousness are mechanisms and risk factors that increase the duration or severity of exposure. Earlier reviews established the importance of this problem in critical care, but they predated several contemporary prevention trials, electronic order interventions, recent meta analyses, and current implementation guidance.^3,4

The burden is clinically substantial. Cohort studies and reviews consistently report exposure keratopathy in sedated, ventilated, and neurologically impaired patients.^5–9 A recent systematic review and meta analysis estimated a pooled prevalence of 34.0% and a pooled incidence of 23.0% among critically ill patients.⁴ Differences in case definition, timing of examination, patient mix, and baseline eye care explain some variation between studies, but the condition is clearly common enough to justify routine prevention.

The mechanism is not confined to critical care. Exposure keratopathy during prolonged general anesthesia follows the same sequence of reduced tear production, absent blinking, and incomplete eyelid closure.^10,11 Low humidity and dry environmental conditions can further destabilize the exposed ocular surface.¹² These parallels reinforce the broader principle that unconscious or heavily sedated patients require active corneal protection.

Baseline vulnerability can also modify risk. Proptosis, shallow orbits, eyelid laxity, preexisting lagophthalmos, chronic ocular surface disease, and previous ocular or adnexal cancer treatment may reduce ocular surface reserve.^13,14 Hormonal change and therapies associated with ocular dryness may provide additional background susceptibility in selected patients, although their independent contribution to ICU exposure keratopathy has not been quantified.¹⁵

The direct economic burden of ICU acquired exposure keratopathy has not been well quantified. Prevention, however, relies mainly on low cost measures such as lubrication, eyelid closure support, and moisture barriers, whereas established microbial keratitis, corneal ulceration, or perforation may require intensive antimicrobial therapy, surgery, prolonged follow up, or transplantation. This contrast provides a practical rationale for prevention, while formal cost-effectiveness studies remain necessary.

This review updates the clinical evidence and extends previous reviews by integrating current comparative trials, bedside screening, pediatric data, nursing workflow, management of established disease, protocol implementation, and a resource based framework for ICUs with different levels of ophthalmic support.

Methods and Review Approach

This article is a narrative clinical review rather than a systematic review or meta analysis. PubMed/MEDLINE was searched for English language publications from January 2000 through 15 September 2026, while selected earlier seminal studies were retained when directly relevant. Reference lists of key reviews and trials were hand searched, and major professional and health system guidance documents were examined. Search concepts included exposure keratopathy, ocular surface disease, corneal injury, intensive care, mechanical ventilation, sedation, lagophthalmos, chemosis, fluorescein, lubrication, ophthalmic ointment, eyelid taping, moisture chamber, polyethylene cover, bandage contact lens, punctal plug, neurotrophic keratopathy, and eye care protocol.

Priority was given to systematic reviews and meta analyses, randomized clinical trials, prospective cohort studies, comparative observational studies, quality improvement reports, and clinically relevant guidance. Case reports were not used to establish routine practice. Sources were selected for direct relevance to critically ill patients, ocular surface injury, prevention, clinical escalation, or implementation. Quantitative pooling was not performed.

Evidence is interpreted according to study design rather than a formal grading system. Systematic reviews, meta analyses, and randomized trials provide the strongest comparative evidence; observational studies inform epidemiology and risk; quality improvement studies inform implementation; and professional guidance supports pragmatic bedside practice. The risk framework proposed later in this review is a clinical synthesis and has not been validated as a predictive scoring system.

Why Critically Ill Patients Develop Ocular Surface Failure

The healthy ocular surface depends on complete eyelid closure, spontaneous blinking, adequate tear secretion and distribution, corneal sensation, epithelial integrity, and antimicrobial components of the tear film. Sedatives and neuromuscular blocking agents reduce blink frequency and orbicularis tone. Mechanical ventilation and reduced consciousness impair eyelid closure and corneal reflexes, while positive pressure ventilation and fluid shifts may contribute to chemosis. Systemic instability may also reduce tear production and epithelial healing.^6–8

