Ophthalmologic Approach to Chemical Burns 

Updated: Sep 18, 2018
Author: Mark Ventocilla, OD, FAAO; Chief Editor: Andrew A Dahl, MD, FACS 

Overview

Background

Chemical injuries to the eye represent one of the true ophthalmic emergencies, wherein time is truly critical. While almost any chemical can cause ocular irritation, serious damage generally results from either strongly basic (alkaline) compounds or strongly acidic compounds. Alkali injuries are more common and can be more clinically challenging, with a significant potential for long-term morbidity. Bilateral ocular 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] See the image below.

Severe chemical injury with early corneal neovascu Severe chemical injury with early corneal neovascularization.

Pathophysiology

The severity of this injury is related to chemical composition, pH, 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 in the cornea. This usually occurs when a strong acid has a pH of less than 4. The hydrogen molecule damages the ocular surface by altering the pH, while the anion causes protein denaturation, precipitation, and coagulation. Protein coagulation creates a barrier and thus 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 are lipophilic and can penetrate cell membranes. They 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, in turn, result in increased intraocular pressure (IOP), sometimes permanent. Additionally, the inflammatory mediators released during this process stimulate the release of prostaglandins, which can further increase IOP.[5] See the image below.

Alkali burn. Note the severe conjunctival reaction Alkali burn. Note the severe conjunctival reaction and stromal opacification blurring iris details inferiorly.

Epidemiology

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] Thus, 90% result from accidental exposures. Safety glasses can help prevent injuries, but industrial accidents often involve chemicals under high pressure. Safety glasses are not of much defense in this setting.

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]

Prognosis

In general, the prognosis of ocular chemical injuries is directly correlated with the severity of insult to the eye and adnexal structures.

Many classification systems and revisions thereof have been aimed at classifying ocular burns in relation to their prognosis, including the following systems: Thoft, Hughes, Roper-Hall, and Pfister.[9]  In essence, all systems aim to quantify the degree of corneal epithelial involvement, the degree of limbal stem cell loss, and the degree of conjunctival involvement.[10]

Injuries can be graded from 0-5, as follows:

  • Grade 0 - Minimal epithelial defect, clear corneal stroma, no limbal ischemia

  • Grade 1 - Partial-complete epithelial defect, clear corneal stroma, no limbal ischemia, corneal epithelial involvement only

  • Grade 2 - Partial-complete epithelial defect, mild stromal haze, none or only mild limbal ischemia

  • Grade 3 - Complete epithelial defect, moderate stromal haze, less than one third of the limbus is ischemic

  • Grade 4 - Complete epithelial defect, stromal haze blurring iris details, one third to two thirds of the limbus is ischemic

  • Grade 5 - Complete epithelial defect, stromal opacification, greater than two thirds of the limbus is ischemic

Grades 0-2 can be expected to heal well with proper care and follow-up examinations.

The course for grades 3-5 is more tenuous and may require surgical intervention, in the form of either limbal stem cell transplantation to regenerate the ocular surface or penetrating keratoplasty to replace the corneal stroma and endothelium. These cases have a much poorer prognosis.

Higher-grade injuries are more susceptible to secondary complications.

Patient Education

If the injury resulted from a preventable accident, proper safety instruction should be provided.

If a patient is left functionally monocular from an injury, the patient should be instructed in the use of safety eyewear (eg, polycarbonate lenses).

For excellent patient education resources, visit eMedicineHealth's First Aid and Injuries Center and Eye and Vision Center. Also, see eMedicineHealth's patient education articles Chemical Burns, Chemical Eye Burns, and Eye Injuries.

 

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:

  • 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, 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.

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)

Complications

Primary complications include the following:

  • Conjunctival inflammation

  • Corneal abrasions

  • 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

 

DDx

Diagnostic Considerations

In the setting of an ocular chemical injury, a full ophthalmic and a full general physical examination should be performed with special attention to the head and neck for signs of other burns to the skin.

Differential Diagnoses

 

Workup

Laboratory Studies

The pH of the ocular surface should be periodically tested. Irrigation should be continued until the pH reaches neutrality.

No other laboratory tests are generally necessary unless other systemic injuries are concurrent.

 

Treatment

Medical Care

Treatment of chemical injuries to the eye requires medical and surgical intervention, both acutely and in the long term, for maximal visual rehabilitation.

