Thursday, October 30, 2025

The Eyes in Critical Illness

 

The Eyes in Critical Illness: A Comprehensive Review for the Intensivist

Dr Neeraj Manikath , claude.ai

Abstract

Ocular complications in critically ill patients represent a frequently overlooked yet significant source of morbidity. The eyes serve both as windows to systemic pathophysiology and as vulnerable organs susceptible to iatrogenic injury in the intensive care unit (ICU). This review examines the spectrum of ocular manifestations in critical illness, from exposure keratopathy to vision-threatening complications, while providing evidence-based strategies for prevention, diagnosis, and management.

Introduction

The human eye, despite its remarkable protective mechanisms, becomes uniquely vulnerable in the critically ill patient. Loss of consciousness, sedation, neuromuscular blockade, and mechanical ventilation disrupt normal protective reflexes, exposing the ocular surface to desiccation and trauma. Studies suggest that 20-42% of ICU patients develop some form of ocular surface disease, with exposure keratopathy being the most common complication.¹ Yet ocular examination remains conspicuously absent from many ICU protocols, leading to preventable vision loss and patient suffering.

Beyond surface complications, the eyes provide invaluable diagnostic information about systemic processes including raised intracranial pressure, embolic phenomena, endocarditis, and coagulopathies. This dual nature—as both diagnostic tool and vulnerable organ—makes ophthalmologic knowledge essential for the modern intensivist.

Epidemiology and Risk Factors

Prevalence of Ocular Complications

The reported incidence of ocular complications in ICU patients varies widely, ranging from 20% to 75% depending on diagnostic criteria and surveillance methods.²,³ Exposure keratopathy represents the most frequent complication, occurring in 60% of mechanically ventilated patients without prophylaxis.⁴ More severe complications including microbial keratitis affect 3-6% of long-stay ICU patients, with associated visual impairment in approximately 40% of these cases.⁵

Risk Stratification

High-risk patients include those with:

  • Glasgow Coma Scale ≤8
  • Neuromuscular blockade
  • Prone positioning
  • Facial edema or burns
  • Prolonged mechanical ventilation (>48 hours)
  • Sedation scores indicating deep sedation
  • Lagophthalmos (incomplete eyelid closure)
  • Positive fluid balance with periorbital edema
  • Chemical or thermal burns to face

Pearl: The "ICU ocular risk score" combining GCS, sedation level, and lagophthalmos can identify patients requiring intensified prophylaxis, though formal validation studies remain limited.

Pathophysiology of Ocular Surface Disease in Critical Illness

The normal eye maintains corneal transparency through a sophisticated tear film comprising lipid, aqueous, and mucin layers, refreshed by spontaneous blinking 15-20 times per minute. Critical illness disrupts this system through multiple mechanisms:

  1. Reduced blink frequency and incomplete closure: Sedation, diminished consciousness, and facial nerve palsy impair the blink reflex. Studies using eyelid monitoring demonstrate that 30-50% of sedated patients have lagophthalmos >2mm, sufficient to cause exposure keratopathy.⁶

  2. Altered tear film composition: Systemic inflammation, dehydration, and medications (particularly anticholinergics and neuromuscular blockers) reduce tear production and alter tear film osmolarity.

  3. Mechanical factors: Prone positioning, poorly fitted oxygen delivery systems, and direct pressure from ventilator tubing or monitoring equipment can traumatize the ocular surface.

  4. Reduced corneal sensation: Sedation, metabolic disturbances, and critical illness polyneuropathy diminish corneal protective reflexes, creating a vicious cycle of unrecognized injury.

Clinical Spectrum of Ocular Complications

Exposure Keratopathy (Keratitis E Lagophthalmia)

This represents the commonest ICU ocular complication, progressing through predictable stages: conjunctival hyperemia and chemosis, punctate epithelial erosions, frank corneal ulceration, and potentially corneal perforation. The inferior third of the cornea is most vulnerable due to preferential exposure.

Oyster: Fluorescein staining reveals subclinical disease in 60% of at-risk patients before clinical signs develop. Consider screening high-risk patients every 48-72 hours.

Chemosis and Periorbital Edema

Aggressive fluid resuscitation, hypoalbuminemia, and prone positioning contribute to periorbital edema. While generally benign, severe chemosis can mechanically prevent eyelid closure and compress the optic nerve (orbit compartment syndrome).

Hack: The "finger pressure test"—inability to close eyelids with gentle finger pressure suggests significant chemosis requiring intervention. Consider head-of-bed elevation, diuresis, and albumin supplementation in hypoalbuminemic patients.

