> Table of Contents > Ocular Chemical Burns
Ocular Chemical Burns
Robert J. Hyde, MD, MA, NRP, FACEP
Patricia Ruth Atchinson, DO
image BASICS
DESCRIPTION
  • Chemical exposure to the eye can result in rapid, devastating, and permanent damage and is one of the true emergencies in ophthalmology.
  • Separate alkaline from acid chemical exposure
    • Alkali burns: more severe. Alkaline compounds are lipophilic, penetrating rapidly into eye tissue; saponification of cells leads to necrosis and may produce injury to lids, conjunctiva, cornea, sclera, iris, and lens (cataracts).
    • Acid burns: Acid usually does not damage internal structures because its associated anion causes protein denaturation, creating a barrier to further acid penetration. (Hydrofluoric acid is an exception to this rule; see below.) Injury is often limited to lids, conjunctiva, and cornea.
  • System(s) affected: nervous, skin/exocrine
  • Synonym(s): chemical ocular injuries
EPIDEMIOLOGY
  • Predominant age: can occur at any age, peak from 20 to 40 years of age
  • Predominant sex: male > female
Incidence
  • Estimated 300/100,000 per year
  • Alkali burns twice as common as acid burns
ETIOLOGY AND PATHOPHYSIOLOGY
  • Acidic compounds
    • Anion leads to protein denaturing and protective barrier formation by coagulation necrosis forming an eschar. This more superficial mechanism of injury tends to have prominent scarring that may lead to vision loss:
      • Hydrofluoric acid is an exception. In its nonionized form, it behaves like an alkaline substance, capable of penetrating the corneal stroma and leading to extensive anterior segment lesions. When ionized, it may combine with intracellular calcium and magnesium to form insoluble complexes, leading to potassium ion movements and cell death. Once systemically absorbed, severe hypocalcemia can occur.
  • Alkaline compounds
    • Lipophilic compounds that penetrate into deep structures on disassociation into cations and hydroxide
    • Hydroxide causes saponification of fatty acids in cell membranes, leading to cell death.
    • Cation causes hydration of glycosaminoglycans, leading to corneal opacification and hydration of collagen, resulting in rapid shortening and thickening of collagen fibrils that leads to an acute elevation in intraocular pressure secondary to shrinking and contraction of the cornea and sclera.
    • Long-term elevation in intraocular pressure may occur from accumulation of inflammatory debris within the trabecular meshwork.
    • Penetration into deep structures may also affect perfusing vessels, leading to ischemia of affected area.

Sources of Alkaline and Acidic Compounds

Alkaline Compounds

Typical Sources

Calcium hydroxide (lime)

Cement, whitewash

Sodium hydroxide (lye)

Drain cleaner, airbags

Potassium hydroxide (lye)

