Chemical (Alkali and Acid) Injury of the Conjunctiva and Cornea

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Article initiated by:
Angela Chang, Danielle Trief, MD, MSc, James Chodosh, MD, MPH, Kathryn Colby MD
All contributors:
Clara Murff, Danielle Trief, MD, MSc, Gary L. Legault, MD, Maria A. Woodward, MD, Colleen Halfpenny, M.D., Anna Murchison, MD, MPH, James Drake Auran, MD, Zeba A. Syed, MD, Grant A. Justin, MD, Ravi Patel, MD, MBA, Henry Bair, MD
Assigned editor:
Gary L. Legault, MD, Ravi Patel, MD, MBA
Review:
Assigned status Up to Date
 by Gary L. Legault, MD on September 2, 2026.


ICD-10
[1]26.6
ICD-9
372.06


Chemical ocular injury requires immediate decontamination and urgent assessment. Early treatment limits continued tissue damage; severe burns may require prolonged medical care and ocular surface reconstruction.

Disease Entity

International Classification of Diseases

ICD-10-CM category T26.6 covers corrosion of the cornea and conjunctival sac. Initial-encounter examples are T26.60XA (unspecified eye), T26.61XA (right eye), and T26.62XA (left eye). The X is a placeholder; laterality is represented by 0, 1, or 2 immediately before it. Use the appropriate seventh character: A for initial encounter, D for subsequent encounter, or S for sequela. Related categories include T26.5 (eyelid and periocular area), T26.7 (corrosion with resulting rupture and destruction of the eyeball), T26.8 (other specified parts of the eye and adnexa), and T26.9 (part unspecified). Select the full code and any additional codes according to the current ICD-10-CM tabular instructions.[1]

This article focuses on chemical (alkali and acid) injury of the conjunctiva and cornea. For an overview of initial care by non-ophthalmologists, see Pre-Ophthalmologist Management of Eye Trauma. Immediate first-response actions are also summarized in the role-based Management sections below.

Epidemiology

Chemical ocular injuries occur in the workplace and at home, and may also result from assault. Exposure patterns vary by population and setting.[2] In a United States emergency-department study using 2010–2013 data, injury rates were highest among children aged 1–2 years.[3] Household cleaners and laundry detergent pods are important sources of pediatric exposure; detergent-pod injuries have also been documented among preschool-aged children.[4] Alkali injuries are generally reported more often than acid injuries.[2]

Etiology

Chemical injuries may result from acidic, alkaline, or neutral agents. Common causes of acid and alkali injuries are listed below.[2][5]

Table 1. Examples of agents associated with acid injuries.[2][5]
Agent Formula Examples of sources
Sulfuric acid H₂SO₄ Lead-acid vehicle batteries
Hydrofluoric acid HF Glass etching and polishing; mineral refining
Acetic acid CH₃COOH Vinegar; concentrated glacial acetic acid
Hydrochloric acid HCl Pool maintenance chemicals
Table 2. Examples of agents associated with alkaline exposures. Injury depends on concentration, contact time, and the product formulation.[2][5][6]
Agent Formula Examples of sources
Ammonia NH₃ Cleaning products; fertilizers; industrial refrigerants
Potassium hydroxide KOH Caustic potash
Sodium hydroxide NaOH Drain cleaners; some airbag deployment residues
Calcium hydroxide Ca(OH)₂ Slaked lime; mortar, cement, and whitewash
Sodium hypochlorite NaOCl Household chlorine bleach and disinfectants

Pathophysiology

Alkali

Alkali agents are lipophilic and therefore penetrate tissues more rapidly than acids. They saponify the fatty acids of cell membranes, penetrate the corneal stroma, and destroy proteoglycan ground substance and collagen bundles. The damaged tissues then secrete proteolytic enzymes, which lead to further damage.[7][8]

Acid

Acids cause injury by denaturing and precipitating tissue proteins. The resulting coagulation can limit deeper penetration, so many acid injuries are less penetrating than alkali injuries.[8] Strong acids can nevertheless cause severe damage. Hydrofluoric acid is an important exception because it can rapidly penetrate the cornea and damage the anterior segment.[9]

Primary Prevention

Prevention includes safe chemical handling, appropriate storage of household products away from children, and eye and face protection selected for the exposure hazard. OSHA standard 1910.133 requires appropriate protection for hazards such as liquid chemicals, acids, and caustic liquids; chemical-splash goggles and additional face protection should be selected according to the workplace hazard assessment.[10] Under OSHA standard 1910.151(c), workplaces where the eyes or body may be exposed to injurious corrosive materials must provide suitable facilities for immediate drenching or flushing within the work area.[11]