Microbial Keratitis

This sight-threatening complication affects 3-6% of long-stay ICU patients, with Pseudomonas aeruginosa, Staphylococcus aureus, and fungal pathogens predominating.⁷ Risk factors include corneal epithelial defects, colonization of respiratory equipment, and immunosuppression.

Clinical presentation: White or yellow corneal infiltrate with overlying epithelial defect, anterior chamber reaction, and hypopyon in severe cases. Requires urgent ophthalmologic consultation.

Pearl: Microbial keratitis in ICU patients often presents atypically due to immunosuppression. Maintain high suspicion in any patient with corneal opacity or infiltrate, regardless of inflammation severity.

Corneal Abrasions and Mechanical Trauma

Direct trauma from endotracheal tube ties, monitoring equipment, or inadvertent contact during patient care causes 10-15% of ICU ocular injuries. These typically present as sudden-onset conjunctival injection and tearing when sedation is lightened.

Retinal and Choroidal Complications

Purtscher retinopathy: Traumatic, embolic, or complement-mediated occlusion of retinal precapillaries causing cotton-wool spots and retinal whitening. Associated with trauma, pancreatitis, fat embolism, and amniotic fluid embolism.

Ischemic optic neuropathy: Both anterior and posterior forms occur in critically ill patients, associated with anemia, hypotension, and prone positioning during surgery. Prevention focuses on maintaining adequate perfusion pressure and hematocrit.

Cytomegalovirus retinitis: Immunosuppressed patients, particularly post-transplant or with advanced HIV, require ophthalmologic surveillance.

Pupillary Abnormalities as Diagnostic Signs

The pupils provide critical diagnostic information:

  • Bilateral fixed dilated pupils: Brain death, severe anoxia, anticholinergic toxicity, hypothermia
  • Bilateral pinpoint pupils: Pontine hemorrhage, opioid overdose, organophosphate poisoning
  • Unilateral mydriasis: Uncal herniation (ipsilateral), direct ocular trauma, Adie's pupil
  • Relative afferent pupillary defect (RAPD): Optic nerve or severe retinal pathology

Hack: The "reverse RAPD" (stronger light response in the affected eye) suggests retrobulbar pathology rather than optic nerve disease—consider orbital compartment syndrome or severe uveitis.

Orbit Compartment Syndrome

This ophthalmologic emergency results from elevated intraorbital pressure (>40 mmHg) causing optic nerve ischemia. Causes include retrobulbar hemorrhage, severe periorbital edema, and orbital cellulitis.

Clinical features: Proptosis, tense orbit, ophthalmoplegia, elevated intraocular pressure, and RAPD. Requires emergent lateral canthotomy and cantholysis if ophthalmology unavailable.

Raised Intracranial Pressure: Ocular Signs

Papilledema develops over hours to days with sustained ICP elevation, presenting as optic disc swelling with blurred margins and obscured vessels. Acute severe elevation may cause disc hemorrhages.

Pearl: Absence of spontaneous venous pulsations on fundoscopy suggests ICP >200 mmH₂O with 80% specificity, though their presence doesn't exclude raised ICP.

Oyster: Bedside ocular ultrasound measuring optic nerve sheath diameter (ONSD) >5mm in adults suggests raised ICP with reasonable sensitivity (90%) and specificity (85%).⁸ Measure 3mm posterior to the globe in two planes.

Prevention Strategies: Evidence-Based Approaches

Standard Prophylaxis

Multiple prophylactic strategies exist, but evidence quality varies:

1. Lubricating ointments: Petroleum-based ointments (e.g., lacrilube) applied every 4-6 hours reduce exposure keratopathy incidence from 60% to 7-15%.⁹ More effective than artificial tear drops due to prolonged corneal contact time.

2. Eyelid taping: Hypoallergenic tape securing complete eyelid closure reduces keratopathy risk. Use horizontal taping across both lids rather than vertical taping.

3. Polyethylene eye covers: Commercial moisture chambers or simple polyethylene covers create a humid microenvironment, reducing tear evaporation. Comparable efficacy to ointments with less visual obstruction when patients wake.

4. Combination approaches: Ointment plus eyelid taping or moisture chambers provides superior protection compared to single interventions, appropriate for highest-risk patients.¹⁰

Hack: Create an improvised moisture chamber using plastic wrap secured with hypoallergenic tape, ensuring no direct pressure on the globe. Change every 12-24 hours to prevent maceration.

