eMedicine Specialties > Ophthalmology > Ophthalmology for the General Practitioner

Burns, Chemical

Author: J Bradley Randleman, MD, Associate Professor, Department of Ophthalmology, Section of Cornea, External Disease and Refractive Surgery, Emory University School of Medicine; Director of Cornea, External Disease and Refractive Surgery Fellowship, Emory University; Physician Member, Section of Ophthalmology, The Emory Clinic
Coauthor(s): Alok S Bansal, MD, Resident Physician, Emory Eye Center; Evan S Loft, MD, Staff Physician, Department of Ophthalmology, Emory University; Geoffrey Broocker, MD, FACS, Chief of Service, Ophthalmology, Professor of Ophthalmology, Department of Ophthalmology, Emory University School of Medicine, Grady Memorial Hospital
Contributor Information and Disclosures

Updated: Apr 7, 2009

Introduction

Background

Chemical injuries to the eye represent one of the true ophthalmic emergencies. While almost any chemical can cause ocular irritation, serious damage generally results from either strongly basic (alkaline) compounds or acidic compounds. Alkali injuries are more common and can be more deleterious. Bilateral chemical exposure is especially devastating, often resulting in complete visual disability. Immediate, prolonged irrigation, followed by aggressive early management and close long-term monitoring, is essential to promote ocular surface healing and to provide the best opportunity for visual rehabilitation.^1,2,3

Pathophysiology

The severity of this injury is related to type, volume, concentration, duration of exposure, and degree of penetration of the chemical. The mechanism of injury differs slightly between acids and alkali.⁴

Acid injury

Acids dissociate into hydrogen ions and anions in the cornea. The hydrogen molecule damages the ocular surface by altering the pH, while the anion causes protein denaturation, precipitation, and coagulation. Protein coagulation generally prevents deeper penetration of acids and is responsible for the ground glass appearance of the corneal stroma following acid injury. Hydrofluoric acid is an exception; it behaves like an alkaline substance because the fluoride ion has better penetrance through the stroma than most acids, leading to more extensive anterior segment disruption.⁴

Alkali injury

Alkaline substances dissociate into a hydroxyl ion and a cation in the ocular surface. The hydroxyl ion saponifies cell membrane fatty acids, while the cation interacts with stromal collagen and glycosaminoglycans. This interaction facilitates deeper penetration into and through the cornea and into the anterior segment. Subsequent hydration of glycosaminoglycans results in stromal haze. Collagen hydration causes fibril distortion and shortening, leading to trabecular meshwork alterations that can result in increased intraocular pressure (IOP). Additionally, the inflammatory mediators released during this process stimulate the release of prostaglandins, which can further increase IOP.⁵

Frequency

United States

Chemical injuries are responsible for approximately 7% of work-related eye injuries treated at US hospital emergency departments.⁶   More than 60% of chemical injuries occur in workplace accidents, 30% occur at home, and 10% are the result of an assault.⁷

Mortality/Morbidity

As many as 20% of chemical injuries result in significant visual and cosmetic disability; only 15% of patients with severe chemical injuries achieve functional visual rehabilitation.

Race

No overall racial predilection exists; however, young black males are more likely to have high-concentration, high-impact alkaline chemical injuries secondary to assault.⁸

Sex

Males are 3 times more likely to experience chemical injuries than females.⁷

Age

Chemical injuries can strike any population; however, most injuries occur in patients aged 16-45 years.^6,7

Clinical

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 when unknown.

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:

• Pain (often extreme)
• Foreign body sensation
• Blurred vision
• Excessive tearing
• Photophobia
• Red eye(s)

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, and IOP. Common physical manifestations of chemical injuries to the eye include the following:

• 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 shrinking the anterior chamber. 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.
• Particles in the conjunctival fornices: This finding is more common with particulate injuries, such as plaster. 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.
• 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.
• 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.
• 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.
• Adnexal damage/scarring: Similar to chemical injuries on other skin areas, this finding can lead to severe exposure problems if eyelid scarring prevents proper closure, thereby exposing an already damaged ocular surface.

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

• Search for CME/CE on This Topic »

• Burns, Ocular (Emergency Medicine)
• Burns, Chemical (Plastic Surgery)
• Burns, Thermal (Plastic Surgery)
• Burns (Pediatrics: Surgery)

• Burns Center
• Chemical Burn Overview
• Chemical Eye Burn Overview
• Chemical Burns Treatment
• Eye and Vision Center
• Chemical Burns Symptoms
• Chemical Burns Causes
• Eye Injuries Overview

• Aggression in Girls May Be Linked to BPA
• Microneedle Patches Could Make Hypodermic Needles Obsolete
• Red Yeast Rice Reduces LDL-Cholesterol Levels in Statin-Intolerant Patients

• Older Adults and Burns
• Emergency Treatment of Severely Burned Pediatric Patients: Current Therapeutic Strategies
• Irritant Contact Dermatitis from Plants

• Gallbladder and Biliary Disease Resource Center