Lagophthalmos is the most visible pathway. Even a small persistent palpebral aperture can expose the inferior cornea to desiccation. Chemosis can mechanically prevent complete closure and elevate conjunctiva above the eyelid margin. Reduced blinking limits tear redistribution and debris clearance. In patients with a low Glasgow Coma Scale (GCS), neurological injury, or deep sedation, warning symptoms may be absent, creating a clinically important interval between disease progression and recognition.^4,9

Mechanical ventilation is both a marker of illness severity and part of a cluster that includes sedation, reduced blink, immobility, facial edema, facial tubing, and prolonged exposure. Prone positioning can add facial edema, ocular compression, incomplete closure, and reduced access for examination.¹⁶ Environmental desiccation from low humidity may further destabilize an already exposed tear film.¹² Figure 1 summarizes the principal pathophysiological sequence.

Figure 1.

Pathophysiological pathway to ICU‑associated ocular surface failure. Critical illness and organ support impair blinking, corneal reflexes, and eyelid closure, while lagophthalmos, chemosis, tear evaporation, and baseline vulnerability promote epithelial injury.

Epidemiology and Risk Factors

Reported rates differ because studies use different definitions, grading systems, patient populations, examination schedules, fluorescein methods, and baseline eye care protocols. Earlier evidence suggested that approximately 20% to 42% of ICU patients may develop exposure keratopathy.³ More recent pooled evidence estimated prevalence at 34.0% and incidence at 23.0%.⁴

Among mechanically ventilated adults, Al-Tamimi et al reported exposure keratopathy in 42.3%, with lower GCS, inotrope use, and longer hospital stay associated with disease.⁸ Lagophthalmos and chemosis also recur as important risk factors across cohort studies.^6,7,9 These observations support direct examination of eyelid closure and ocular surface status rather than relying on severity of illness alone.

Pediatric patients require specific surveillance. Hartford et al documented exposure keratopathy across several ICU populations, including pediatric care.⁹ In a prospective pediatric ICU cohort, ocular surface disease was present in 15% of children at admission and occurred during hospitalization in 32.2% of those who underwent repeated examinations. Under a dynamic care protocol, 8.6% had ocular surface disease at the final assessment, and no severe infiltrates, ulcers, or scars were reported.¹⁷ Pediatric practice should therefore be informed by age‑specific evidence rather than assumed to mirror adult care completely.

Additional factors that may modify susceptibility include perioperative exposure after prolonged anesthesia, dry ambient air or directed oxygen flow near the ocular surface, supine or prone positioning, proptosis, eyelid laxity, and preexisting ocular surface disease. Cancer‑related ocular surface compromise and treatment‑associated dryness may further reduce reserve in selected patients. These factors should be considered baseline or contextual modifiers unless stronger ICU‑specific evidence demonstrates independent risk. Table 1 summarizes clinically relevant risk factors and their implications.

Table 1.

Risk Factors for Exposure Keratopathy in the ICU and Their Clinical Implications

Risk Factor	Mechanism	Clinical Implication
Mechanical ventilation	Often accompanies sedation, reduced blinking, facial edema, and prolonged exposure.6–9	Examine eyelid closure and ocular surface status daily; consider scheduled prophylaxis.
Reduced consciousness	Limits symptom reporting, blinking, and protective responses.6–9	Treat marked impairment, including GCS of 8 or less, as high risk.
Sedation or neuromuscular blockade	Reduces orbicularis tone and blink frequency and can prevent complete closure.6–8	Use lubrication together with reliable closure or a moisture chamber when exposure is present.
Lagophthalmos	Produces direct and persistent corneal exposure.6,7,9	Initiate a closure strategy and reassess closely.
Chemosis	Conjunctival swelling may mechanically prevent full eyelid closure.6,8,9	Escalate protection when chemosis is severe or prevents closure.
Dry ambient air or directed oxygen	Can increase tear evaporation and surface desiccation.12	Minimize avoidable airflow toward the eye and strengthen moisture preservation.
Supine or prone positioning	Positioning can alter exposure; prone care can add edema, pressure, and reduced access.16	Inspect before and after repositioning and avoid direct globe pressure.
Anatomical predisposition	Proptosis, shallow orbits, eyelid laxity, or baseline lagophthalmos reduce protective reserve.	Identify at admission and use a lower threshold for prophylaxis.
Preexisting ocular surface compromise	Previous ocular or adnexal surgery, cancer therapy, dry eye, or epithelial disease can reduce baseline reserve.13–15	Document baseline status and consider early ophthalmology input.
Perioperative exposure	General anesthesia reduces blinking and tear stability.10,11	Continue ocular protection when vulnerable patients transition from the operating room to the ICU.
Prolonged ICU stay	Increases cumulative exposure and opportunity for epithelial injury.5,8	Continue surveillance throughout prolonged ventilation or reduced consciousness.
Poor protocol adherence	Missed lubrication, closure, or reassessment can increase preventable harm.18	Use simple checklists, handover prompts, education, and audit.