Risk-Stratified Protocols

Low-risk patients (conscious, intact blink reflex, expected ICU stay <48 hours):

  • Artificial tears every 4 hours while awake
  • Clinical assessment daily

Moderate-risk patients (sedated, mechanically ventilated, intact eyelid closure):

  • Lubricating ointment every 4 hours
  • Clinical assessment every 48 hours
  • Consider eyelid taping during prone positioning

High-risk patients (GCS ≤8, lagophthalmos, facial burns, prolonged NMB):

  • Lubricating ointment every 2-4 hours
  • Eyelid taping or moisture chambers
  • Fluorescein staining every 48-72 hours
  • Consider ophthalmology consultation for prophylaxis

Diagnostic Approach

Bedside Examination

Systematic examination requires only basic equipment:

  1. External inspection: Assess eyelid closure, periorbital edema, proptosis, and symmetry
  2. Eyelid eversion: Check for foreign bodies or chalazia in unconscious patients
  3. Fluorescein staining: 1-2 drops of fluorescein with cobalt blue light reveals epithelial defects as bright green staining
  4. Pupillary assessment: Size, symmetry, light response, and RAPD testing
  5. Fundoscopy: Evaluate optic disc, vessels, and retina through dilated pupils if safe

Pearl: Perform fluorescein examination under ultraviolet or cobalt blue light in a darkened environment. Punctate staining (multiple small dots) suggests early exposure keratopathy; geographic staining indicates established ulceration.

Advanced Imaging

Ocular ultrasound: Point-of-care ultrasound assesses:

  • Optic nerve sheath diameter (raised ICP)
  • Lens position (globe rupture)
  • Vitreous hemorrhage or detachment
  • Retinal detachment

CT orbits: Indicated for suspected orbital fracture, foreign body, or compartment syndrome.

Ophthalmologic consultation: Required for microbial keratitis, suspected globe rupture, acute vision loss, or orbit compartment syndrome.

Management of Established Complications

Exposure Keratopathy

Mild (punctate epithelial erosions):

  • Increase lubrication frequency to every 2 hours
  • Ensure complete eyelid closure with taping/moisture chambers
  • Reassess in 24-48 hours

Moderate (corneal ulceration without infection):

  • Intensive lubrication (hourly)
  • Consider temporary tarsorrhaphy if prolonged ICU stay expected
  • Ophthalmology consultation

Severe (deep ulceration, descemetocele, perforation):

  • Emergency ophthalmology consultation
  • Tissue adhesive or penetrating keratoplasty may be required

Microbial Keratitis

Management principles:

  • Urgent ophthalmology consultation for corneal scraping and culture
  • Broad-spectrum fortified topical antibiotics:
    • Vancomycin 25-50 mg/mL (Gram-positive coverage)
    • Tobramycin or gentamicin 9-14 mg/mL (Gram-negative coverage)
  • Administer every 30-60 minutes initially, then taper based on response
  • Avoid corticosteroids until infection controlled
  • Systemic antibiotics if scleral involvement or endophthalmitis suspected

Hack: If ophthalmology unavailable and microbial keratitis strongly suspected, initiate moxifloxacin 0.5% drops hourly as temporizing measure while arranging transfer.

Orbit Compartment Syndrome

Requires immediate intervention:

  1. Medical management (if mild, IOP 30-40 mmHg):

    • Elevate head of bed 30-45 degrees
    • Mannitol 1-2 g/kg IV or hypertonic saline
    • Acetazolamide 500 mg IV
    • Timolol 0.5% drops twice daily
  2. Surgical decompression (if severe, IOP >40 mmHg, or vision threatened):

    • Lateral canthotomy and cantholysis
    • Can be performed at bedside by trained intensivists
    • Provides immediate 30-40% volume expansion of orbit

Pearl: When performing canthotomy, use straight scissors to make a 1-2 cm horizontal incision through the lateral canthus to the bony orbital rim, then cut the inferior crus of the lateral canthal tendon. Improper technique risks incomplete decompression.

Special Populations

Prone Positioning for ARDS

Prone positioning increases ocular complications through multiple mechanisms: direct pressure, dependent edema accumulation, and impaired venous drainage. Incidence of exposure keratopathy reaches 85% in prone patients without prophylaxis.¹¹

Preventive strategies:

  • Meticulous face positioning with specialized prone pillows
  • Eyes should hang freely without pressure
  • Increase lubrication frequency to every 2 hours
  • Check eye position with each repositioning
  • Consider moisture chambers over simple lubrication

Burns and Facial Trauma

Facial burns require specialized care:

  • Early ophthalmology consultation
  • Aggressive lubrication (every 1-2 hours)
  • Consider temporary tarsorrhaphy for severe lagophthalmos
  • Monitor for symblepharon (conjunctival adhesions) formation
  • Vitamin A supplementation may aid corneal healing

Post-Cardiac Arrest

Retinal and optic nerve ischemia may occur during prolonged arrest. Pupillary examination provides prognostic information, though medications confound interpretation. Consider ophthalmologic examination in survivors to assess for ischemic damage affecting visual recovery.

