The Wills Eye Manual

Chapter 3. Trauma

3.1 Chemical Burn

Treatment should be instituted IMMEDIATELY, even before testing vision, unless an open globe is suspected.

NOTE: This includes alkali (e.g., lye, cements, plasters, airbag powder, bleach, ammonia), acids (e.g., battery acid, pool cleaner, vinegar), solvents, detergents, and irritants (e.g., mace).

Emergency Treatment

1. Copious but gentle irrigation using saline or Ringer lactate solution. Tap water can be used in the absence of these solutions and may be more efficacious in inhibiting elevated intracameral pH than normal saline for alkali burns. NEVER use acidic solutions to neutralize alkalis or vice versa as acid-base reactions themselves can generate harmful substrates and cause secondary thermal injuries. An eyelid speculum and topical anesthetic (e.g., proparacaine) may be placed prior to irrigation. Upper and lower fornices must be everted and irrigated. After exclusion of open globe injury, particulate matter should be flushed or manually removed. Manual use of intravenous tubing connected to an irrigation solution best facilitates the irrigation process.

2. Wait 5 to 10 minutes after irrigation is stopped to allow the dilutant to be absorbed; then check the pH in the fornices using litmus paper. Irrigation is continued until neutral pH is achieved (i.e., 7.0 to 7.4). The pH should be read before the litmus paper dries.

3. Conjunctival fornices should be swept with a moistened cottontipped applicator to remove any sequestered particles of caustic material and necrotic conjunctiva, especially in the case of a persistently abnormal pH. If there is concern for retained material, double eversion of the eyelids with Desmarres eyelid retractors may be performed to identify and remove particles in the deep fornix.

4. Acidic or basic foreign bodies embedded in the conjunctiva, cornea, sclera, or surrounding tissues may require surgical excision.

NOTE: The volume of irrigation fluid required to reach neutral pH varies with the chemical and with the duration of the chemical exposure. The volume required may range from a few liters to many liters (over 10 L).

MILD TO MODERATE BURNS

Signs

Critical. Corneal epithelial defects range from scattered superficial punctate keratopathy (SPK), to focal epithelial loss, to sloughing of the entire corneal epithelium. No significant areas of perilimbal ischemia are seen (i.e., no blanching of the conjunctival or episcleral vessels).

Other. Focal areas of conjunctival epithelial defect, chemosis, hyperemia, hemorrhages, or a combination of these; mild eyelid edema; mild anterior chamber (AC) reaction; first- and second-degree burns of the periocular skin with or without lash loss.

NOTE: If you suspect a corneal epithelial defect but do not see one with fluorescein staining, repeat the fluorescein application to the eye. Sometimes the defect is slow to take up the dye. If the entire epithelium sloughs off, only Bowman membrane remains, which may take up fluorescein poorly.

Workup

1. History: Time of injury? Specific type of chemical? Time from exposure until irrigation started? Duration, amount, and type of irrigation? Eye protection? Sample of agent, package/label, or material safety data sheets are helpful in identifying and treating the exposing agent.

2. Slit lamp examination with fluorescein staining. Eyelid eversion to search for foreign bodies. Evaluate for and diagram conjunctival and corneal epithelial defects and ulcerations. Check the intraocular pressure (IOP). In the presence of a distorted cornea, IOP may be most accurately measured with a Tono-Pen, pneumotonometer, or rebound tonometer. Gentle palpation may be used if necessary.

Treatment

1. See Emergency Treatment above.

2. Consider cycloplegic (e.g., cyclopentolate 1% or 2%, homatropine 5% b.i.d. to t.i.d.) if significant photophobia, pain, or AC inflammation. If limbal ischemia is suspected, avoid phenylephrine because of its vasoconstrictive properties.

3. Frequent (e.g., q1-2h while awake) use of preservative-free artificial tear drops, artificial tear, or antibiotic ointment (e.g., erythromycin, bacitracin) depending on presence and size of corneal and/or conjunctival epithelial defects.

4. Consider topical steroids (e.g., prednisolone acetate 1% q.i.d.) as adjunctive treatment with topical antibiotic (e.g., trimethoprim/polymyxin B or fluoroquinolone drops q.i.d.) for a week even if epithelial defect is present, especially for an alkali injury.

