Trauma
Ocular trauma is a leading cause of blindness in developed countries. Trauma may occur in industrial settings, during sports activities, or at home. Most patients affected are young males, and the majority of cases are anterior segment injuries.
CHEMICAL BURNS
An ocular chemical burn is an emergency requiring immediate irrigation with water or saline solution at the site of injury for at least 30 minutes. Mechanical removal of foreign particles should also be performed. These actions should be repeated at the emergency room after quickly checking the pH of the tears, even before taking a detailed history or performing a complete eye examination.
If initial evaluation shows potentially life-threatening respiratory or gastrointestinal involvement, these conditions should be attended to first.
Etiology
• Alkali: Examples include sodium hydroxide (lye), calcium hydroxide (lime, cement, and plaster), and ammonia.
• Acids: sulfuric acid (battery fluid)
• Mace (chloroacetophenone) and teargas
• Organic solvents
• Detergents
Symptoms
• Pain, redness, tearing, decreased vision
Signs
• Mild to moderate
▪ Burns and edema of the eyelid
▪ Conjunctival injection, chemosis, abrasion
▪ Punctate or large epithelial defects on the cornea (Fig. 11-1A)
▪ Mild anterior chamber activity
• Severe
▪ Burns of the skin of the eyelids
▪ Chemosis, conjunctival necrosis, conjunctival ischemia (sludging or absence of blood flow through conjunctival vessels) (Fig. 11-1B-E, eFig. 11-1B and C)
▪ Scleral/limbal ischemia
▪ Significant anterior chamber activity
▪ Corneal epithelial defects, edema, or melting (Fig. 11-1F)
▪ Poor or no view of the anterior chamber because of corneal haze (Fig. 11-1G, eFig. 11-1G)
▪ Intraocular pressure (IOP) may be low, normal, or elevated in acute stages.
▪ The degree of limbal ischemia and corneal haziness carries prognostic importance.
Treatment
• Mild cases may be treated on an outpatient basis. Severe injuries may require hospitalization.
• Copious irrigation with normal saline through an IV infusion set for at least 30 minutes and repeated every 30 minutes until neutral pH is reached. Consider using an agent with high neutralizing capacity such as Cederroth eye wash.
• Mechanical removal of foreign particles and debridement of necrotic tissues should be performed with a cotton-tipped applicator or jeweler’s forceps under topical anesthesia.
• Frequent instillation of preservative-free tear drops (q1h)
• Cycloplegics (e.g., cyclopentolate 1%, scopolamine 0.25%, or atropine 1% t.i.d.)
• Topical antibiotic ointment (e.g., erythromycin, bacitracin, or tetracycline) q2h if an eye patch is not used. Pressure patching may aid in reepithelialization.
• Control IOP if it is elevated, either with topical drops or with oral carbonic anhydrase inhibitors.
• For injuries with significant inflammation and without risk of corneal melting, topical corticosteroid (e.g., dexamethasone 0.1% or prednisolone 1%) q1-2h may be used during the first week, tapered during the second week, and increased after epithelial healing if necessary. A combined antibiotic-corticosteroid (e.g., tobramycin 0.3%-dexamethasone 0.1% ointment) q1-2h can also be used.
• Topical acetylcysteine 10% drops q.i.d. may help control collagenase activity and corneal melting.
• High-dose vitamin C 1 g PO t.i.d. and topical ascorbate 10% drops q1-6h may be helpful in severe alkali burns.
• Doxycycline 100 mg PO b.i.d. can be used to decrease collagenase activity.
• Early amniotic membrane graft or amniotic membrane on a scleral ring (e.g., ProKera) may be beneficial in severe cases.
• If there is symblepharon formation, daily sweeping of the fornices with a cotton-tipped applicator or glass rod can be performed under topical anesthesia to break the adhesions. Alternatively, a scleral shell may be used.
• For progressive corneal melting or perforation, tissue adhesive, amniotic membrane graft, limbal stem cell graft, lamellar patch graft, or penetrating keratoplasty may be necessary.