Diagnosis

History

Begin irrigation immediately after a chemical exposure and obtain the history during or after decontamination. Do not delay irrigation to identify the agent or obtain a detailed history. Ask about the substance and concentration, time and duration of exposure, prior rinsing and its duration, high-pressure or penetrating mechanisms, contact lenses, and eye protection. The product label or safety data sheet may help identify the agent. In the United States, Poison Control can be reached at 1-800-222-1222. Assess associated skin, inhalational, and systemic exposures while ocular decontamination continues.[12][13]

Physical Examination

For an isolated chemical exposure, begin irrigation immediately unless an open globe injury is known or strongly suspected. If pH paper is immediately available, check the ocular surface pH of both eyes without delaying irrigation. Continue irrigation until the pH is physiologic (approximately 7.0–7.2). Pause for at least 5 minutes before rechecking, so the measurement reflects the ocular surface rather than the irrigating fluid. If the pH remains abnormal or rebounds, resume irrigation and look for retained chemical material. Repeat pH checks after apparent normalization to confirm stability.[14][15]

After decontamination, document visual acuity and the extent and depth of injury, including corneal epithelial loss and haze, conjunctival involvement, and limbal involvement or ischemia. These findings help grade the burn and estimate prognosis.[16]

Once an open globe injury has been excluded, a trained clinician should inspect the palpebral fissures, evert the eyelids, and remove retained material from the conjunctival fornices. Examine the palpebral and bulbar conjunctiva and cornea with fluorescein and cobalt blue illumination. Retained particles can continue to cause damage despite irrigation. Measure intraocular pressure (IOP) only when globe integrity permits; chemical injury may cause acute or chronic pressure elevation.[15][17]

Classification

Two commonly used classification systems are the Roper-Hall (modified Hughes) classification[18][19] and the Dua classification.[20] Roper-Hall grades the injury by corneal involvement and limbal ischemia. Dua uses limbal involvement in clock hours and the percentage of conjunctival involvement. A trial comparing their prognostic value found that the Dua system better distinguished outcomes in severe burns.[16] Record the underlying findings and the classification used; reporting both systems can support comprehensive documentation.

Figure 1. Roper-Hall and Dua classification systems and examples of burn severity.

Role of Imaging

Imaging is not routinely required for an isolated ocular chemical injury and must not delay irrigation. A high-pressure or penetrating mechanism, suspected intraocular foreign body, or associated orbital injury requires urgent specialist assessment and appropriate trauma imaging. Avoid ocular pressure, tonometry, and ocular ultrasound when an open globe injury is suspected; see Ruptured Globe.[21]

Symptoms

The most common symptoms are severe pain, epiphora, blepharospasm, and reduced visual acuity.

Management

Irrigation and Early Management

Chemical ocular injury is an emergency. For an isolated chemical exposure, begin copious irrigation immediately with clean water or an immediately available suitable irrigating solution. Continue through transfers of care. Do not wait for a detailed history, visual acuity testing, imaging, an ideal fluid, or ophthalmology arrival.[12][14] The special precautions for a known or strongly suspected open globe are described below.

Early irrigation limits contact time, removes the offending substance, and helps restore physiologic ocular surface pH. Several liters and prolonged irrigation may be required. In clinical care, use a stable physiologic pH and removal of retained material to guide the endpoint, rather than a fixed volume or elapsed time alone.[14][22]

When feasible, support the patient’s head and tilt it toward the affected side. Use a gentle stream directed from the nasal side outward, away from the unaffected eye. Gently hold the lids open without pressure on the globe; encourage blinking and looking in different directions to expose the conjunctival sacs. Avoid transferring chemicals from contaminated hands or equipment to the eye.[12][23]

Irrigation lenses, eyelid specula, ophthalmic topical anesthetics, and subsequent medications are clinician-directed interventions and are discussed in the ED Physician and Ophthalmologist and Medical Therapy sections. Preparing these interventions must not delay immediate irrigation for an isolated chemical exposure.

