Chemical Injuries of the Cornea

1. Pathophysiology

Alkali Burns (more severe)

• Stromal proteoglycan disruption - corneal edema and opacification
• Limbal stem cell destruction - loss of regenerative capacity
• Iris, ciliary body, and trabecular meshwork damage
• IOP rise (inflammatory debris, trabecular damage) or fall (ciliary body injury)

Acid Burns (relatively self-limiting)

Irritants

Clinical Stages (McCulley Classification)

2. Clinical Assessment

Symptoms

• Severe pain, photophobia, blepharospasm
• Epiphora (tearing)
• Reduced or lost visual acuity

Signs on Examination

• Conjunctival/scleral hyperemia or blanching (ischemia)
• Corneal epithelial defect (fluorescein staining)
• Corneal haze or opacification (stromal edema)
• Limbal pallor/ischemia (key prognostic sign)
• Anterior chamber reaction
• Altered IOP (high or low)
• In severe cases: iris/pupil obscuration, lens opacification

3. Grading Systems

A. Roper-Hall Classification (1965, modification of Hughes/Balen)

B. Dua Classification (2001)

Limbal involvement is documented by fluorescein staining and/or limbal ischemia and recorded as clock hours - a more objective measure. Surviving conjunctival epithelium is important because it can provide cover to the cornea.

4. Emergency Management

Step 1: Copious Irrigation (Cornerstone of Treatment)

• Begin immediately - even before assessment - using any non-caustic liquid available
• At least 1-2 liters of normal saline or lactated Ringer's solution; up to 20 liters may be needed for severe burns
• If IV fluids unavailable: tap water, shower, drinking fountain are all acceptable
• Duration: Minimum 30 minutes of continuous irrigation
• Use a Morgan Lens or IV tubing through lid speculum for effective delivery
• Sweep all fornices with a moistened cotton swab to remove particulate matter (especially lime/cement particles which continue releasing alkali)
• Check conjunctival pH after irrigation and again 30 minutes later - target pH 7.5-8.0
• If pH remains abnormal, continue irrigation until normalized

Step 2: Assessment After Irrigation

• Visual acuity
• Slit-lamp examination with fluorescein staining
• Dilated fundoscopy
• IOP measurement
• Grade the injury (Roper-Hall or Dua)
• Immediate ophthalmology referral

Step 3: Acute Medical Management (Grade-Based)

• Preservative-free lubricating drops and ointment
• Topical steroids (e.g., prednisolone 1% QID for 1 week then taper) - reduce inflammation
• Prophylactic topical antibiotics (e.g., ciprofloxacin QID)
• Cycloplegic agents (e.g., cyclopentolate 1% TID) - for comfort and preventing posterior synechiae
• IOP-lowering agents as needed

• Intensive topical steroids (prednisolone 1% every 1-2 hours)
• Ascorbic acid (Vitamin C) 10% topically every 2 hours - promotes collagen synthesis, reduces corneal ulceration risk
• Oral ascorbic acid (2 g/day) - systemic antioxidant support
• Topical citrate 10% every 2 hours - inhibits neutrophil migration and collagenase activity
• Tetracycline derivatives (oral doxycycline 100 mg BD) - matrix metalloproteinase inhibitor, prevents corneal melting
• Systemic steroids (oral prednisolone) for severe inflammation
• Bandage contact lens or amniotic membrane for epithelial defects
• Tarsal conjunctival sweeping and lysis of any symblepharon formation

Step 4: Surgical Interventions in the Acute Phase

• Amniotic membrane transplantation (AMT): Applied acutely (within 48-72 hours) to promote re-epithelialization, reduce inflammation and scarring
• Tenonplasty/peritomy: Restores limbal blood supply in extensive ischemia
• Debridement of necrotic tissue

5. Long-Term Complications

Ocular Surface Complications

1. Limbal Stem Cell Deficiency (LSCD): The most significant complication. Loss of limbal stem cells leads to:
   • Conjunctivalization of the cornea (conjunctival epithelium replaces corneal epithelium)
   • Persistent epithelial defects and recurrent breakdown
   • Fibrovascular pannus formation
   • Deep corneal vascularization
   • Chronic ocular surface inflammation
2. Corneal Scarring and Opacification: Stromal fibrosis from the healing response - major cause of visual loss
3. Dry Eye / Neurotrophic Keratopathy: Destruction of conjunctival goblet cells and corneal nerves leads to severe aqueous and mucin deficiency; impaired corneal sensation causes poor epithelial healing
4. Persistent Epithelial Defects: Especially in LSCD; risk of secondary infections and corneal ulceration/perforation