Abbreviations: GCS, Glasgow Coma Scale; ICU, intensive care unit.

Clinical Spectrum and Ophthalmic Assessment

The clinical spectrum begins with dryness, conjunctival injection, tear film instability, and punctate epithelial erosions. Persistent exposure may progress to a larger epithelial defect, sterile ulceration, microbial keratitis, stromal thinning, scarring, perforation, endophthalmitis, and permanent visual impairment. In selected patients, persistent epithelial breakdown may acquire features of neurotrophic keratopathy with impaired healing. Because many ICU patients cannot reliably report pain, photophobia, or reduced vision, surveillance cannot depend on symptoms.

Bedside assessment should include eyelid position and closure, spontaneous blink, lagophthalmos, chemosis, conjunctival injection, discharge, corneal clarity, and visible epithelial defect. Fluorescein staining with cobalt blue illumination or a portable slit lamp improves detection. In one prospective study, ICU clinicians using fluorescein and a pen torch with a blue filter achieved 77.8% sensitivity and 96.7% specificity for keratopathy compared with ophthalmologist examination using a portable slit lamp.¹⁹ This finding supports structured screening where continuous ophthalmology coverage is unavailable.

Patients at high risk should be reassessed daily, or more often when epithelial disease is progressing. When daily specialist review is not possible, trained bedside staff can document eyelid closure and fluorescein findings, and serial photography may assist communication with ophthalmology if institutional privacy and imaging standards are met.

Urgent ophthalmology review is indicated for corneal opacity, infiltrate, epithelial defect, ulceration, purulent discharge, severe chemosis that prevents closure, rapid deterioration, suspected microbial keratitis, or failure of basic protection. When microbial keratitis or corneal ulceration is suspected, corneal sampling should be obtained when feasible without delaying treatment, and empiric intensive topical antimicrobial therapy should begin promptly according to local microbiology, severity, and corneal specialist guidance.

Persistent epithelial defects or neurotrophic keratopathy that fail conventional exposure correction and lubrication may require specialist therapies. Cenegermin has randomized trial evidence for neurotrophic keratopathy, whereas topical insulin has emerging supportive evidence for persistent epithelial defects and related ocular surface disorders.^20,21 These therapies are not routine ICU prophylaxis and should not displace correction of exposure, infection control, and timely specialist management.

Prevention Strategies

Lubrication

Artificial tears can supplement the tear film in mild disease, but aqueous drops have short retention and may evaporate rapidly when the cornea remains exposed. Ointments persist longer and reduce evaporation, which makes them practical for scheduled prophylaxis in sedated or ventilated patients, although transient blur can complicate frequent pupillary assessment.

Comparative evidence generally favors longer retention or combined approaches over drops alone. A 2024 systematic review found that polyethylene covers, gels, and ointments were broadly protective, whereas aqueous drops and adhesive tape used alone were less consistently effective.²²

Mechanical Eyelid Closure

Eyelid taping directly addresses lagophthalmos and is inexpensive, but technique is important. The eyelids should be gently closed without pressure on the globe, tape should not contact the cornea, skin trauma should be minimized, and closure should be checked again after repositioning. Taping alone does not correct tear film instability.