Regardless of the underlying chemical involved, common goals of management include the following: (1) removing the offending agent, (2) promoting ocular surface healing, (3) eliminating inflammation, (4) preventing infection, and (5) controlling IOP.

Remove inciting chemical (irrigation)

Immediate copious irrigation remains the single most important therapy for treating chemical injuries. If available, the eye should be anesthetized prior to irrigation.

Ideally, the eye should be irrigated with a sterile balanced buffered solution, such as normal saline solution or Ringer's lactate solution. However, immediate irrigation with even plain tap water is preferred over waiting for the ideal fluid.

The irrigation solution must contact the ocular surface. This is best achieved with a special irrigating tubing (eg, Morgan lens) or a lid speculum. Irrigation should be continued until the pH of the ocular surface is neutralized, to a range of 7.0-7.2, usually requiring 1-2 liters of fluid. Monitor the pH at 15- to 20-minute intervals after stabilization to ensure that no further particles are present to continue changing the pH. Once irrigation is finished, a complete thorough eye examination should be performed. Care should be taken to examine the fornices and under the upper lids via tarsal eversion for residual particles.

Promote ocular surface (epithelial) healing

Once the inciting chemical has been completely removed, epithelial healing can begin. Chemically injured eyes have a tendency to poorly produce adequate tears; therefore, artificial tear supplements play an important role in healing. Topical antibiotic ointment should be applied frequently to help the surface heal and to prevent secondary infection. Topical steroids are also needed to control inflammation, which facilitates epithelial healing.

Ascorbate plays a fundamental role in collagen remodeling, leading to an improvement in corneal healing. It may also prevent or delay corneal ulceration. It is available in topical and oral forms. Oral tetracycline class antibiotics (tetracycline, minocycline, doxycycline) may also decrease the risk of corneal melting through inhibition of matrix metalloproteinases.

Placement of a therapeutic bandage contact lens until the epithelium has regenerated can be helpful in some patients.[11]

Amniotic membrane transplant in eyes with acute ocular burns promotes faster healing of epithelial defects in patients with moderate grade burns.[12] Amniotic membranes have anti-inflammatory, antimicrobial, anticollagenolytic, and growth factor properties that can enhance epithelial rejuvenation. The Prokera (Bio-Tissue) brand device is a sutureless office-based amniotic membrane that has been proven to be extremely useful in acute moderate chemical injuries.

No long-term advantage of amniotic membrane transplant is evident when compared with medical and mechanical release of adhesions in terms of final visual outcome, appearance of symblepharon, and corneal vascularization in a controlled clinical setting.[12]

Eliminate inflammation

Inflammatory mediators released from the ocular surface at the time of injury cause tissue necrosis, neovascularization, and scarring and attract further inflammatory reactants.

This robust inflammatory response not only inhibits reepithelialization but also increases the risk of corneal ulceration and perforation.

Controlling inflammation with topical steroids can help break this inflammatory cycle. Prednisolone acetate 1% should be used 4 times daily for 1 week in a mild chemical burn. Difluprednate and loteprednol etabonate are also extremely useful topical steroid preparations for chemical ocular-surface disease. The steroid dose should be increased to hourly dosing in more severe burns. Steroids should be discontinued or tapered rapidly by 10-14 days to avoid corneal melting.

Acetylcysteine (10% or 20% Mucomyst prepared in a certified compounding pharmacy) can inhibit collagenase to reduce corneal ulceration, yet its clinical use is currently controversial.

Prevent infection

When the corneal epithelium is absent, the eye is much more susceptible to infection.

Prophylactic topical antibiotics are warranted during the initial treatment stages. Ointment preparations such as bacitracin may be soothing to the patient but difficult to administer and somewhat blurring. Topical moxifloxacin (Vigamox) is preservative-free and offers broad-spectrum coverage. Polymyxin B trimethoprim (PolyTrim) and besifloxacin (Besivance) are also well-tolerated and broad-spectrum.

Control IOP

The use of aqueous suppressants is advocated to reduce IOP secondary to chemical injuries, both as an initial therapy and during the later recovery phase, if IOP is high (>30 mm Hg).

Control pain

Severe chemical burns can be extremely painful.

Ciliary spasm can be managed with topical cycloplegic agents; however, oral pain medication may be necessary initially to control pain.