Bystanders

First ensure scene safety and avoid further exposure. Call for emergency assistance and begin eye irrigation as soon as it is safe to do so. Do not rub the eye. Copious early irrigation has been associated with less severe alkali injury and shorter healing times.[24] A visibly penetrating injury or protruding object requires the open globe precautions below; do not manipulate or remove an embedded object.[21]

Use clean running water immediately if sterile saline or another suitable irrigating solution is not at hand. Do not wait to obtain a preferred product. Do not apply acids or alkalis to neutralize the exposure, because this can worsen injury.[12][24]

Continue irrigation while awaiting emergency responders and during transfer of care when feasible. Remove contact lenses only if this can be done readily without delaying irrigation or manipulating a suspected penetrating injury. Pass on the exposure time, substance, and rinsing already performed. Provide the container or safety data sheet if readily available, without delaying treatment.[12][25]

EMS and First Responders

Initiate irrigation on scene and continue irrigation during transport, using normal saline, lactated Ringer’s solution, or clean water if a sterile solution is unavailable. Unless an open globe injury is known or strongly suspected, irrigation takes priority over a comprehensive eye examination. A fixed duration does not establish adequate decontamination; continue until handoff or a protocol-directed assessment confirms a stable physiologic pH.[14][26]

First responders must follow their current local protocols and authorized scope of practice. Contact-lens removal and ophthalmic topical anesthetics may facilitate irrigation when permitted and safe. Lid eversion, fornix sweeping, and insertion of an irrigation lens require appropriate training and exclusion of an open globe injury. Medication or equipment preparation must not delay irrigation.[15]

Known or strongly suspected open globe with chemical contamination: do not apply pressure, remove a protruding object, insert an irrigation lens, or irrigate the open globe. Decontaminate surrounding skin without directing fluid into the wound, protect the eye with a rigid shield that does not touch the globe or protruding object, and obtain immediate ophthalmology/trauma and toxicology guidance. Do not withhold prompt irrigation for an ordinary chemical splash solely because of a hypothetical concern for globe rupture. See Ruptured Globe.[15][21]

ED Physician and Ophthalmologist

In clinical care, an ophthalmic topical anesthetic such as proparacaine or tetracaine can improve tolerance of irrigation. Use an ocular formulation; lidocaine prepared for intravenous injection should not be used as an eyedrop. After excluding an open globe, a trained clinician may use an eyelid speculum or irrigation lens. An irrigation lens does not replace inspection and removal of retained particles.[15][21] Continue irrigation until the ocular surface pH is approximately 7.0–7.2 and remains physiologic after a pause of at least 5 minutes. Resume irrigation if the pH is abnormal or rebounds.[14][15]

After excluding an open globe, evert the lids and inspect the conjunctival fornices for caustic particles. A trained clinician can remove visible material with sterile cotton-tipped applicators moistened with irrigating fluid. Recheck pH after particle removal and repeat inspection if the pH fails to remain normal.[15][23]

Types of Irrigating Fluid

Prompt irrigation is more important than selection of a particular fluid. Clean tap water is appropriate for immediate first aid. In clinical settings, normal saline, lactated Ringer’s solution, or balanced salt solution may be used when immediately available.[12][14]

Differences in sterility, tonicity, availability, and comfort may influence the choice of fluid. A small clinical comparison found better patient tolerance of balanced salt solution than of several other tested solutions.[27] Such differences should not be used to postpone irrigation with readily available clean water or saline.

Specialized buffered or amphoteric eyewashes, including Diphoterine, have been studied in experimental and clinical settings.[28][29] Their reported effects depend on the product and study conditions; the available evidence does not establish one universally preferred solution for all exposures. Avoid extrapolating laboratory neutralization ratios into a clinical irrigation-volume requirement.

Do not delay irrigation to obtain balanced salt solution, Diphoterine, or another specific product.

Medical Therapy

Mild to moderate injuries (Roper-Hall grades I and II) often respond to medical therapy. Treatment aims to restore the epithelium, support collagen synthesis, limit collagen breakdown, and control inflammation.[5] The medications below are prescribed and monitored by the treating clinician, preferably with ophthalmology involvement; they are not bystander first-aid measures.