Structural Complications

1. Symblepharon and Ankyloblepharon: Adhesion between the palpebral and bulbar conjunctiva (symblepharon) or between the lids (ankyloblepharon); causes restricted ocular movements, entropion, lagophthalmos, and chronic surface damage
2. Entropion/Ectropion: Cicatricial lid changes - in-turning or out-turning of the lids causing chronic corneal irritation and exposure
3. Fornix shortening and obliteration: Loss of the conjunctival cul-de-sac

Pressure-Related

1. Secondary Glaucoma: Occurs in 15-55% of patients with severe burns. Mechanisms include:
   • Contraction of anterior segment structures
   • Inflammatory debris in trabecular meshwork
   • Direct trabecular meshwork damage
   • Grades III-IV have significantly higher IOP and are more likely to need glaucoma surgery
2. Hypotony: Ciliary body damage can cause chronically low IOP and phthisis bulbi

Other

1. Cataract: Direct chemical injury to the lens (especially with alkali penetration)
2. Corneal vascularization: Deep stromal vessels that compromise corneal immune privilege (relevant for future transplantation)
3. Phthisis bulbi: End-stage atrophy of the globe in the most severe cases

6. Long-Term Surgical Rehabilitation

Key Points Summary

• Alkali burns are more dangerous than acid burns due to ongoing saponification and deeper penetration
• Immediate copious irrigation is the single most important intervention - neutralize the chemical and remove particulates
• The Roper-Hall (Grade I-IV) and Dua (Grade I-VI) classifications guide prognosis and management
• Dua classification is superior for severe burns as it incorporates conjunctival involvement
• Medical management escalates from lubrication/antibiotics (mild) to ascorbate, citrate, tetracyclines, and amniotic membrane (severe)
• Long-term complications - LSCD, glaucoma, dry eye, symblepharon, and scarring - require prolonged follow-up and staged surgical rehabilitation

Chemical Injuries of the Cornea

1. Pathophysiology

Alkali Burns (more severe)

• Stromal proteoglycan disruption - corneal edema and opacification
• Limbal stem cell destruction - loss of regenerative capacity
• Iris, ciliary body, and trabecular meshwork damage
• IOP rise (inflammatory debris, trabecular damage) or fall (ciliary body injury)

Acid Burns (relatively self-limiting)

Irritants

Clinical Stages (McCulley Classification)

2. Clinical Assessment

Symptoms

• Severe pain, photophobia, blepharospasm
• Epiphora (tearing)
• Reduced or lost visual acuity

Signs on Examination

• Conjunctival/scleral hyperemia or blanching (ischemia)
• Corneal epithelial defect (fluorescein staining)
• Corneal haze or opacification (stromal edema)
• Limbal pallor/ischemia (key prognostic sign)
• Anterior chamber reaction
• Altered IOP (high or low)
• In severe cases: iris/pupil obscuration, lens opacification

3. Grading Systems

A. Roper-Hall Classification (1965, modification of Hughes/Balen)

B. Dua Classification (2001)

Limbal involvement is documented by fluorescein staining and/or limbal ischemia and recorded as clock hours - a more objective measure. Surviving conjunctival epithelium is important because it can provide cover to the cornea.

4. Emergency Management

Step 1: Copious Irrigation (Cornerstone of Treatment)

• Begin immediately - even before assessment - using any non-caustic liquid available
• At least 1-2 liters of normal saline or lactated Ringer's solution; up to 20 liters may be needed for severe burns
• If IV fluids unavailable: tap water, shower, drinking fountain are all acceptable
• Duration: Minimum 30 minutes of continuous irrigation
• Use a Morgan Lens or IV tubing through lid speculum for effective delivery
• Sweep all fornices with a moistened cotton swab to remove particulate matter (especially lime/cement particles which continue releasing alkali)
• Check conjunctival pH after irrigation and again 30 minutes later - target pH 7.5-8.0
• If pH remains abnormal, continue irrigation until normalized

Step 2: Assessment After Irrigation

• Visual acuity
• Slit-lamp examination with fluorescein staining
• Dilated fundoscopy
• IOP measurement
• Grade the injury (Roper-Hall or Dua)
• Immediate ophthalmology referral