Surgical Care

Surgical intervention may be required if the above medical treatments do not result in epithelial healing within a few weeks.

Remove inciting chemical

After instilling topical anesthesia, sweep the fornices with a moist sterile cotton swab to remove any retained foreign material.

This technique is especially important when particulate matter (eg, plaster or cement) is responsible for the injury.

Promote ocular surface healing

See the list below:

  • Debridement of necrotic conjunctival/corneal tissue

  • Temporary amniotic membrane patching[13]

Limbal stem cell transplant, either autologous from a fellow healthy eye or allograft from a living relative or cadaver

See the list below:

  • Cultivated corneal epithelial stem cell sheet transplantation[14, 15, 16, 17]

  • Lysis of conjunctival symblepharon; adhesions are a later finding, and they can be managed with repeated lysis using a glass rod or a sterile cotton swab

Prevent infection

Cyanoacrylate tissue adhesive may be applied for the treatment of small corneal perforations or descemetoceles threatening perforation.

Visual rehabilitation

See the list below:

  • Penetrating keratoplasty with or without cataract extraction[18]

  • Keratoprosthesis

Control IOP

Glaucoma filtering surgery or aqueous tube shunt placement may be used for cases of increased IOP refractory to medical management. Both require intact conjunctiva, which is more likely to be found superiorly after chemical exposure.

Consultations

In most instances, patients present to non-ophthalmologists for their immediate care. At a minimum, patients with mild chemical injuries should have follow-up care arranged with an ophthalmologist. Any patient with a moderate-to-serious injury should be immediately evaluated and followed appropriately by an ophthalmologist. Other medical personnel may be needed as determined by the extent of the extraocular injuries sustained.

Prevention

Education and training regarding the prevention of chemical exposures in the workplace can help prevent chemical injuries to the eye.

Persons who may be exposed to chemicals in the workplace are advised to wear safety goggles.

Further Outpatient Care

Close follow-up care is mandatory in the first weeks following a severe chemical injury to assess epithelial regeneration and corneal melting, to change medications, to control inflammation and IOP, and to prevent secondary infection. Patients should be under the care of an ophthalmologist during this critical period.

Further Inpatient Care

In patients with severe chemical injuries, short hospitalization may be warranted to closely monitor IOP, corneal integrity, medication use, and pain control.

Inpatient & Outpatient Medications

See the list below:

  • Prednisolone acetate 1%, loteprednol etabonate, or difluprednate (1 gtt qid)
  • Erythromycin or bacitracin ophthalmic ointment (4-8 times/d)
  • Homatropine 5% or scopolamine 0.25% (1 gtt tid)
  • Ascorbate (500 mg PO qid)
  • Levobunolol hydrochloride 0.5% (1 gtt bid) or acetazolamide (500 mg PO bid) - Pressure-lowering agents, such as levobunolol and acetazolamide, are indicated only if IOP is increased (>30 mm Hg).

Transfer

After completing initial irrigation and treatment, patients should be transferred to facilities that have ophthalmologists available to assume their care.

 

Medication

Medication Summary

Medical therapy following irrigation in chemical injuries is geared toward promoting epithelial healing, preventing infection, eliminating inflammation, preventing glaucomatous damage from increased IOP, and controlling pain.

Epithelial healing is promoted through aggressive lubrication, ascorbate replenishment, and judicious use of topical corticosteroids. Artificial tears and ointments are especially important with severely scarred and exposed eyes, best recommended in a preservative-free form in anticipation of frequent prolonged use. Ascorbate, both oral and topical, aids in the synthesis of collagen fibrils. Topical steroids decrease ocular surface inflammation, facilitating new epithelial cell growth and ocular surface regeneration. The presence of epithelial defects and corneal exposure necessitates the use of prophylactic topical antibiotics to prevent infection in the already compromised eye.

Antibiotic ointments can serve the dual purpose of providing lubrication and preventing infection. Broad-spectrum antibiotic coverage is required to most effectively minimize infection risk.

Moderate and severe injuries often stimulate an increase in IOP due to anterior chamber inflammation and collagen fibril shortening. This condition is treated most effectively with aqueous suppressants, especially oral carbonic anhydrase inhibitors and topical beta-adrenergic blockers.