Standard Treatments

Antibiotics: A topical antibiotic ointment such as erythromycin four times daily provides lubrication and prophylaxis against superinfection. More severe injuries, particularly those with an epithelial defect, may warrant a topical fluoroquinolone.[5][30]

Cycloplegic agents: Atropine or cyclopentolate may reduce pain from ciliary spasm.[5][30]

Artificial tears: Use preservative-free lubricating drops generously for comfort and ocular surface support.[5][30]

Topical corticosteroids: Early treatment can suppress inflammation and limit inflammatory tissue damage.[31] Mild injuries may be treated with prednisolone acetate 1% four times daily; more severe injuries may require hourly dosing initially. Reassess frequently and individualize the taper after the first week according to epithelial healing and inflammation. Prolonged intensive use requires close monitoring for stromal thinning, infection, and IOP elevation.[30][32]

Other Treatments

Ascorbic acid: Ascorbate supports collagen synthesis and may be depleted after a severe chemical injury. Specialist regimens include topical sodium ascorbate 10% hourly while awake and oral vitamin C, up to 2 g four times daily in adults.[5][30] Experimental studies associate ascorbate supplementation with reduced ulceration after alkali injury.[33] High-dose systemic vitamin C requires assessment of renal function and other contraindications; avoid this high-dose regimen in patients with renal impairment.[34]

Doxycycline: Tetracyclines may reduce collagenolysis through effects on matrix metalloproteinases and inflammatory pathways, independently of antimicrobial activity.[35][36] Oral doxycycline is a specialist adjunct in selected burns. Review pregnancy, lactation, pediatric age, allergies, and drug interactions before prescribing. Product labeling warns of effects on developing teeth and bone, particularly during later pregnancy and in children aged 8 years or younger; the adult regimen below should not be applied automatically to these patients.[37]

Citrate drops: Neutrophils contribute proteolytic enzymes that can damage corneal stromal collagen after alkali injury.[38] Citrate chelates calcium and may reduce neutrophil activity and collagenolysis. Its use is an adjunct selected by the treating ophthalmologist.[39][40]

Medroxyprogesterone acetate 1%: This has been described as a specialist adjunct or an alternative when prolonged corticosteroid use raises concerns about stromal healing.[2][15] Much of its mechanistic evidence comes from animal studies.[41][42] Choice and timing should be individualized by a cornea specialist rather than based on an automatic substitution after a fixed number of days.

Platelet-rich plasma eyedrops: Small clinical studies have reported faster epithelialization in selected chemical burns. Preparation, availability, and evidence vary; this is a specialist adjunct rather than a routine first-line treatment.[43]

Surgical Treatments

Debridement of necrotic epithelium: An ophthalmologist may remove nonviable tissue because it can sustain inflammation and impede epithelialization. The extent and timing depend on tissue viability and the severity of the burn.[5]

Conjunctival/Tenon advancement (tenonplasty): Severe limbal ischemia and necrosis can lead to sterile corneal ulceration. After assessment and debridement of nonviable tissue, advancement of vascularized conjunctival and Tenon tissue may help restore blood supply and support epithelial recovery.[44]

Figure 2. Severe alkali injury with limbal ischemia.

Amniotic membrane transplantation (AMT): AMT may provide ocular surface coverage, improve comfort, and support epithelial healing. Sutureless ring-mounted devices such as Prokera permit rapid placement, although extensive conjunctival injury may require broader surgical coverage.[45][46][47] A 2022 Cochrane review evaluated two randomized controlled trials of AMT added to medical treatment within the first 7 days after an ocular burn. Evidence of benefit in moderate burns was uncertain because of bias and imprecision; for severe burns, no important benefit was demonstrated. AMT remains a specialist adjunct, and these findings do not establish a routine benefit for every burn.[48][49]

Limbal stem cell transplantation: Severe chemical injury can cause limbal stem cell deficiency, impairing corneal epithelial renewal and permitting conjunctivalization. In unilateral disease, an autograft may be obtained from the healthy fellow eye after careful donor-eye assessment. In bilateral disease, living-related or cadaveric allografts are options and generally require systemic immunosuppression and specialist monitoring.[50][51][52][53] When possible, reconstructive transplantation should be delayed until ocular surface inflammation is controlled.[53][54]

Cultivated oral mucosal epithelial transplantation (COMET): Autologous buccal mucosal epithelial cells may be cultivated and transplanted to reconstruct the ocular surface in selected severe cases. Because the tissue is autologous, graft-related systemic immunosuppression is not required.[55][56]

Boston keratoprosthesis: In selected eyes with severe scarring, limbal stem cell deficiency, or repeated graft failure, a keratoprosthesis may offer visual rehabilitation. Candidacy depends on ocular surface, lid, glaucoma, and posterior segment status and the ability to maintain lifelong follow-up. The device itself does not require systemic immunosuppression.[57][58]

Recommended Treatment

Treatment is individualized according to injury severity and evolving clinical findings. The following is an example of an ophthalmologist-directed initial regimen for adults, organized by Roper-Hall grade.[5][30] It follows immediate decontamination and assessment of globe integrity. Doses and duration require adjustment for contraindications, age, renal function, epithelial healing, infection risk, and IOP. Compounded drops and surgical procedures require specialist supervision.

