Consequences of blunt trauma to the eye range from eyelid to orbital injury.

Eyelids: Eyelid contusions (which result in black eyes) are more cosmetically than clinically significant, although more serious injuries may sometimes accompany them and should not be overlooked. Uncomplicated contusions are treated with ice packs to inhibit swelling during the first 24 to 48 h, followed by hot compresses to aid absorption of the hematoma.

Minor lid lacerations not involving the lid margin or tarsal plate may be repaired with nylon (or, in children, plain gut) 6-0 or 7-0 sutures. Lacerations of the lid margin are best repaired by an ophthalmic surgeon to ensure accurate apposition and to avoid a notch in the contour. Complicated lid lacerations, which include those of the medial portion of the lower or upper eyelid (possibly involving the lacrimal canaliculus), through-and-through lacerations, those in which the patient has ptosis, and those that expose orbital fat or involve the tarsal plate, should also be repaired by an ophthalmic surgeon.

Globe: Trauma may cause the following:

• Conjunctival, anterior chamber, and vitreous hemorrhage
• Retinal hemorrhage, edema, or detachment
• Laceration of the iris
• Cataract
• Dislocated lens
• Glaucoma
• Globe rupture (laceration)

Evaluation can be difficult when massive lid edema or laceration is present. Even so, unless the need for immediate eye surgery is obvious (necessitating evaluation by an ophthalmologist as soon as possible), the lid is opened, taking care not to exert pressure on the globe, and as complete an examination as possible is conducted. At a minimum, the following are noted:

• Visual acuity
• Pupillary responses
• Extraocular movements
• Anterior chamber depth or hemorrhage
• Presence of red reflex

An analgesic or, after obtaining any surgical consent, an anxiolytic may be given to facilitate examination. Gentle and careful use of eyelid retractors or an eyelid speculum makes it possible to open the lids. If a commercial instrument is not available, the eyelids can be separated with makeshift retractors fashioned by opening a paperclip to an S shape, then bending the U-shaped ends to 180°. Globe laceration should be suspected with any of the following:

• A corneal or scleral laceration is visible.
• Aqueous humor is leaking (positive Seidel sign).
• The anterior chamber is very shallow (eg, making the cornea appear to have folds) or very deep (due to rupture posterior to the lens).
• The pupil is irregular.

If globe laceration is suspected, measures that can be taken before an ophthalmologist is available consist of applying a protective shield (see Eye Trauma: Treatment) and combating possible infection with systemic antimicrobials as for intraocular foreign bodies (see Eye Trauma: Intraocular foreign bodies). Topical antibiotics are avoided. Vomiting, which can increase intraocular pressure (IOP) and contribute to extravasation of ocular contents, is suppressed using antiemetics as needed. Because fungal contamination of open wounds is dangerous, corticosteroids are contraindicated until after wounds are closed surgically. Tetanus prophylaxis is indicated after open globe injuries. Very rarely, after laceration of the globe, the uninjured, contralateral eye becomes inflamed (sympathetic ophthalmia—see Uveitis and Related Disorders: Sympathetic Ophthalmia) and may lose vision to the point of blindness unless treated. The mechanism is an autoimmune reaction; corticosteroid drops can prevent the process and may be prescribed by an ophthalmologist.

Hyphema (anterior chamber hemorrhage): Hyphema may be followed by recurrent bleeding, glaucoma, and blood staining of the cornea, any of which may result in permanent vision loss. Symptoms are of associated injuries unless the hyphema is large enough to obstruct vision. Direct inspection typically reveals layering of blood or the presence of clot or both in the anterior chamber. Layering is seen as a meniscus-like blood level in the dependent (usually inferior) part of the anterior chamber. Microhyphema, a less severe form, may be detectable by direct inspection as haziness in the anterior chamber or by slit-lamp examination as suspended RBCs.

An ophthalmologist should attend to the patient as soon as possible. The patient is placed on bed rest with the head elevated 30 to 45° and is given an eye shield to protect the eye from further trauma (see Eye Trauma: Corneal Abrasions and Foreign Bodies). Patients who are at high risk of recurrent bleeding (eg, those with large hyphemas, bleeding diatheses, anticoagulant use, or sickle cell disease), who have IOP that is difficult to control, or who are likely to be nonadherent to recommended treatment may be hospitalized. Oral and topical NSAIDs are contraindicated because they may contribute to recurrent bleeding.

