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Chemical Burns

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Title: Chemical Burns

Author: E Anne Shepherd, 4^th Year Medical Student, University of Tennessee Health Science Center

Text:

The first step in assessing a patient who is believed to have suffered a chemical injury to the eye is to obtain a history of the incident and identify the offending chemical. This should NOT delay treatment though. Key to emergency treatment is irrigation, irrigation, irrigation. If the patient calls from home, advise them to irrigate their eye(s) with clean water for a minimum of thirty minutes before coming in. If the patients is presenting to the emergency room, isotonic saline or lactate ringer solution should be used to irrigate. Irrigation should be continued until a neutral pH is achieved; this could require up to 20 liters. Adequate irrigation is significantly easier when the patient’s ocular surface is anesthetized with topical anesthetics such as 1% proparacaine.  Remember that these drops are toxic to the eye when used for extended periods.  The patient should NEVER be prescribed or given topical anesthetics for pain control.  Once adequate irrigation is completed a thorough ophthalmic exam is necessary to assess the damage. It is important pay attention to the fornices, visual acuity, intraocular pressure and assess for limbal blanching.

If the chemical composition of the insulting agent is unknown and cannot be identified poison control can be contacted for more information. Items commonly causing injury to eye are listed below.

Table 1. Etiologies of common acid burns:

Table 2. Etiologies of common alkali burns:

In general, alkali burns are more harmful and cause more damage than acid burns. Alkali solutions are lipophilic and therefor penetrate the eye more rapidly and have the potential to deposit in the ocular tissues. Acids, on the other hand, cause precipitation of proteins which creates a barrier and prevents further damage in most cases. If the damage to the cornea is severe enough in either an acid or alkali burn, there can be destruction to the limbal stem cells causing limbal stem cell deficiency (link). Loss of these stem cells creates opacification and neovasculatization of the cornea. Other complications that can arise are increased intraocular pressure from inflammatory changes and direct damage to the trabecular meshwork, scarring and forniceal shortening, lifelong dryness from loss of goblet cells, and symblepharon formation from epithelial destruction (see Image 1).

Treatment includes antibiotic eye drops, cycloplegic/mydriaic drops for comfort, topical lubricants like artificial tears, and pressure lower drops, if necessary. Achieving corneal epithelization is important to prevent further inflammation and corneal damage. In severe burns that are complicated by persistent corneal epithelial defects, this can be aided by bandage contact lens, botox induced ptosis, or amniotic membrane grafts.

Images:

Image 1: Anterior symblepharon after a severe alkali burn. Symblepharon are prevented by not allowing the non-epithelialized surfaces of the cornea/sclera and the conjunctiva to come in continuous contact.

Image 2. Neovascularization of the cornea with diffuse corneal edema. This can present after both severe acid and alkali burns and are due to damage to limbal stem cells.

References:

Augsburger JJ, Corrêa ZM. Chapter 19. Ophthalmic Trauma. In: Riordan-Eva P, Cunningham ET, Jr. eds. Vaughan & Asbury’s General Ophthalmology, 18e New York, NY: McGraw-Hill; 2011.

Singh P, Tyagi M, Kumar Y, Gupta KK, Sharma PD. Ocular chemical injuries and their management. Oman Journal of Ophthalmology. 2013;6(2):83-86. doi:10.4103/0974-620X.116624.

Identifier: Moran_CORE_23919