Ophthalmologic Approach to Chemical Burns Clinical Presentation

Updated: Oct 08, 2019
  • Author: Mark Ventocilla, OD, FAAO; Chief Editor: Andrew A Dahl, MD, FACS  more...
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Presentation

History

Most often, the patient gives a history of a liquid or a gas being splashed or sprayed into the eyes or of particles falling into the eyes. Query the patient regarding the specific nature of the chemical and the mechanism of injury (eg, simple splash vs high-velocity blast). The local poison control center can be an invaluable resource in determining the exact nature of the chemical composition, when unknown, particularly with obscure commercial products.

Regardless of the specific mechanism of injury, the patient's complaints are frequently related to the severity of the exposure. Common complaints elicited are as follows:

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Physical

A thorough physical examination should be deferred until the affected eye is irrigated copiously, and the pH of the ocular surface is neutralized. Topical anesthetic drops may be used to aid in patient comfort and cooperation. After irrigation, a thorough eye examination is performed with special attention given to clarity and integrity of the cornea, degree of limbal ischemia, concomitant retained foreign bodies, conjunctival trauma, lid trauma, and IOP. Common physical manifestations of chemical injuries to the eye are discussed below.

Decreased visual acuity: Initial visual acuity can be decreased because of corneal epithelial defects, haze, increased lacrimation, or discomfort. In moderate-to-severe chemical burns seen soon after the injury, the corneal haze may be minimal on presentation with good vision, but it can increase significantly with time, severely reducing vision.

Increased IOP: An immediate rise in IOP may result from collagen deformation and shortening, thereby reducing the anterior chamber depth. Prolonged elevation of IOP is directly related to the degree of anterior segment inflammation.

Conjunctival inflammation: Varying degrees of conjunctival hyperemia and chemosis are possible, and even a mild chemical injury can elicit an exuberant conjunctival response. Prolonged or severe conjunctival inflammation must be aggressively treated owing to the significant risk of substantia propria cicatrization, trichiasis and entropion, symblepharon (usually more severe inferiorly), punctal stenosis, and severe dry eye due to obliteration of the lacrimal ductules and goblet cells.

Particles in the conjunctival fornices: This finding is more common with particulate injuries, such as wet plaster or concrete. If not removed, the residual particles can serve as a reservoir for continued chemical release and injury. These particles must be removed before ocular surface healing can begin.

Perilimbal ischemia: The degree of limbal ischemia (blanching) is perhaps the most significant prognostic indicator for future corneal healing because the limbal stem cells are responsible for repopulating the corneal epithelium. In general, the greater the extent of blanching, the worse the prognosis. However, the presence of intact perilimbal stem cells does not guarantee normal epithelial healing. The extent of blanching should be documented in terms of clock hours involved. Limbal ischemia also portends trabecular meshwork damage, eventual peripheral anterior synechiae, and recalcitrant glaucoma.

Corneal epithelial defect: Corneal epithelial damage can range from mild diffuse punctate epithelial keratitis (PEK) to a complete epithelial defect. A complete epithelial defect may not take up fluorescein dye as rapidly as in a routine corneal abrasion; therefore, it may be missed. If an epithelial defect is suspected but not found on the initial evaluation, the eye should be reexamined after several minutes. The size of the defect should be recorded so as to document response to treatment on subsequent visits.

Conjunctival epithelial defect: Conjunctival epithelial damage is found more commonly than corneal defects because milder burns manifest first inferiorly where chemicals aggregate with gravity and less rapid turnover from reflex blinking and squeezing.

Stromal haze: Haze can range from a clear cornea (grade 0) to a complete opacification (grade 5) with no view into the anterior chamber.

Corneal perforation: A very rare finding at presentation, it is more likely to occur after the initial presentation (from days to weeks) in severely injured eyes that have poor healing capacity. It may also result from a simultaneous penetrating injury.

Anterior chamber inflammatory reaction: This can vary from trace cell and flare to a vigorous fibrinoid anterior chamber reaction. Generally, this finding is more common with alkaline injuries because of the greater depth of penetration. Uveitis is generally another very poor prognostic sign.

Adnexal damage/scarring: Similar to chemical injuries on other skin areas, this finding can lead to severe exposure problems if eyelid scarring prevents proper lid closure, thereby exposing an already damaged ocular surface. Lagophthalmos should be addressed early and aggressively by a surgeon experienced in oculoplastics.

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Causes

Common sources of alkali are as follows: [9]

  • Cleaning products (eg, ammonia)

  • Fertilizers (eg, ammonia)

  • Drain cleaners (eg, lye)

  • Cement, plaster, mortar (eg, lime)

  • Airbag rupture (eg, sodium hydroxide)

  • Fireworks (eg, magnesium hydroxide)

  • Potash (eg, potassium hydroxide)

Common sources of acids are as follows: [9]

  • Battery acid (eg, sulfuric acid)

  • Bleach (eg, sulfurous acid)

  • Glass polish (eg, hydrofluoric; behaves like alkali)

  • Vinegar (eg, acetic acid)

  • Chromic acid (brown discoloration of conjunctiva)

  • Nitric acid (yellow discoloration of conjunctiva)

  • Hydrochloric acid (used to clean swimming pools)

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Complications

Primary complications include the following:

  • Conjunctival inflammation

  • Corneal haze and edema

  • Acute rise in IOP

  • Corneal melting and perforations

Secondary complications include the following:

  • Secondary glaucoma

  • Secondary cataract

  • Bulbar conjunctival scarring

  • Lid scarring, trichiasis, and entropion

  • Corneal thinning and perforation

  • Complete ocular surface disruption with corneal scarring and vascularization

  • Corneal ulceration (sterile or infectious)

  • Complete globe atrophy (phthisis bulbi): See the image below.

    Complete cicatrization of the corneal surface foll Complete cicatrization of the corneal surface following chemical injury.
  • Secondary severe dry eye (long-term) due to loss of conjunctival goblet cells and lacrimal ductules

  • Tarsal conjunctival scarring, leading to symblepharon formation, trichiasis, and cicatricial ectropion or ectropion

  • Complete ocular surface disruption with corneal scarring, keratinization, and vascularization due to loss of limbal stem cells

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