5. Oral pain medication (e.g., acetaminophen with or without codeine) as needed.

6. If IOP is elevated, acetazolamide 250 mg p.o. q.i.d., acetazolamide 500 mg sequel p.o. b.i.d., or methazolamide 25 to 50 mg p.o. b.i.d. or t.i.d. may be given. Electrolytes, especially potassium, should be monitored in patients on these medications. Add a topical beta-blocker (e.g., timolol 0.5% b.i.d.) if additional IOP control is required. Alpha-agonists should be avoided because of their vasoconstrictive properties, especially if limbal ischemia is present.

Follow Up

Initially daily, then every few days until corneal epithelial defect is healed. Topical steroids should be initiated if there is significant inflammation. Monitor for corneal epithelial breakdown, stromal thinning, and infection.

SEVERE BURNS

Signs (in addition to the above)

(See Figure 3.1.1.)

FIGURE 3.1.1 Alkali burn.

Critical. Pronounced chemosis and conjunctival blanching, corneal edema and opacification, a moderate to severe AC reaction (may not be appreciated if the cornea is opaque).

Other. Increased IOP, second- and third-degree burns of the surrounding skin, and local necrotic retinopathy as a result of direct penetration of alkali through the sclera.

Workup

Same as for mild-to-moderate burns.

Treatment

1. See Emergency Treatment above.

2. Hospital admission may be needed for close monitoring of IOP and corneal healing.

3. Debride necrotic tissue containing foreign matter.

4. Cycloplegic (e.g., cyclopentolate 1% or 2% b.i.d. to t.i.d., homatropine 5% b.i.d. to t.i.d., or atropine 1% daily to b.i.d.). Avoid phenylephrine due to vasoconstriction.

5. Topical antibiotic (e.g., trimethoprim/polymyxin B or fluoroquinolone drops q.i.d.; erythromycin or bacitracin ointment q.i.d. to q2h while awake). Caution with ciprofloxacin and large epithelial defects as it can precipitate in the cornea.

6. Topical steroid (e.g., prednisolone acetate 1% or dexamethasone 0.1% q.i.d. to q2h while awake) with concurrent antibiotic coverage even in the presence of an epithelial defect, especially if significant AC or corneal inflammation is present. May use a combination antibiotic/steroid such as tobramycin/dexamethasone drops or ointment q1-2h while awake.

7. lOP-lowering medications as above if the IOP is increased or cannot be determined.

8. Frequent (e.g., q1h while awake) use of preservative-free artificial tears or gel if not using frequent ointments.

9. Oral tetracyclines and vitamin C may also reduce collagenolysis and stromal melting (e.g., doxycycline 100 mg p.o. b.i.d. and vitamin C 1,000 mg p.o. daily).

10. Lysis of conjunctival adhesions b.i.d. by sweeping the fornices may be helpful. If symblepharon begins to form despite attempted lysis, consider using an amniotic membrane ring (e.g., ProKera Plus Ring) or scleral shell to maintain the fornices.

11. In severe cases with large areas of epithelial loss on the bulbar and forniceal conjunctival surfaces, consider suturing a very large amniotic membrane into the fornices.

12. Other considerations:

• For poorly healing epithelial defects, a therapeutic soft contact lens, collagen shield, amniotic membrane graft (e.g., sutured/glued or self-retained membrane), or tarsorrhaphy may be considered.

 Ascorbate and citrate for alkali burns has been reported to speed healing time and allow better visual outcome. Administration has been studied intravenously (i.v.), orally (ascorbate 500 to 2,000 mg daily), and topically (ascorbate 10% q1h). Caution in patients with renal compromise secondary to potential renal toxicity.

 If any melting of the cornea occurs, other collagenase inhibitors may be used (e.g., acetylcysteine 10% to 20% drops q4h while awake).

 Topical biologic fluids including autologous serum tears, platelet-rich plasma, umbilical cord serum, and amniotic membrane suspensions may be useful to promote epithelialization.

 If the melting progresses (or the cornea perforates), consider cyanoacrylate tissue adhesive. An emergency patch graft or corneal transplantation may be necessary; however, the prognosis for grafts is better if performed long after initial injury (over 12 to 18 months).