Temporary tarsorrhaphy can protect severe or refractory exposure, but it is often impractical in the ICU because disease may be bilateral and repeated pupillary or neurological examinations may be required. Nonsurgical closure methods are therefore preferable for routine prophylaxis, with tarsorrhaphy reserved for selected refractory cases under ophthalmology supervision.

Moisture Chamber Approaches

Moisture chambers and transparent polyethylene covers reduce evaporation and create a humid microenvironment while preserving visual access to the eye. A meta analysis of seven randomized trials found less corneal damage with moisture chambers than with lubrication overall (risk ratio 0.27, 95% confidence interval 0.11 to 0.67). The difference was not statistically significant when moisture chambers were compared specifically with lubricating ointment (risk ratio 0.81, 95% confidence interval 0.51 to 1.29). The overall certainty of evidence was low, so these findings support selection according to exposure severity, workflow, and availability rather than a universal hierarchy.²³

Commercial moisture chambers are not available in all settings. Transparent, single patient polyethylene film may be a practical alternative when approved by local infection prevention policy and monitored for skin integrity, displacement, and contamination.

Combined and Adjunctive Approaches

Combined therapy is reasonable when exposure and tear film instability coexist. In a randomized trial of 156 intubated ICU patients, polyethylene cover plus ophthalmic ointment reduced corneal abrasion more effectively than polyethylene cover alone or polyethylene cover plus artificial tears.²⁴ Other randomized studies support ointment, polyethylene cover, or combined approaches over routine care, saline, or taping alone.^25–27

A randomized pilot trial found that bandage contact lenses and punctal plugs reduced keratopathy more effectively than lubrication alone in selected mechanically ventilated patients, with healing of some existing lesions in the bandage lens group.²⁸ These are specialist adjuncts. A bandage lens can desiccate or increase microbial risk when exposure persists or monitoring is inadequate, and a punctal plug does not correct incomplete eyelid closure.

Hydrogel dressings have also been evaluated for ocular surface protection.²⁹ Overall, no single product is sufficient for every patient. The most defensible strategy is care matched to risk that preserves moisture, achieves reliable eyelid closure, avoids pressure on the globe, and permits repeated examination. Table 2 compares the main preventive options.

Table 2.

Comparison of Preventive and Adjunctive Interventions for Critically Ill Patients

Intervention	Strengths	Limitations	Best Use
Artificial tears	Accessible and useful for mild dryness.	Short retention and frequent dosing; less effective when exposure persists.	Low to moderate risk with preserved eyelid closure.22
Ophthalmic ointment	Longer retention and reduced evaporation; practical for scheduled prophylaxis.	Transient blur can complicate pupil checks; contamination risk if shared.	Moderate to high risk, particularly in ventilated or sedated patients.22–25
Eyelid taping	Directly addresses lagophthalmos and is inexpensive.	Can cause skin injury or incomplete closure if applied poorly; globe pressure must be avoided.	Lagophthalmos when staff are trained and closure can be checked.
Polyethylene cover or moisture chamber	Creates a humid environment, is transparent, and reduces evaporation.	Can dislodge; infection prevention and replacement procedures are required.	High risk exposure, chemosis, or poor blink.22,23,26,27
Ointment plus cover or closure	Addresses both tear film instability and exposure.	Requires reliable technique and supplies.	Patients with substantial exposure or multiple risk factors.24
Bandage contact lens	Pilot randomized evidence suggests preventive and healing benefit.	Requires ophthalmology oversight; desiccation and infection are concerns if monitoring is poor.	Selected patients with refractory epithelial disease.28
Punctal plug	Reduces tear drainage and showed benefit in a pilot trial.	Does not correct exposure; specialist placement and follow up are required.	Selected patients under ophthalmology supervision.28
Temporary tarsorrhaphy	Provides strong mechanical closure in severe exposure.	Limits examination and may be impractical when disease is bilateral or pupil checks are frequent.	Selected severe or refractory cases.
Protocol or order set	Improves consistency, documentation, and accountability.	Effect depends on adherence, education, and audit.	All ICUs; paper tools are suitable when electronic systems are unavailable.5,30–32

Abbreviation: ICU, intensive care unit.