Drain cleaner

Ammonia

Cleaning agents

Ammonium hydroxide

Fertilizers

Acidic Compounds

Typical Sources

Sulfuric acid

Car batteries

Sulfurous acid

Bleach

Hydrochloric acid

Chem labs, swimming pools

Acetic acid

Vinegar

Hydrofluoric acid

Glass polish

RISK FACTORS
  • Construction work (plaster, cement, whitewash)
  • Use of cleaning agents (drain cleaners, ammonia)
  • Automobile battery explosions (sulfuric acid)
  • Industrial work, including work in industrial chemical laboratories
  • Alcoholism
  • Any risk factor for assault (˜10% of injuries due to deliberate assault)
GENERAL PREVENTION
Safety glasses to safeguard eyes
COMMONLY ASSOCIATED CONDITIONS
Facial (including eyelids) cutaneous chemical or thermal burns
image DIAGNOSIS
PHYSICAL EXAM
  • Acidic compound may present with a ground-glass appearance secondary to superficial scar formation.
  • Alkaline compounds may present with corneal opacification secondary to glycosaminoglycan hydration; however, severe acid burns may also present with this finding.
  • Mild burns
    • Blurry vision
    • Eyelid skin erythema and edema
    • Corneal epithelial defects or superficial punctate keratitis
    • Conjunctival chemosis, hyperemia, and hemorrhages without perilimbal ischemia
    • Mild anterior chamber reaction
  • Moderate to severe burns
    • Reduced vision
    • 2nd- and 3rd-degree burns of eyelid skin
    • Corneal edema and opacification
    • Corneal epithelial defects
    • Marked conjunctival chemosis and perilimbal blanching
    • Moderate anterior chamber reaction
    • Increased intraocular pressure
    • Local necrotic retinopathy
DIFFERENTIAL DIAGNOSIS
  • Thermal burns
  • Ocular cicatricial pemphigoid
  • Other causes of corneal opacification
  • Ultraviolet radiation keratitis
DIAGNOSTIC TESTS & INTERPRETATION
Not necessary unless suspicion of intraocular or orbital foreign body is present. In this case, CT should be used and MRI is contraindicated.
Diagnostic Procedures/Other
  • Measure pH of tear film with litmus paper or electronic probe:
    • Irrigating fluid with nonneutral pH (e.g., normal saline has pH of 4.5) may alter results.
  • Careful slit-lamp exam, fundus ophthalmoscopy, tonometry, and measurement of visual acuity
  • Full extent of damage from alkali burns may not be apparent until 48 to 72 hours after exposure.
Test Interpretation
  • Corneal epithelial defects or superficial punctate keratitis, edema, opacification
  • Conjunctival chemosis, hyperemia, and hemorrhages
  • Perilimbal ischemia
  • Anterior chamber reaction
  • Increased intraocular pressure
image TREATMENT
Copious irrigation and removal of corneal or conjunctival foreign bodies are always the initial treatment (1,2,3)[A]:
  • Passively open patient's eyelid and have patient look in all directions while irrigating.
  • Be sure to remove all reservoirs of chemical from the eyes.
  • Continue irrigation until the tear film and superior/inferior cul-de-sac is of neutral pH (7 ± 0.1) and pH is stable (2)[C]:
    • Severe burns should be irrigated for at least 15 minutes to as much as 2 to 4 hours; this irrigation should not be interrupted during transportation to hospital (2)[C].
    • Irrigation via Morgan lens (polymethylmethacrylate scleral lens) is a good way to achieve continuous irrigation over a prolonged period of time.
    • It is impossible to overirrigate.
  • Initial pH testing should be done on both eyes even if the patient claims to only have unilateral ocular pain/irritation so that a contralateral injury is not neglected.
  • P.727