Follow Up

These patients need to be monitored closely, either as inpatients or daily initially as outpatients. Topical steroids should be tapered after 7 to 14 days, because they can promote corneal melting. If prolonged anti-inflammatory treatment is needed, consider switching to medroxyprogesterone acetate 1% to prevent corneal stromal melting. Long-term use of preservative-free artificial tears q1-6h and lubricating ointments q.h.s. to q.i.d. may be required. A severely dry eye may require a tarsorrhaphy or a conjunctival flap. Conjunctival or limbal stem cell transplantation from the fellow eye may be performed in unilateral injuries that fail to heal within several weeks to several months.

SUPER GLUE (CYANOACRYLATE) INJURY TO THE EYE

NOTE: Rapid-setting super glues harden quickly on contact with moisture.

Treatment

1. If the eyelids are glued together, they can often be separated with gentle traction. Lashes may need to be cut to separate the eyelids. Misdirected lashes, hardened glue mechanically rubbing the cornea, and glue adherent to the cornea should be carefully removed with fine forceps. Copious irrigation with warm normal saline, warm compresses, or ointment may be used to loosen hardened glue on the eyelids, eyelashes, cornea, or conjunctiva.

2. Epithelial defects are treated as corneal abrasions (see 3.2, Corneal Abrasion).

3. Warm compresses q.i.d. may help remove any remaining glue stuck in the lashes that did not require urgent removal.

4. If complete removal of glue is not possible from the eyelid margin, a bandage contact lens may be applied along with topical antibiotic drop therapy until the glue falls off.

Follow Up

Initially daily, then every few days until all corneal epithelial defects are healed.

3.2 Corneal Abrasion

Symptoms

Sharp pain, photophobia, foreign body sensation, tearing, discomfort with blinking, blurred vision, and history of scratching or hitting the eye

Signs

(See Figure 3.2.1.)

FIGURE 3.2.1 Corneal abrasion with fluorescein staining.

Critical. Epithelial defect that stains with fluorescein; absence of underlying corneal opacification (presence of which indicates infection or inflammation).

Other. Conjunctival injection, swollen eyelid, and mild AC reaction.

Differential Diagnosis

• Recurrent erosion (see 4.2, Recurrent Corneal Erosion).

 Herpes simplex keratitis (see 4.15, Herpes Simplex Virus).

 Confluent SPK (see 4.1, Superficial Punctate Keratopathy).

 Ultraviolet keratopathy (see 4.7, Ultraviolet Keratopathy).

 Exposure keratopathy (see 4.5, Exposure Keratopathy).

 Neurotrophic keratopathy (see 4.6, Neurotrophic Keratopathy).

 Chemical burn (see 3.1, Chemical Burn).

Workup

1. Slit lamp examination: Use fluorescein dye, measure the size (e.g., height and width) of the abrasion, and diagram its location. Evaluate for foreign body, infiltrate (underlying corneal opacification), AC reaction, hyphema, corneal laceration, and penetrating trauma.

2. Evert the eyelids to ensure that no foreign body is present, especially in the presence of vertical or linear abrasions.

Treatment

1. Antibiotic

 Noncontact lens wearer: Antibiotic ointment (e.g., erythromycin, bacitracin, or bacitracin/polymyxin B q2-4h while awake) or antibiotic drops (e.g., polymyxin B/trimethoprim or a fluoroquinolone q.i.d.). Abrasions secondary to fingernails or vegetable matter should be covered with a fluoroquinolone drop (e.g., ofloxacin, moxifloxacin, besifloxacin) or ointment (e.g., ciprofloxacin) at least q.i.d.

 Contact lens wearer: Must have antipseudomonal coverage (i.e., fluoroquinolone). May use antibiotic ointment or antibiotic drops at least q.i.d.

NOTE: The decision to use drops versus ointment depends on the needs of the patient. Ointments offer better barrier and lubricating function between eyelid and abrasion but tend to blur vision temporarily. They may be used to augment drops at bedtime. We prefer frequent ointments.

2. Cycloplegic agent (e.g., cyclopentolate 1% to 2% b.i.d. or t.i.d.) for traumatic iritis, which may develop 24 to 72 hours after trauma. Avoid steroid use for iritis with epithelial defects because it may impede epithelial healing and increase infection risk. Avoid use of long-acting cycloplegics for small abrasions to allow for faster visual recovery.

3. Patching is rarely necessary and can cause a serious abrasion if not applied properly. Patching should be avoided in all contact lens-related corneal abrasions due to higher risk of infection.