Protocolized ICU Eye Care and Quality Improvement

Protocolized care is one of the strongest implementation lessons in this field. Kousha et al used a two phase prospective cohort design and reported a marked reduction in exposure keratopathy after introduction of a risk based eye care protocol.⁵ Education programs have also improved recognition and standardized care.³⁰

Nursing adherence is central because the effect of lubrication or eyelid closure depends on correct and repeated application. Inconsistent compliance with eye care has been associated with ocular complications in ICU patients.¹⁸ Education should therefore explain that apparently minor exposure can progress to irreversible corneal injury and should link bedside adherence to a concrete patient safety outcome.

Electronic medical record interventions can improve consistency where digital systems are available. Swiston et al found greater use of ophthalmic ointment after an electronic order protocol, although the observed reduction in exposure keratopathy was not statistically significant.³¹ A more recent protocol study across several ICU types reported a significant overall decrease in exposure keratopathy after implementation, while also showing that correct prophylaxis administration remained incomplete.³² Electronic prompts can initiate prevention, but education, auditing, and nursing ownership are required to sustain it.

A practical protocol should define who is screened, what findings are documented, which intervention is used at each risk level, how often the eyes are reassessed, when ophthalmology is contacted, and how adherence is audited. In resource-constrained hospitals, the same principles can be implemented with paper checklists, bedside reminders, nursing charts, handover prompts, and brief multidisciplinary review.

Implementation in Resource-Constrained ICUs

Resource‑constrained ICUs may have limited ophthalmology coverage, shortages of lubricants, no portable slit lamp, limited access to cobalt blue illumination, high nursing workload, and inconsistent documentation. Professional guidance nonetheless emphasizes regular examination, basic ocular surface protection, and early escalation.^33,34 The essential actions are simple: identify patients at risk, inspect eyelid closure, lubricate exposed eyes, secure safe closure, reduce evaporation, and refer promptly when warning signs appear.

A basic bundle can use sterile ocular lubricant where available, gentle eyelid closure, hypoallergenic tape applied without globe pressure, and a transparent single patient moisture barrier when locally approved. Single patient materials reduce cross contamination. Infection prevention policy should address handling, replacement frequency, and contamination of ointment tubes or covers. Routine saline washing should not be regarded as a substitute for tear film protection.

Where ophthalmologists are not on site, escalation criteria should be explicit. An epithelial defect, corneal opacity, suspected infiltrate, purulent discharge, severe chemosis that prevents closure, trauma, chemical exposure, or persistent redness despite protection should trigger urgent ophthalmology assessment or teleophthalmology consultation when appropriate. The demonstrated feasibility of fluorescein screening by trained ICU clinicians supports early detection where specialist access is intermittent.¹⁹

Embedding eye care within broader quality improvement work is consistent with integrated eye care and global eye health priorities.^35,36 Table 3 presents a resource based implementation framework.

Table 3.

Resource-Based ICU Eye Care Framework

Resource Level	Minimum Actions	Escalation Criteria
Basic ICU without on site ophthalmology	Daily assessment of eyelid closure, blink, chemosis, and corneal clarity; sterile lubricant; safe eyelid closure; approved transparent moisture barrier; single patient materials.	Corneal opacity, epithelial defect, infiltrate, purulent discharge, severe chemosis, trauma, chemical exposure, or failure to improve.
Intermediate ICU with periodic ophthalmology support	Risk assessment at admission; scheduled prophylaxis; fluorescein examination by trained staff; serial photography when permitted; regular compliance audit.	Persistent staining, lagophthalmos, suspected microbial keratitis, or deterioration despite protocol.
Advanced ICU with electronic systems and ophthalmology access	Electronic prophylaxis prompts or order set; nursing documentation each shift; portable slit lamp when available; defined referral pathway; quality dashboard.	Ulceration, infiltrate, progressive epithelial defect, refractory exposure, or need for procedural treatment.
All settings	Educate staff; avoid direct globe pressure; maintain infection prevention; review eye status during handover; assign responsibility for prophylaxis and reassessment.	Escalate early rather than waiting for advanced corneal disease.