Nursing and Multidisciplinary Considerations

Implementing effective eye care requires:

  1. Nursing protocols: Clear written guidelines for eye care frequency and techniques
  2. Education: Regular training on eye examination and prophylaxis application
  3. Documentation: Standardized assessment tools integrated into ICU flowsheets
  4. Quality metrics: Track exposure keratopathy and microbial keratitis rates as ICU quality indicators
  5. Multidisciplinary rounds: Include eye care in daily ICU checklists

Oyster: Create laminated cards with fluorescein staining images showing mild, moderate, and severe keratopathy for nursing reference. Empower nurses to escalate care based on examination findings.

Future Directions and Research Gaps

Despite the frequency of ocular complications, high-quality randomized trials remain scarce. Priority areas include:

  • Large multicenter trials comparing prophylactic strategies
  • Standardized grading systems for ICU-related eye disease
  • Investigation of novel prophylaxis (humidified oxygen, specialized contact lenses)
  • Long-term visual outcomes following ICU-acquired eye disease
  • Cost-effectiveness analyses of intensive prevention protocols

Conclusion

Ocular complications represent a significant yet preventable source of morbidity in critically ill patients. The intensivist must recognize the eyes as vulnerable organs requiring systematic assessment and prophylaxis. Risk stratification allows tailored interventions, while early recognition and appropriate management prevent vision-threatening complications. Implementing robust eye care protocols improves patient outcomes and should be considered a fundamental component of comprehensive ICU care.

As we pursue excellence in critical care, we must ensure that the windows to the soul—and the world—remain clear for our patients' recovery and return to meaningful life.


References

  1. Mercieca F, Suresh P, Morton A, Tullo A. Ocular surface disease in intensive care unit patients. Eye (Lond). 1999;13(Pt 2):231-236.

  2. Imanaka H, Taenaka N, Nakamura J, et al. Ocular surface disorders in the critically ill. Anesth Analg. 1997;85(2):343-346.

  3. Ezra DG, Lewis G, Healy M, et al. Preventing exposure keratopathy in the critically ill: a prospective study comparing eye care regimens. Br J Ophthalmol. 2005;89(8):1068-1069.

  4. Kuruvilla S, Peter J, David S, et al. Incidence and risk factor evaluation of exposure keratopathy in critically ill patients: A cohort study. J Crit Care. 2015;30(2):400-404.

  5. Rosenberg JB, Eisen LA. Eye care in the intensive care unit: narrative review and meta-analysis. Crit Care Med. 2008;36(12):3151-3155.

  6. Werli-Alvarenga A, Ercole FF, Herdman TH, Chianca TC. Lagophthalmos and dry eye in ICU patients: evidence-based care. Intensive Crit Care Nurs. 2013;29(5):248-256.

  7. Kirwan JF, Potamitis T, El-Kasaby H, et al. Microbial keratitis in intensive care. BMJ. 1997;314(7087):433-434.

  8. Rajajee V, Vanaman M, Fletcher JJ, Jacobs TL. Optic nerve ultrasound for the detection of raised intracranial pressure. Neurocrit Care. 2011;15(3):506-515.

  9. Kalhori RP, Ehsaei A, Daneshgar F, et al. Different nursing care methods for prevention of keratopathy among intensive care unit patients. Glob J Health Sci. 2016;8(7):212-217.

  10. Kousha O, Kousha Z, Paddle J. Incidence, risk factors and impact of protocolised care on exposure keratopathy in critically ill adults: A two-phase prospective cohort study. Crit Care. 2018;22(1):5.

  11. So HM, Lee CC, Leung AK, et al. Comparing the effectiveness of polyethylene covers with lanolin eye ointment to prevent corneal abrasions in critically ill patients: A randomized controlled study. Int J Nurs Stud. 2008;45(11):1565-1571.


Key Pearls Summary:

  • Screen high-risk patients with fluorescein every 48-72 hours
  • ONSD >5mm suggests raised ICP with 90% sensitivity
  • Prone positioning increases keratopathy risk to 85%—intensify prophylaxis
  • Microbial keratitis in ICU often presents atypically due to immunosuppression
  • Absence of spontaneous venous pulsations suggests ICP >200 mmH₂O
  • Risk-stratify all ICU admissions for ocular complications within 24 hours

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