Inflamed eyes often experience ciliary spasm, which can be painful. This spasm is blocked by relatively long-acting mydriatic cycloplegics. In severe chemical injuries, oral pain medication may be required to comfort the patient.

Topical antibiotics

Class Summary

Prevent ocular surface infection and effectively lubricate the eye.

Erythromycin ophthalmic

Macrolide broad-spectrum antibiotic.

Ciprofloxacin HCl (Ciloxan)

Fluoroquinolone broad-spectrum bacteriocidal antibiotic.

Carbonic anhydrase inhibitors

Class Summary

Carbonic anhydrase inhibitors reduce aqueous humor production, thereby reducing IOP.

Methazolamide (Neptazane)

Reduces aqueous humor formation by inhibiting the enzyme carbonic anhydrase, which results in decreased IOP.

Acetazolamide (Diamox)

Decreases secretion of aqueous humor through the same mechanism as methazolamide, lowering IOP.

Cycloplegic mydriatics

Class Summary

Cycloplegic mydriatics reduce pain by blocking ciliary spasm, and they reduce intraocular inflammation by stabilizing the blood-aqueous barrier. Drugs from this category are chosen based on their duration of action. Intermediate-acting compounds, such as homatropine or scopolamine, are preferred to short-acting compounds, such as tropicamide, or extremely long-acting compounds, such as atropine sulfate. Recently, the availability of standard generic and proprietary topical cycloplegics has been plagued by shortages.

Homatropine (Isopto Homatropine)

Blocks responses of sphincter muscle of iris and muscle of ciliary body to cholinergic stimulation, producing pupillary dilation (mydriasis) and paralysis of accommodation (cycloplegia).

Induces mydriasis in 10-30 min and cycloplegia in 30-90 min. These effects last up to 48 h.

Scopolamine ophthalmic (Isopto Hyoscine)

Anticholinergic agent that blocks constriction of sphincter muscle of iris and ciliary body muscle, which, in turn, results in mydriasis (dilation) and cycloplegia (paralysis of accommodation). These effects last up to 5 days.

Ascorbate

Class Summary

Critical cofactor necessary for collagen fibril synthesis. Released from the damaged cornea and the anterior chamber, and it must be replenished to promote corneal wound healing.

Ascorbic acid (Ce-vi-sol, Cecon, Cevi-Bid)

Water-soluble vitamin that serves as a cofactor regulating collagen synthesis.

Beta-adrenergic blockers

Class Summary

Topical beta-blockers reduce aqueous humor production, which then reduces IOP.

Timolol maleate 0.25%, 0.5% (Betimol, Istalol, Timoptic, Timoptic XE)

May reduce elevated and normal IOP, with or without glaucoma, by reducing production of aqueous humor or by outflow facilitation.

Levobunolol hydrochloride 0.25%, 0.5% (Betagan)

Nonselective beta-adrenergic blocking agent that lowers IOP by reducing aqueous humor production and possibly increasing outflow of aqueous humor.

Betaxolol ophthalmic (Betoptic S)

Selectively blocks beta 1-adrenergic receptors with little or no effect on beta 2-receptors. Reduces IOP by reducing production of aqueous humor.

Topical corticosteroids

Class Summary

Steroids decrease ocular surface inflammatory response, facilitating earlier epithelial healing and regeneration. These medications should be tapered after 7-10 days because of the risk of corneal melting with prolonged use. Should inflammation persist, systemic anti-inflammatory agents, including oral steroids (prednisone), should be considered.

Prednisolone acetate 1% (Pred Forte, Econopred)

Decreases corneal inflammation and neovascularization, uveitis, and anterior segment inflammation.

Fluorometholone acetate 0.1% (FML, FML Forte, Flarex)

Decreases corneal inflammation and neovascularization, uveitis, and anterior segment inflammation.

Rimexolone 1% (Vexol)

Decreases corneal inflammation and neovascularization, uveitis, and anterior segment inflammation.

Loteprednol etabonate 0.5% (Lotemax)

Decreases corneal inflammation and neovascularization, uveitis, and anterior segment inflammation. Reduces risk of steroid-induced IOP elevation.

Difluprednate 0.05% (Durezol)

Decreases corneal inflammation and neovascularization, uveitis, and anterior segment inflammation. Considered the strongest topical steroid, contains less toxic preservative sorbitol, and more likely to induce significant IOP elevations than other topical steroids.