Complications
• Corneal haze or scarring
• Infectious keratitis
• Dry eyes
• Symblepharon
• Cicatricial entropion or ectropion
• Trichiasis or distichiasis
• Punctal stenosis or occlusion
• Limbal stem cell deficiency
• Pannus formation
• Cataract
• Glaucoma
Prognosis
• Dismal to excellent, depending on the severity of the injury (Fig. 11-1H, eFig. 11-1H). In general, alkaline substances cause the most severe injuries because they penetrate ocular tissues easily.
 FIGURE 11-1. Chemical burn. A. A mild acid injury caused a large corneal abrasion, which has been stained with yellow fluorescein dye. There is minimal to no conjunctival blanching, and the cornea is essentially clear. Mild chemical burns generally resolve without serious consequences. B. A sulfuric acid injury occurred to this patient’s right eye. There is a large central and inferior corneal epithelial defect and mild inferior conjunctival blanching. |
 FIGURE 11-1. (continued) C. This eye withstood a battery acid (sulfuric acid) injury. There is moderate conjunctival blanching and mucus adherent to the conjunctiva and cornea. D. The left eye of the patient seen in B has a much more extensive sulfuric acid injury. The epithelium is necrotic and has already sloughed off of the superior cornea. There is extensive conjunctival and scleral blanching inferiorly and nasally. |
 FIGURE 11-1. (continued) E. High-magnification view of the eye seen in D demonstrating ischemia of the conjunctiva and sclera. There is segmentation of the red blood cells, indicating lack of blood flow. The greater the degree of ischemia, the worse is the prognosis. F. A severe lye (sodium hydroxide) injury caused extensive ischemic damage in the lower two-thirds of the eye. The cornea has undergone necrosis centrally, leading to a perforation requiring an emergency corneal transplant. This alkali injury eventually resulted in enucleation. |
 FIGURE 11-1. (continued) G. Twelve days after a severe alkali injury, the conjunctiva and sclera remain blanched, and the cornea is opaque. There has been no reepithelialization of the damaged cornea or conjunctiva. H. Many years after a severe chemical burn, the cornea remains totally scarred and vascularized. |
THERMAL AND ELECTRICAL BURNS
THERMAL BURNS
Thermal burns can be mild to severe and can occur at any age. Cigarette burns are not uncommon in small children, whose eyes may be at hand level of a person holding a cigarette.
Etiology
• Curling irons
• Cigarettes, especially children
• Flames
• Hot liquids
• Molten metals
Symptoms
• Pain, redness, decreased vision
Signs
• Thermal burns on skin of eyelids
• Conjunctival injection, chemosis, epithelial defects (eFig. 11-2A1 and 2)
• Punctate or large epithelial defects on cornea
• A white area of cauterized epithelium (Fig. 11-2A)
• In severe cases
▪ Anterior chamber reaction
▪ Corneal haze and edema
▪ Limbal or scleral ischemia, corneal or scleral perforation (Fig. 11-2B)
Treatment
• Removal of foreign bodies and debridement of devitalized tissues
• Topical antibiotic ointment to prevent infection and to lubricate the ocular surface (e.g., erythromycin, bacitracin, polymyxin B/bacitracin, ciprofloxacin q2-6h)
• Cycloplegics (e.g., cyclopentolate 1% or scopolamine 0.25% t.i.d.)
• Pressure patching, lateral tarsorrhaphy, or amniotic membrane graft should be considered for large or nonhealing epithelial defects.
• Topical corticosteroids (similar to use in chemical burns) to reduce inflammation and prevent symblepharon formation during the first 1 to 2 weeks, bearing in mind that they can potentiate corneal melting.
Complications
• Corneal scarring
• Irregular astigmatism
• Decreased vision
• Infectious keratitis
Prognosis
• Depends on the severity of the injury, especially the exact cause of the burn and duration of contact. Short-contact burns, such as those from curling irons and cigarettes, have an excellent prognosis. Molten metal that adheres to the cornea causes a much more substantial injury. Eyelid damage can cause exposure problems and long-term difficulties with corneal healing.