4. Consider a short course of topical nonsteroidal anti-inflammatory drug (NSAID) drops (e.g., ketorolac 0.4% to 0.5% q.i.d. for 3 days) for pain control. Avoid in patients with other ocular surface disease. Oral acetaminophen, NSAIDs, or narcotics (in severe cases) can also be used for pain control.

NOTE: Never prescribe topical anesthetics (e.g., proparacaine, tetracaine) for analgesia, as this may delay epithelial healing and increase infection and ulceration risk.

5. Debride loose or hanging epithelium because it may inhibit healing. A cotton-tipped applicator soaked in topical anesthetic (e.g., proparacaine) or sterile jeweler’s forceps (used with caution) may be utilized.

6. Bandage contact lenses may be used to improve comfort and protect the epithelium during healing. Contact lenses are rarely used in the emergency room setting out of concern for patient compliance and follow up. If a bandage contact lens is placed, patients should use prophylactic topical antibiotics (e.g., polymyxin B/trimethoprim or a fluoroquinolone q.i.d.) and should be monitored closely for epithelial healing and contact lens replacement. Do not use for abrasions associated with contact lens wear or if any concern for infection exists.

Follow Up

Noncontact Lens Wearer

1. If patched or given bandage contact lens, the patient should return in 24 hours (or sooner if symptoms worsen) for reevaluation.

2. Central or large corneal abrasion: Return the next day to determine if the epithelial defect is improving. If the abrasion is healing, may see 2 to 3 days later. Instruct patient to return sooner if symptoms worsen. Revisit every 3 to 5 days until healed.

3. Peripheral or small abrasion: Return 2 to 5 days later. Instruct patient to return sooner if symptoms worsen. Revisit every 3 to 5 days until healed.

Contact Lens Wearer

Close follow up until the epithelial defect resolves, and then treat with topical antibiotic (e.g., fluoroquinolone drops) for an additional 1 or 2 days. The patient may resume contact lens wear after the eye feels normal for a week after cessation of a proper medication course. A new contact lens should be used at that time.

3.3 Corneal and Conjunctival Foreign Bodies

Symptoms

Foreign body sensation, tearing, pain, and redness.

Signs

(See Figure 3.3.1.)

FIGURE 3.3.1 Corneal metallic foreign body with rust ring.

Critical. Conjunctival or corneal foreign body with or without a rust ring.

Other. Conjunctival injection, eyelid edema, mild AC reaction, and SPK. A small infiltrate may surround a corneal foreign body; it is usually reactive and sterile. Vertically oriented linear corneal abrasions or SPK may indicate a foreign body under the upper eyelid.

Workup

1. History: Determine the mechanism of injury (e.g., metal striking metal, power tools or weed-whackers, direct pathway with no safety glasses, distance of the patient from the instrument of injury, etc.). Attempt to determine the size, shape, velocity, force, and composition of the object. Always keep in mind the possibility of an intraocular foreign body (IOFB).

2. Document visual acuity before any procedure is performed. One or two drops of topical anesthetic may be necessary to facilitate the examination.

3. Slit lamp examination: Locate and assess the depth of the foreign body. Examine closely for possible entry sites (rule out selfsealing lacerations), pupil irregularities, iris tears and transillumination defects (TIDs), lens capsular perforations, lens opacities, hyphema, AC shallowing (or deepening in scleral perforations), and asymmetrically low IOP in the involved eye.

NOTE: There may be multiple foreign bodies with injuries due to power equipment or explosive debris.

If there is no evidence of perforation, evert the eyelids and inspect the fornices for additional foreign bodies. Double everting the upper eyelid with a Desmarres eyelid retractor may be necessary. Carefully inspect conjunctival lacerations to rule out an underlying scleral laceration or perforation. Measure and diagram the dimensions of any corneal or scleral infiltrate and the degree of any AC reaction for monitoring therapy response and progression of possible infection.

NOTE: An infiltrate accompanied by a significant AC reaction, purulent discharge, or extreme conjunctival injection and pain should be cultured to rule out infection, treated aggressively with antibiotics, and followed closely (see 4.11, Bacterial Keratitis).

4. Dilate the eye and examine the posterior segment for possible IOFB (see 3.15, Intraocular Foreign Body).

5. Consider B-scan ultrasonography, computed tomography (CT) scan of the orbit (axial, coronal, and parasagittal views, 1-mm sections), or ultrasound biomicroscopy (UBM) to exclude an intraocular or intraorbital foreign body. While we prefer a CT scan, a plain film x-ray can also be used to rule out radiodense foreign bodies. Avoid magnetic resonance imaging (MRI) if there is a history of possible metallic foreign body.