  • Use whatever nontoxic fluid is available for irrigation on scene. In hospital, sterile water, normal saline, normal saline with bicarbonate, balanced salt solution (BSS), or lactated Ringer solution may be used:
    • No therapeutic difference in effectiveness has been noted between types of solutions (1)[C].
  • A topical anesthetic can be used to provide patient comfort (e.g., proparacaine, tetracaine).
  • Sweep the conjunctival fornices every 12 to 24 hours to prevent adhesions (2)[C].
  • Eye patching may relieve pain but has not been shown to improve outcomes (4)[C].
MEDICATION
First Line
  • Further treatment (depending on severity and associated conditions)
    • Topical prophylactic antibiotics: any broad-spectrum agent (e.g., bacitracin-polymyxin B [Polysporin] ointment q2-4h, ciprofloxacin [Ciloxan] drops q2-4h, chloramphenicol [Chloroptic] ointment q2-4h) (1)[C]:
      • Some experts suggest that systemic tetracycline 250 mg PO q6h and especially derivatives such as doxycycline 100 mg PO BID may be beneficial to encourage healing of persistent corneal epithelial defects by inhibiting metalloproteinases (5)[C].
    • Tear substitutes: hydroxypropyl methylcellulose (HypoTears PF, Refresh Plus) drops q4h, carboxymethylcellulose (Refresh PM) ointment at bedtime (1)[C]:
      • Most beneficial in those with impaired tear production (elderly patients)
    • Cycloplegics for photophobia and/or uveitis: cyclopentolate 1% TID or scopolamine 1/4% BID (1)[C]
    • Antiglaucoma for elevated intraocular pressure: latanoprost (Xalatan) 0.005% q24h, timolol (Timoptic) 0.5% BID, or levobunolol (Betagan) 0.5% BID, and/or acetazolamide (Diamox) 125 to 250 mg PO q6h, or methazolamide (Neptazane) 25 to 50 mg PO BID, and/or IV mannitol 20% 1 to 2 g/kg as needed (1)[C]
    • Corticosteroids for intraocular inflammation: prednisolone (Pred-Forte) 1% or equivalent q1-4h for 7 to 10 days; if severe, prednisone 20 to 60 mg PO daily for 5 to 7 days. Taper rapidly if epithelium is intact by this time (1)[C]:
      • Use of corticosteroids >10 days may do harm by inhibiting repair and cause corneoscleral melt (1,6)[C].
    • Vitamin C (ascorbic acid) 500 mg PO QID and topical 10% ascorbate solution in artificial tears reduces the incidence of corneal thinning and ulceration (2)[C].
    • Acetylcysteine (Mucomyst) 10-20% topically q4h to promote wound healing (2)[C]
  • Precautions
    • Timolol and levobunolol: history of heart failure (HF) or chronic obstructive pulmonary disease (COPD)
    • Acetazolamide and methazolamide: history of nephrolithiasis or metabolic acidosis
    • Mannitol: history of HF or renal failure
    • Scopolamine: history of urinary retention
    • Topical corticosteroids must be used with caution in the presence of damaged corneal epithelium because iatrogenic infection can occur. Daily follow-up or consultation with an ophthalmologist is recommended.
SURGERY/OTHER PROCEDURES
  • Goal of subacute treatment is restoration of the normal ocular surface anatomy, control of glaucoma, and restoration of corneal clarity.
  • Surgical options include the following:
    • Débridement of necrotic tissue (1)[C]
    • Conjunctival/tenon advancement (tenoplasty) to restore vascularity in severe burns (1)[C]
    • Tissue adhesive (e.g., isobutyl cyanoacrylate) for impending or actual corneal perforation of
      • Tectonic keratoplasty for acute perforation >1 mm (1)[C]
    • Limbal autograft transplantation for epithelial stem cell restoration (1)[C]
    • Amniotic membrane transplantation (6)[C] or umbilical cord serum drops (*)[B] to promote epithelial regeneration (6)[C]
    • Conjunctival or mucosal membrane transplant to restore ocular surface in severe injury (1)[C]
    • Lamellar or penetrating keratoplasty for tectonic stabilization or visual rehabilitation (1)[C]
INPATIENT CONSIDERATIONS
Admission Criteria/Initial Stabilization
Based on ophthalmologic consultation and concomitant burn injuries
image ONGOING CARE
FOLLOW-UP RECOMMENDATIONS
Patient Monitoring
  • Depending on severity of ocular injury
    • From daily to weekly visits initially
  • May be inpatient
  • If on mannitol or prednisone, consider frequent serum electrolytes.
PATIENT EDUCATION
  • Safety glasses
  • Need for immediate ocular irrigation with any available water following chemical exposure to the eyes
PROGNOSIS
  • Depends on severity of initial injury: Increased limbal involvement in clock hours and greater percentage of conjunctival involvement correlate with poorer prognosis (Dua classification system).
  • For mildly injured eyes, complete recovery is the norm.
  • For severely injured eyes, permanent loss of vision is not uncommon.
REFERENCES
1. Wagoner MD. Chemical injuries of the eye: current concepts in pathophysiology and therapy. Surv Ophthalmol. 1997;41(4):275-313.
2. Singh P, Tyagi M, Kumar Y, et al. Ocular chemical injuries and their management. Oman J Ophthalmol. 2013;6(2):83-86.
3. Eslani M, Baradaran-Rafii A, Movahedan A, et al. The ocular surface chemical burns. J Ophthalmol. 2014;2014:196827.
4. Chau JP, Lee DT, Lo SH. A systematic review of methods of eye irrigation for adults and children with ocular chemical burns. Worldviews Evid Based Nurs. 2012;9(3):129-138.
5. Spector J, Fernandez WG. Chemical, thermal, and biological ocular exposures. Emerg Med Clin North Am. 2008;26(1):125-136.
6. Ralph RA. Tetracyclines and the treatment of corneal stromal ulceration: a review. Cornea. 2000;19(3):274-277.
Additional Reading
&NA;
  • Fish R, Davidson RS. Management of ocular thermal and chemical injuries, including amniotic membrane therapy. Curr Opin Ophthalmol. 2010;21(4):317-321.
  • Gicquel JJ. Management of ocular surface chemical burns. Br J Ophthalmol. 2011;95(2):159-161.
  • Lin A, Patel N, Yoo D, et al. Management of ocular conditions in the burn unit: thermal and chemical burns and Stevens-Johnson syndrome/toxic epidermal necrolysis. J Burn Care Res. 2011;32(5):547-560.
  • Roblin I, Urban M, Flicoteau D, et al. Topical treatment of experimental hydrofluoric acid skin burns by 2.5% calcium gluconate. J Burn Care Res. 2006;27(6):889-894.
  • Sharma N, Lathi SS, Sehra SV, et al. Comparison of umbilical cord serum and amniotic membrane transplantation in acute ocular chemical burns. Br J Ophthalmol. 2015;99(5):669-673.
See Also
&NA;
Burns
Codes
&NA;
ICD10
  • T26.50XA Corrosion of unsp eyelid and periocular area, init encntr
  • T26.60XA Corrosion of cornea and conjunctival sac, unsp eye, init
  • S05.00XA Inj conjunctiva and corneal abrasion w/o fb, unsp eye, init
Clinical Pearls
&NA;
  • Prompt irrigation of all chemical burns, even prior to arrival to the emergency department, is essential to ensure best outcomes. It is impossible to overirrigate.
  • All patients with chemical injuries to their eyes should have urgent ophthalmology consultation and/or referral.