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Chapter: Ophthalmology: Ocular Trauma

Chemical Injuries in Eye

Chemical Injuries in Eye
Chemical injuries can be caused by a variety of substances such asacids, alkalis, detergents, solvents, adhesives, and irritants like tear gas. Severity may range from slight irritation of the eye to total blindness.

Chemical Injuries


Chemical injuries can be caused by a variety of substances such asacids, alkalis, detergents, solvents, adhesives, and irritants like tear gas. Severity may range from slight irritation of the eye to total blindness.

Chemical injuries are among the most dangerous ocular injuries. First aid at the site of the accident is crucial to minimize the risk of severe sequelae such as blindness.

As a general rule, acid burns are less dangerous than alkali burns. This is because most acids do not act deeply. Acids differ from alkalis in that they cause immediate coagulation necrosis in the superficial tissue. This has the effect of preventing the acid from penetrating deeper so that the burn is effec-tively a self-limiting process. However, some acids penetrate deeply like alka-lis and cause similarly severe injuries. Concentrated sulfuric acid (such as from an exploding car battery) draws water out of tissue and simultaneously develops intense heat that affects every layer of the eye. Hydrofluoric acid and nitric acid have a similar penetrating effect.

Alkalis differ from most acids in that they can penetrate by hydrolyzingstructural proteins and dissolving cells. This is referred to as liquefactivenecrosis. They then cause severe intraocular damage by alkalizing theaqueous humor.


Epiphora, blepharospasm, and severe pain are the primarysymptoms. Acid burns usually cause immediate loss of visual acuity due to the superficial necrosis. In alkali injuries, loss of visual acuity often manifests itself only several days later.

Clinical picture and diagnostic considerations:

Proper diagnosis of thecause and severity of the burn is crucial to treatment and prognosis.

Alkali burns may appear less severe initially than acid burns but they lead to blindness.

Morphologic findings and the resulting prognosis can vary greatly depending on the severity and duration of exposure to the caustic agent. This informa-tion is summarized in Table 18.2.


First aid rendered at the scene of the accident often decides thefate of the eye. The first few seconds and minutes and resolute action by per-sons at the scene are crucial. Immediate copious irrigation of the eye may be performed with any watery solution of neutral pH, such as tap water, mineral water, soft drinks, coffee, tea, or similar liquids. Milk should be avoided as it the increases penetration of the burn by opening the epithelial barrier. A sec-ond person must rigorously restrain the severe blepharospasm to allow effec-tive irrigation. A topical anesthetic to relieve the blepharospasm will rarely be available at the scene of the accident. Coarse particles (such as lime particles in a lime injury) should be flushed and removed from the eye. Only after these actions have been taken should the patient be brought to an ophthalmologist or eye clinic.

Chronology of treatment of chemical injuries:

First aid at the scene of the accident (coworkers or family members):

–  Restrain blepharospasm by rigorously holding the eyelids open.

– Irrigate the eye within seconds of the injury using tap water, mineral water, soft drinks, coffee, tea, or similar liquids. Carefully remove coarse particles from the conjunctival sac.

–  Notify the rescue squad at the same time.

–  Transport the patient to the nearest ophthalmologist or eye clinic.

Treatment by the ophthalmologist or at the eye clinic:

– Administer topical anesthesia to relieve pain and neutralize blepharospasm.

– With the upper and lower eyelids fully everted, carefully remove small particles such as residual lime from the superior and inferior conjuncti-val fornices under a microscope using a moist cotton swab.

– Flush the eye with a buffer solution. Long-term irrigation using an irri-gating contact lens may be indicated (the lens is connected to a cannula to irrigate the eye with a constant stream of liquid).

–  Initiate systemic pain therapy if indicated.

Additional treatment on the ward in an eye clinic:

The following therapeutic measures for severe chemical injuries are usu-ally performed on the ward:

–  Continue irrigation.

– Initiate topical cortisone therapy (dexamethasone 0.1% eyedrops and prednisolone 1% eyedrops).

–  Administer subconjunctival steroids.

– Immobilize the pupil with atropine 1% eyedrops or scopolamine 0.25% eyedrops twice daily.

– Administer anti-inflammatory agents (two oral doses of 100 mg indomethacin or diclofenac) or 50 – 200 mg systemic prednisolone.

–  Administer oral and topical vitamin C to neutralize cytotoxic radicals.

– Administer 500 mg of oral acetazolamide (Diamox) to reduce intraocu-lar pressure as prophylaxis against secondary glaucoma.

– Administer hyaluronic acid for corneal care to promote re-epithelial-ization and stabilize the physiologic barrier.

–  Administer topical antibiotic eyedrops.

– Debride necrotic conjunctival and corneal tissue and make radial inci-sions in the conjunctiva (Passow’s method) to drain the subconjunctival edema.

Additional surgical treatment in the presence of impaired wound heal-ing following extremely severe chemical injuries:

– A conjunctival and limbal transplantation (stem cell transfer) can replace lost stem cells that are important for corneal healing. This will allow re-epithelialization.

–  Where the cornea does not heal, cyanoacrylate glue can be used toattach a hard contact lens (artificial epithelium) to promote healing.

– A Tenon’s capsuloplasty (mobilization and advancement of a flap of subconjunctival tissue of Tenon’s capsule to cover defects) can help to eliminate conjunctival and scleral defects.

Late surgical treatment after the eye has stabilized:

– Lysis of symblepharon (symblepharon refers to adhesions between the palpebral and bulbar conjunctiva; see also prognosis and complica-tions) to improve the motility of the globe and eyelids.

– Plastic surgery of the eyelids to the release the globe. This should be only performed 12 to 18 months after the injury).

– Where there is total loss of the goblet cells, transplantation of nasal mucosa usually relieves pain (the lack of mucus is substituted by goblet cells from the nasal mucosa).

– Penetrating keratoplasty  may be performed to restore vision. Because the traumatized cornea is highly vascularized (Fig. 18.10), these procedures are plagued by a high incidence of graft rejection. A clear cornea can rarely be achieved in a severely burned eye even with a HLA-typed corneal graft and immunosuppressive ther-apy.

Prognosis and possible complications:

The degree of ischemia of the con-junctiva and the limbal vessels is an indicator of the severity of the injury and the prognosis for healing (see Table 18.2). The greater the ischemia of the con-junctiva and limbal vessels, the more severe the burn will be. The most severeform of chemical injury presents as a “cooked fish eye” (Fig. 18.11) for which the prognosis is very poor, i.e., blindness is possible.

Moderate to severe chemical injuries involving the bulbar and palpe-bral conjunctiva can result in symblepharon (adhesions between the palpebral and bulbar conjunctiva; Fig. 18.12). Inflammatory reactions in the ante-rior chamber secondary to chemical injuries can lead to secondary glau-coma.


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