Treatment

Corneal Foreign Body (Superficial or Partial Thickness)

1. Apply topical anesthetic (e.g., proparacaine). Remove the corneal foreign body with a foreign body spud or fine forceps such as jeweler’s forceps at a slit lamp. Multiple superficial foreign bodies may be more easily removed by irrigation.

FIGURE 3.3.2 Burr removal of metallic rust ring.

NOTE: If there is concern for full-thickness corneal foreign body, exploration and removal should be performed in the operating room.

2. Remove the rust ring as completely as possible on the first visit. This may require an ophthalmic burr (see Figure 3.3.2). It is sometimes safer to leave a deep, central rust ring to allow time for the rust to migrate to the corneal surface, at which point it can be removed more easily.

3. Measure and diagram the size of the resultant corneal epithelial defect.

4. Treat as indicated for corneal abrasion (see 3.2, Corneal Abrasion).

NOTE: Erythromycin ointment should not be used for residual epithelial defects from corneal foreign bodies as it does not provide strong enough antibiotic coverage.

5. Alert the patient to return as soon as possible if there is any worsening of symptoms.

6. Counsel patient about protective eye wear.

Conjunctival Foreign Body

1. Remove foreign body under topical anesthesia.

 Multiple or loose superficial foreign bodies can often be removed with saline irrigation.

 A foreign body can be removed with a cotton-tipped applicator soaked in topical anesthetic or with fine forceps. For deeply embedded foreign bodies, consider pretreatment with a cotton-tipped applicator soaked in phenylephrine 2.5% to reduce conjunctival bleeding.

 Small, relatively inaccessible, buried subconjunctival foreign bodies may sometimes be left in the eye without harm unless they are infectious or proinflammatory. Occasionally, they will surface with time, at which point they may be removed more easily. Conjunctival excision is sometimes indicated.

 Check the pH if an associated chemical injury is suspected (e.g., alkali from fireworks). See 3.1, Chemical Burn.

2. Sweep the conjunctival fornices with a cotton-tipped applicator soaked with a topical anesthetic to remove any remaining pieces.

3. See 3.4, Conjunctival Laceration if there is a significant conjunctival laceration.

4. A topical antibiotic (e.g., bacitracin ointment, trimethoprim/polymyxin B drops, or fluoroquinolone drops q.i.d.) may be used.

5. Preservative-free artificial tears may be given as needed for irritation.

Follow Up

1. Corneal foreign body: Follow up as with corneal abrasion (see 3.2, Corneal Abrasion). If residual rust ring remains, reevaluate in 24 hours.

2. Conjunctival foreign body: Follow up as needed, or in 1 week if residual foreign bodies were left in the conjunctiva.

3.4 Conjunctival Laceration

Symptoms

Pain, redness, and/or foreign body sensation, with a history of trauma.

Signs

Fluorescein staining of the conjunctiva. The conjunctiva may be torn and rolled up on itself. Exposed white sclera may be noted. Conjunctival and subconjunctival hemorrhages are often present.

Workup

1. History: Determine the nature of the trauma and whether a ruptured globe or intraocular or intraorbital foreign body may be present. Evaluate the mechanism for possible foreign body involvement, including size, shape, and velocity of object.

2. Complete ocular examination, including careful exploration of the sclera (after topical anesthesia, e.g., proparacaine or viscous lidocaine) in the region of the conjunctival laceration to rule out scleral laceration or subconjunctival foreign body. The entire area of sclera under the conjunctival laceration must be inspected. Since the conjunctiva is mobile, inspect a wide area of the sclera under the laceration. Use a proparacaine-soaked, sterile cottontipped applicator to manipulate the conjunctiva. Irrigation with saline may be helpful in removing scattered debris. A Seidel test may be helpful (see Appendix 5, Seidel Test to Detect a Wound Leak). Cellulose surgical spears may be helpful for detecting vitreous through a wound. Dilated fundus examination, especially evaluating the area underlying the conjunctival injury, must be carefully performed with indirect ophthalmoscopy.