Grade I

  • Topical erythromycin ointment or a comparable antibiotic ointment four times daily.
  • Prednisolone acetate 1% four times daily, with reassessment and taper directed by the treating ophthalmologist.
  • Preservative-free artificial tears as needed.
  • For pain, consider a short-acting cycloplegic such as cyclopentolate, up to three times daily as appropriate.

Grade II

  • Topical fluoroquinolone four times daily, selected according to the epithelial defect and infection risk.
  • Prednisolone acetate 1% hourly while awake initially. Reassess frequently and plan the taper after approximately 7–10 days according to inflammation and epithelial recovery. A persistent defect at 10–14 days warrants specialist reassessment of intensive steroid therapy and stromal integrity; do not automatically substitute another drug based on elapsed time alone.
  • A long-acting cycloplegic such as atropine, prescribed by the treating ophthalmologist.
  • Oral vitamin C, 2 g four times daily in selected adults; assess renal function and avoid this high-dose regimen in renal impairment.
  • Oral doxycycline, 100 mg twice daily in selected adults. Review contraindications and the pregnancy, lactation, and pediatric cautions described above.[37]
  • Compounded sodium ascorbate 10% drops hourly while awake when indicated.
  • Preservative-free artificial tears as needed.
  • Specialist debridement of nonviable epithelium as appropriate. Tissue adhesive may be needed for focal stromal thinning or impending perforation.

Grade III

  • Use the grade II measures with more intensive specialist monitoring and treatment as indicated.
  • Consider early AMT when appropriate, recognizing the uncertainty in trial evidence. Extensive ocular surface involvement may require a membrane that covers the conjunctival fornices and palpebral conjunctiva, rather than a cornea-only device.[47][48]

Grade IV

  • Use the grade II/III measures with urgent cornea-specialist assessment.
  • Severe ischemia or necrosis may require early surgical intervention. Tenonplasty may help reestablish vascular supply; AMT and other reconstructive measures should be selected according to the extent of injury and tissue viability.[44][48]

Stages of Ocular Recovery

The stages of ocular recovery after a chemical injury are summarized below.[5][9]

Table 3. Stages of ocular recovery after chemical injury. Timing and recovery vary with injury severity.[5][9][13][53][58]
Phase Time after injury Clinical course
Initial At presentation Assess corneal, limbal, and conjunctival involvement after immediate decontamination to grade injury severity.
Acute First week Epithelial recovery begins where viable limbal stem cells remain. Treatment supports epithelial healing and controls inflammation.
Early repair Days 7–21 Mild injuries may re-epithelialize; severe injuries may have persistent epithelial defects and stromal ulceration. Continue to monitor epithelial healing and stromal integrity.
Late repair After day 21 Severe limbal stem cell deficiency may cause persistent epithelial defects, conjunctivalization, ulceration, and scarring. Ocular surface reconstruction may be required, and visual recovery is variable.

Figure 3. Grade II burn approximately 1 month after injury, with focal thinning treated with tissue adhesive and a bandage contact lens.

Figure 4. Final appearance of the same grade II burn, with focal conjunctivalization.

Clinical photographs courtesy of Dr. Kathryn Colby (Massachusetts Eye and Ear Infirmary).

Follow-up

Severe chemical burns generally require daily assessment initially. Consider admission when intensive treatment cannot be delivered reliably, when the patient is a child requiring supervised care, or when associated injuries or systemic exposure warrant it. Lengthen follow-up intervals as the surface stabilizes, while maintaining long-term surveillance for glaucoma, dry eye, limbal stem cell deficiency, and cicatricial complications.[5][17][58]

Other Long-Term Complications

Glaucoma

Glaucoma is an important complication of severe ocular chemical injury. Mechanisms include inflammatory and structural damage to the trabecular meshwork and other anterior segment tissues.[59] In one clinical series, more severe burns (Roper-Hall grades III and IV) were associated with higher presenting IOP and greater need for long-term glaucoma medication or surgery than grades I and II.[17] Monitor IOP when globe integrity permits and treat pressure elevation with ophthalmology guidance.