 FIGURE 11-2. Thermal injury. A. A curling iron briefly touched this cornea, causing coagulation of the corneal epithelium and turning it white. It can be removed mechanically or it will slough off naturally. Generally, these eyes recover without sequelae because the length of time the heat is in contact with the cornea is minimal. Electrical injury. B. An electrical injury caused a localized area of scleral melt with uveal prolapse. Additionally, the electrical injury produced necrosis of a large portion of upper eyelid tissue, resulting in severe exposure. The eye was treated with a scleral patch graft and eyelid skin grafting. |
ELECTRICAL BURNS
Ocular electrical burns usually result from electrical injuries to the head or a lightning strike. In addition to corneal and scleral burns, they can cause acute uveitis. The lens is frequently involved, and cataracts may develop months to years later. Eyelid damage can cause exposure problems and long-term difficulties with corneal healing.
ULTRAVIOLET KERATOPATHY (ARC WELDER FLASH)
Severe, painful punctate keratopathy can result hours after exposure to significant levels of ultraviolet light.
Etiology
• Usually caused by welding or using a sunlamp without proper protective eyewear. Milder forms can also be seen in patients with significant sun exposure, such as after a day at the beach or after skiing.
Symptoms
• Symptoms usually develop 6 to 10 hours after the exposure.
• Pain, photophobia, foreign body sensation, tearing, redness, and decreased vision
Signs
• Spasm of eyelids in severe cases
• Punctate epithelial erosions, especially in the interpalpebral regions (Fig. 11-3)
• Eyelid edema, conjunctival hyperemia
Treatment
• Preservative-free artificial tears q2-3h
• Topical antibiotic drops (e.g., a fluoroquinolone) t.i.d. to q.i.d. and antibiotic ointment (e.g., erythromycin, tetracycline, bacitracin, polymyxin B/bacitracin, or ciprofloxacin) at bedtime. For more severe cases, topical antibiotic ointment 4 to 8 times a day will provide more lubrication and comfort.
• Cycloplegics (e.g., cyclopentolate 1% or scopolamine 0.25% t.i.d.)
• Pressure patching or a bandage soft contact lens for severe epithelial erosions
• Emphasize to the patient the importance of protective eyewear.
Complications
• Rarely, infectious keratitis
CORNEAL ABRASION
Corneal abrasions result from corneal surface trauma that causes removal of a portion of the epithelial layer.
Etiology
• Mechanical trauma (e.g., fingernail, paper edge, tree branch)
• Chemical injuries, medicamentosa keratitis
• Foreign body
• Contact lens
• Misdirected eyelashes
• Neurotrophic or exposure keratopathy
• Iatrogenic (e.g., after removal of corneal sutures, epithelial debridement)
Symptoms
• Pain, especially upon blinking; foreign-body sensation; photophobia; tearing; redness; often decreased vision
• Topical anesthetic drops relieve the pain (and facilitate the eye examination).
Signs
• Epithelial defect that may be detected grossly or at the slit lamp. It is easily seen with fluorescein dye using cobalt blue light (Fig. 11-4, eFig. 11-4A1 and 2).
Treatment
• Search for and remove any foreign body in the conjunctival fornices and under the upper eyelid.
• Epilate any misdirected eyelashes.
• Topical antibiotic ointment (e.g., erythromycin, tetracycline, bacitracin, polymyxin B/bacitracin, or ciprofloxacin) q2-6h. Topical antibiotic drops may be used if the abrasion is small or if the patient finds that ointments blur vision.
• Cycloplegics (e.g., cyclopentolate 1% or scopolamine 0.25% t.i.d.)
• Pressure patching or a bandage soft contact lens is occasionally used for large defects. Small defects generally do not require patching or bandage soft contact lens.
• For traumatic or contact lens-induced abrasions, bandage contact lenses and patching are relatively contraindicated because they increase the risk of infection. A topical antibiotic with good gram-negative coverage (e.g., a fluoroquinolone, tobramycin, gentamicin, polymyxin B/neomycin/gramicidin) should be used.
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