Abbreviation: ICU, intensive care unit.

Pragmatic Risk Stratification and Escalation

The following framework is intended to simplify bedside decisions and has not been validated as a predictive score. It should be adapted to local staffing, equipment, and ophthalmology access.

Low Risk

Patients with complete eyelid closure, spontaneous blinking, a clear cornea, and no clinically important chemosis can undergo routine observation with at least daily reassessment while the risk persists. Lubrication may be used according to symptoms or local prophylaxis policy.

Moderate Risk

Patients with reduced blinking, mild chemosis, sedation, early incomplete closure, directed oxygen or dry airflow near the eye, or preexisting ocular surface vulnerability should receive scheduled lubricant drops or ointment. Eyelid closure should be documented and reassessed at least daily, with stronger protection added if exposure persists.

High Risk

Patients with deep sedation during mechanical ventilation, a GCS of 8 or less, neuromuscular blockade, lagophthalmos, severe chemosis, prone positioning, absent blink, or positive fluorescein staining should receive ointment together with reliable eyelid closure support or a moisture chamber. Direct globe pressure should be avoided, reassessment should occur daily or more often if deterioration is evident, and ophthalmology input should be obtained for epithelial defect, infiltrate, opacity, or refractory exposure.

For quality improvement, ICUs can monitor the proportion of ventilated or deeply sedated patients with a documented eye examination, the proportion of high‑risk patients who receive prescribed prophylaxis, adherence to scheduled lubrication and closure measures, and the rate of exposure keratopathy or corneal injury per ICU admission or ventilator day. These measures convert eye care from an optional bedside task into an auditable patient safety process. Figure 2 links clinical progression with practical prevention and escalation points.

Figure 2.

Clinical progression and prevention of ICU‑associated exposure keratopathy. Early ocular surface injury can progress to epithelial breakdown, microbial keratitis, structural damage, and visual loss; surveillance, lubrication, eyelid closure or moisture chamber protection, and timely ophthalmology referral can interrupt progression.

Research Gaps and Future Directions

Important gaps remain. Definitions of exposure keratopathy, corneal abrasion, ocular surface disease, and epithelial injury differ between studies; follow‑up intervals and grading systems are inconsistent; many trials are small and single center; and adherence, nursing time, cost, post‑ICU visual outcomes, and implementation in resource‑constrained settings are rarely measured. Pediatric, neurologic, burn, trauma, oncologic, and prolonged prone positioning populations require more focused evidence.

Future studies should use standardized definitions, pragmatic multicenter designs, resource‑based prevention bundles, cost‑effectiveness analyses, and implementation outcomes. Digital prompts, teleophthalmology, serial fluorescein imaging, and simplified nurse led screening warrant further evaluation. Patient‑centered outcomes should include visual function, ocular discomfort after recovery, corneal scarring, need for surgery, and quality of life.

Conclusion

Exposure keratopathy in the ICU is common, frequently silent, and potentially threatening to vision. Contemporary pooled evidence estimates a prevalence of approximately 34% and an incidence of 23% among critically ill patients, although rates vary according to population, definition, and prevention protocol.⁴ Critical illness and organ support can disrupt eyelid closure, blinking, tear film stability, and epithelial protection, allowing progression from punctate injury to infection, ulceration, scarring, and, in a subset of patients, irreversible visual loss.

The central clinical message is prevention. Scheduled assessment, lubrication, reliable eyelid closure or moisture chamber protection, staff education, and early specialist escalation can reduce avoidable injury, although not every corneal complication in critically ill patients can be prevented. A pragmatic framework adapted to local resources can make ICU eye care measurable and reproducible. Ophthalmologists, intensivists, and nurses should treat ocular surface protection as a shared patient safety responsibility so that survival from critical illness is not followed by avoidable corneal morbidity.

Disclosure

The author reports no conflicts of interest in this work.