IOP can rise acutely (within hours, usually in patients with sickle cell disease or trait) or months to years later. Thus, IOP is monitored daily for several days and then regularly over subsequent weeks and months and if symptoms develop (eg, eye ache, decreased vision, nausea—similar to symptoms of acute angle-closure glaucoma). If pressure rises, timololSome Trade Names
BLOCADREN
TIMOPTIC
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0.5% bid, brimonidineSome Trade Names
ALPHAGAN
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0.2% or 0.15% bid, or both are given. Response to treatment is determined by pressure, often checked every 1 or 2 h until controlled or until a significant rate of reduction is demonstrated; thereafter, it is usually checked once or twice daily. Mydriatic drops (eg, scopolamineSome Trade Names
TRANSDERM SCOP
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0.25% tid or atropineSome Trade Names
ATROPEN
ATROPINE-CARE
SAL-TROPINE
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1% tid for 5 days) and topical corticosteroids (eg, prednisoloneSome Trade Names
ORAPRED
PRELONE
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acetate 1% 4 to 8 times/day for 2 to 3 wk) are often given.

If bleeding is recurrent, an ophthalmologist should be consulted for management. Administration of aminocaproic acidSome Trade Names
AMICAR
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50 to 100 mg/kg po q 4 h (not exceeding 30 g/day) for 5 days may reduce recurrent bleeding, and miotic or mydriatic drugs must also be given. Rarely, recurrent bleeding with secondary glaucoma requires surgical evacuation of the blood.

Blowout fracture: Blowout fracture occurs when blunt trauma forces the orbital contents through one of the most fragile portions of the orbital wall, typically the floor. Medial and roof fractures also can occur. Symptoms include diplopia, enophthalmos, inferiorly displaced globe, hypesthesia of the cheek and upper lip (due to infraorbital nerve injury), and subcutaneous emphysema. Epistaxis, lid edema, and ecchymosis may occur. Diagnosis is best made using CT with thin cuts through the facial bones. If diplopia or cosmetically unacceptable enophthalmos persists beyond 2 wk, surgical repair is indicated. Patients should be told to avoid blowing the nose to prevent subcutaneous dissection of air. Using a topical vasoconstrictor for 2 to 3 days may alleviate epistaxis.

Key Points

• Consult an ophthalmologist if an eyelid laceration is complicated (eg, through the margin, tarsal plate, or canaliculus, causing ptosis, or exposing orbital fat).
• Globe trauma may cause iris laceration, cataract, lens dislocation, glaucoma, vitreous hemorrhage, or retinal damage (hemorrhage, detachment, or edema).
• Suspect globe rupture if trauma results in a visible corneal or scleral laceration, leaking aqueous humor, an unusually shallow or deep anterior chamber, or an irregular pupil.
• Hyphema, best diagnosed by slit-lamp examination, requires bed rest with head elevation at 30 to 45° and close monitoring of intraocular pressure.
• Refer patients for surgical repair of blowout fractures that cause > 2 wk of diplopia or unacceptable enophthalmos.

Posttraumatic Iridocyclitis

(Traumatic Anterior Uveitis; Traumatic Iritis)

Posttraumatic iridocyclitis is an inflammatory reaction of the uvea and iris, typically developing within 3 days of blunt eye trauma.

Symptoms of posttraumatic iridocyclitis include tearing, throbbing ache and redness of the eye, photophobia, and blurred vision. The pupil may be dilated. Diagnosis is by history, symptoms, and slit-lamp examination, which typically reveals flare (due to an increase in protein content of the aqueous humor from the inflammatory exudate) and WBCs in the anterior chamber. Treatment involves a cycloplegic (usually scopolamineSome Trade Names
TRANSDERM SCOP
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0.25% tid or homatropineSome Trade Names
ISOPTO
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5% tid). Topical corticosteroids (eg, prednisoloneSome Trade Names
ORAPRED
PRELONE
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acetate 1% 4 to 8 times/day) are often used to shorten symptom duration.

Last full review/revision September 2012 by Kathryn Colby, MD, PhD

Content last modified November 2012