Dry Eye

Chemical injury may destroy conjunctival goblet cells and disrupt the mucin component of the tear film, causing chronic ocular surface disease and dry eye.[5][13] Discomfort, visual disturbance, and recurrent surface damage can substantially affect quality of life even after initial healing.[60]

Damage to Eyelids or Palpebral Conjunctiva

Conjunctival and eyelid injury may lead to forniceal shortening, symblepharon, and cicatricial entropion or ectropion. Management includes control of inflammation and individualized ocular surface or lid reconstruction. Selected cases may require amniotic membrane or oral mucosal grafting after appropriate specialist assessment.[5][58][61]

References

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  45. ↑ Shafto CM. A simple method of inserting amniotic membrane grafts into the conjunctival sac. Br J Ophthalmol. 1950;34(7):445-446.
  46. ↑ Baum J. Thygeson lecture. Amniotic membrane transplantation: why is it effective? Cornea. 2002;21(4):339-341.
  47. ↑ 47.0 47.1 Kheirkhah A, Johnson DA, Paranjpe DR, Raju VK, Casas V, Tseng SCG. Temporary sutureless amniotic membrane patch for acute alkaline burns. Arch Ophthalmol. 2008;126(8):1059-1066.
  48. ↑ 48.0 48.1 48.2 Clare G, Bunce C, Tuft S. Amniotic membrane transplantation for acute ocular burns. Cochrane Database Syst Rev. 2022;9:CD009379. doi:10.1002/14651858.CD009379.pub3.
  49. ↑ Tandon R, Gupta N, Kalaivani M, Sharma N, Titiyal JS, Vajpayee RB. Amniotic membrane transplantation as an adjunct to medical therapy in acute ocular burns. Br J Ophthalmol. 2011;95(2):199-204.
  50. ↑ Huang T, Wang Y, Zhang H, Gao N, Hu A. Limbal allografting from living-related donors to treat partial limbal deficiency secondary to ocular chemical burns. Arch Ophthalmol. 2011;129(10):1267–1273. doi:10.1001/archophthalmol.2011.251.
  51. ↑ Morgan S, Murray A. Limbal autotransplantation in the acute and chronic phases of severe chemical injuries. Eye (Lond). 1996;10(Pt 3):349-354.
  52. ↑ Tsai RJ, Tseng SC. Human allograft limbal transplantation for corneal surface reconstruction. Cornea. 1994;13(5):389-400.
  53. ↑ 53.0 53.1 53.2 Liang L, Sheha H, Tseng SCG. Long-term outcomes of keratolimbal allograft for total limbal stem cell deficiency using combined immunosuppressive agents and correction of ocular surface deficits. Arch Ophthalmol. 2009;127(11):1428-1434. doi:10.1001/archophthalmol.2009.263.
  54. ↑ Samson CM, Nduaguba C, Baltatzis S, Foster CS. Limbal stem cell transplantation in chronic inflammatory eye disease. Ophthalmology. 2002;109(5):862-868.
  55. ↑ Ma D, Kuo M-T, Tsai Y-J, et al. Transplantation of cultivated oral mucosal epithelial cells for severe corneal burn. Eye (Lond). 2009;23(6):1442-1450.
  56. ↑ Nakamura T, Inatomi T, Sotozono C, Amemiya T, Kanamura N, Kinoshita S. Transplantation of cultivated autologous oral mucosal epithelial cells in patients with severe ocular surface disorders. Br J Ophthalmol. 2004;88(10):1280-1284.
  57. ↑ Khan B, Dudenhoefer EJ, Dohlman CH. Keratoprosthesis: an update. Curr Opin Ophthalmol. 2001;12(4):282-287.
  58. ↑ 58.0 58.1 58.2 58.3 Tuft SJ, Shortt AJ. Surgical rehabilitation following severe ocular burns. Eye (Lond). 2009;23(10):1966-1971.
  59. ↑ Paterson CA, Pfister RR. Intraocular pressure changes after alkali burns. Arch Ophthalmol. 1974;91(3):211-218.
  60. ↑ Le Q, Chen Y, Wang X, Li Y, Hong J, Xu J. Vision-related quality of life in patients with ocular chemical burns. Invest Ophthalmol Vis Sci. 2011;52(12):8951-8956.
  61. ↑ Kheirkhah A, Ghaffari R, Kaghazkanani R, Hashemi H, Behrouz MJ, Raju VK. A combined approach of amniotic membrane and oral mucosa transplantation for fornix reconstruction in severe symblepharon. Cornea. 2013;32(2):155-160.
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