 

Questions & Answers

Overview

What are the types of chemical burns to the eye?

Which factors affect the severity of chemical burns to the eye?

What is the pathophysiology of acid burns to the eye?

What is the pathophysiology of alkali burns to the eye?

What is the prevalence of chemical burns to the eye in the US?

What is the morbidity of chemical burns to the eye?

What are the racial predilections of chemical burns to the eye?

What are the sexual predilections of chemical burns to the eye?

Which age groups have the highest prevalence of chemical burns to the eye?

What is the prognosis of chemical burns to the eye?

How are chemical burns to the eye graded?

What is included in patient education about chemical burns to the eye?

Presentation

Which clinical history findings are characteristic of chemical burns to the eye?

What are the signs and symptoms of chemical burns to the eye?

What is included in the physical exam to assess chemical burns to the eye?

What is the clinical presentation of decreased visual acuity in chemical burns to the eye?

What causes increased intraocular pressure (IOP) in chemical burns to the eye?

What is the clinical presentation of conjunctival inflammation in chemical burns to the eye?

What is the clinical presentation of particles in the conjunctival fornices in chemical burns to the eye?

What is the clinical presentation of perilimbal ischemia in chemical burns to the eye?

What is the clinical presentation of corneal epithelial defect in chemical burns to the eye?

What is the clinical presentation of conjunctival epithelial defect in chemical burns to the eye?

What is the clinical presentation of stromal haze in chemical burns to the eye?

What is the clinical presentation of corneal perforation in chemical burns to the eye?

What is the clinical presentation of anterior chamber inflammatory reaction in chemical burns to the eye?

What is the clinical presentation of adnexal damage or scarring in chemical burns to the eye?

What are the common alkali sources of chemical burns to the eye?

What are the common acids sources of chemical burns to the eye?

What are primary complications of chemical burns to the eye?

What are the complications of chemical burns to the eye?

DDX

Which is the focus of the physical exam to assess chemical burns to the eye?

What are the differential diagnoses for Ophthalmologic Approach to Chemical Burns?

Workup

What is the role of lab testing in the evaluation of chemical burns in the eye?

Treatment

How are chemical burns to the eye treated?

What is the role of irrigation in the treatment of chemical burns to the eye?

How is ocular surface (epithelial) healing promoted following chemical burns to the eye?

How is inflammation reduced following chemical burns to the eye?

How are infections prevented following chemical burns to the eye?

How is increased intraocular pressure (IOP) treated following chemical burns to the eye?

How is pain managed following chemical burns to the eye?

What is the role of surgery in the treatment of chemical burns to the eye?

How is an inciting chemical removed from the eye?

Which surgical treatments are used to promote ocular surface healing following chemical burns to the eye?

What is the role of stem cells in the treatment of chemical burns to the eye?

What is the role of cyanoacrylate tissue adhesive in the treatment of chemical burns to the eye?

What is the role of visual rehabilitation in the treatment of chemical burns to the eye?

What is the role of surgery in the treatment of increased intraocular pressure (IOP) following chemical burns to the eye?

Which specialist consultations are beneficial to patients with chemical burns to the eye?

How are chemical burns to the eye prevented?

What is included in the long-term monitoring of patients with chemical burns to the eye?

When is inpatient care indicated in the treatment of chemical burns to the eye?

Which medications are used in the treatment of chemical burns to the eye?

When is patient transfer indicated for the treatment of chemical burns to the eye?

Medications

What is the role of drug treatment for chemical burns to the eye?

Which medications in the drug class Topical corticosteroids are used in the treatment of Ophthalmologic Approach to Chemical Burns?

Which medications in the drug class Beta-adrenergic blockers are used in the treatment of Ophthalmologic Approach to Chemical Burns?

Which medications in the drug class Ascorbate are used in the treatment of Ophthalmologic Approach to Chemical Burns?

Which medications in the drug class Cycloplegic mydriatics are used in the treatment of Ophthalmologic Approach to Chemical Burns?

Which medications in the drug class Carbonic anhydrase inhibitors are used in the treatment of Ophthalmologic Approach to Chemical Burns?

Which medications in the drug class Topical antibiotics are used in the treatment of Ophthalmologic Approach to Chemical Burns?