Step 3: Acute Medical Management (Grade-Based)

• Preservative-free lubricating drops and ointment
• Topical steroids (e.g., prednisolone 1% QID for 1 week then taper) - reduce inflammation
• Prophylactic topical antibiotics (e.g., ciprofloxacin QID)
• Cycloplegic agents (e.g., cyclopentolate 1% TID) - for comfort and preventing posterior synechiae
• IOP-lowering agents as needed

• Intensive topical steroids (prednisolone 1% every 1-2 hours)
• Ascorbic acid (Vitamin C) 10% topically every 2 hours - promotes collagen synthesis, reduces corneal ulceration risk
• Oral ascorbic acid (2 g/day) - systemic antioxidant support
• Topical citrate 10% every 2 hours - inhibits neutrophil migration and collagenase activity
• Tetracycline derivatives (oral doxycycline 100 mg BD) - matrix metalloproteinase inhibitor, prevents corneal melting
• Systemic steroids (oral prednisolone) for severe inflammation
• Bandage contact lens or amniotic membrane for epithelial defects
• Tarsal conjunctival sweeping and lysis of any symblepharon formation

Step 4: Surgical Interventions in the Acute Phase

• Amniotic membrane transplantation (AMT): Applied acutely (within 48-72 hours) to promote re-epithelialization, reduce inflammation and scarring
• Tenonplasty/peritomy: Restores limbal blood supply in extensive ischemia
• Debridement of necrotic tissue

5. Long-Term Complications

Ocular Surface Complications

1. Limbal Stem Cell Deficiency (LSCD): The most significant complication. Loss of limbal stem cells leads to:
   • Conjunctivalization of the cornea (conjunctival epithelium replaces corneal epithelium)
   • Persistent epithelial defects and recurrent breakdown
   • Fibrovascular pannus formation
   • Deep corneal vascularization
   • Chronic ocular surface inflammation
2. Corneal Scarring and Opacification: Stromal fibrosis from the healing response - major cause of visual loss
3. Dry Eye / Neurotrophic Keratopathy: Destruction of conjunctival goblet cells and corneal nerves leads to severe aqueous and mucin deficiency; impaired corneal sensation causes poor epithelial healing
4. Persistent Epithelial Defects: Especially in LSCD; risk of secondary infections and corneal ulceration/perforation

Structural Complications

1. Symblepharon and Ankyloblepharon: Adhesion between the palpebral and bulbar conjunctiva (symblepharon) or between the lids (ankyloblepharon); causes restricted ocular movements, entropion, lagophthalmos, and chronic surface damage
2. Entropion/Ectropion: Cicatricial lid changes - in-turning or out-turning of the lids causing chronic corneal irritation and exposure
3. Fornix shortening and obliteration: Loss of the conjunctival cul-de-sac

Pressure-Related

1. Secondary Glaucoma: Occurs in 15-55% of patients with severe burns. Mechanisms include:
   • Contraction of anterior segment structures
   • Inflammatory debris in trabecular meshwork
   • Direct trabecular meshwork damage
   • Grades III-IV have significantly higher IOP and are more likely to need glaucoma surgery
2. Hypotony: Ciliary body damage can cause chronically low IOP and phthisis bulbi

Other

1. Cataract: Direct chemical injury to the lens (especially with alkali penetration)
2. Corneal vascularization: Deep stromal vessels that compromise corneal immune privilege (relevant for future transplantation)
3. Phthisis bulbi: End-stage atrophy of the globe in the most severe cases

6. Long-Term Surgical Rehabilitation

Key Points Summary

• Alkali burns are more dangerous than acid burns due to ongoing saponification and deeper penetration
• Immediate copious irrigation is the single most important intervention - neutralize the chemical and remove particulates
• The Roper-Hall (Grade I-IV) and Dua (Grade I-VI) classifications guide prognosis and management
• Dua classification is superior for severe burns as it incorporates conjunctival involvement
• Medical management escalates from lubrication/antibiotics (mild) to ascorbate, citrate, tetracyclines, and amniotic membrane (severe)
• Long-term complications - LSCD, glaucoma, dry eye, symblepharon, and scarring - require prolonged follow-up and staged surgical rehabilitation

• Color-coded headings and section dividers
• All 4 tables (McCulley stages, Roper-Hall, Dua classification, Surgical rehabilitation)
• Graded management steps and long-term complications
• Sources listed at the bottom