3. Consider a CT scan of the orbit without contrast (axial, coronal, and parasagittal views, 1-mm sections) to exclude an intraocular or intraorbital foreign body. B-scan ultrasound or UBM may be helpful.

4. Exploration of the site in the operating room under general anesthesia may be necessary when a ruptured globe is suspected, especially in children.

Treatment

In case of a ruptured globe or penetrating ocular injury, see 3.14, Ruptured Globe and Penetrating Ocular Injury. Otherwise,

1. Antibiotic ointment (e.g., erythromycin, bacitracin, or bacitracin/polymyxin B q.i.d.). A pressure patch may rarely be used for the first 24 hours for comfort.

2. Most lacerations will heal without surgical repair. Some large lacerations (>1 to 1.5 cm) may be sutured with 8-0 polyglactin 910 (e.g., Vicryl) or 6-0 plain gut. When suturing, take care not to bury folds of conjunctiva or incorporate Tenon capsule into the wound. Avoid suturing the plica semilunaris or caruncle to the conjunctiva.

Follow Up

If there is no concomitant ocular damage, patients with large conjunctival lacerations are reexamined within 1 week. Patients with small injuries are seen at longer intervals and instructed to return immediately if symptoms worsen.

3.5 Traumatic Iritis

Symptoms

Dull, aching, or throbbing pain, photophobia, tearing, occasionally floaters, and onset of symptoms usually within 1 to 3 days of trauma.

Signs

Critical. White blood cells (WBCs) and flare in the AC (seen under high-power magnification by focusing into the AC with a small, bright, tangential beam from the slit lamp).

Other. Pain in the traumatized eye when light enters either eye (consensual photophobia); lower (due to ciliary body shock/shutdown) or higher (due to inflammatory debris and/or trabeculitis) IOP than fellow eye; smaller, poorly dilating pupil or larger pupil (often due to iris sphincter tears) in the traumatized eye; perilimbal conjunctival injection; decreased vision.

Differential Diagnosis

 Nongranulomatous anterior uveitis: No history of trauma, or the degree of trauma is not consistent with the level of inflammation. See 12.1, Anterior Uveitis (Iritis/Iridocyclitis).

 Traumatic microhyphema or hyphema: Red blood cells (RBCs) in the AC. See 3.6, Hyphema and Microhyphema.

 Traumatic corneal abrasion: May have an accompanying sterile AC reaction. See 3.2, Corneal Abrasion.

 Traumatic retinal detachment: May produce an AC reaction or demonstrate pigment in the anterior vitreous. See 11.3, Retinal Detachment.

Workup

Complete ophthalmic examination, including IOP measurement and dilated fundus examination.

Treatment

Cycloplegic agent (e.g., cyclopentolate 1% or 2% b.i.d. to t.i.d.). May use a steroid drop (e.g., prednisolone acetate 0.125% to 1% q.i.d.). Avoid topical steroids if an epithelial defect is present.

Follow Up

1. Recheck in 5 to 7 days.

2. If resolved, discontinue the cycloplegic agent and taper steroid drops if using.

3. Around 1 month after trauma, perform gonioscopy to look for angle recession and indirect ophthalmoscopy with scleral depression to detect retinal breaks or detachment.

3.6 Hyphema and Microhyphema

TRAUMATIC HYPHEMA

Symptoms

Pain, blurred vision, and history of blunt or penetrating trauma.

Signs

(See Figure 3.6.1.)

FIGURE 3.6.1 Hyphema.

Clotted or unclotted blood in the AC, usually visible without a slit lamp. A total (100%) hyphema may be black or red. When black, it is called an “8-ball" or “blackball” hyphema, indicating deoxygenated blood; when red, the circulating blood cells may settle with time to become less than a 100% hyphema.

Workup

1. History: Mechanism (including force, velocity, type, and direction) of injury? Protective eyewear? Time of injury? Recent intraocular surgery? Time and extent of visual loss? Maximal visual compromise usually occurs at the time of injury; decreasing vision over time suggests a rebleed or continued bleed (which may cause an IOP rise). Use of anticoagulant medications (e.g., aspirin, NSAIDs, warfarin, or clopidogrel)? Personal or family history of sickle cell disease or trait? Coagulopathy symptoms (e.g., bloody nose blowing, bleeding gums with tooth brushing, easy bruising, bloody stool)?

2. Ocular examination: First rule out a ruptured globe (see 3.14, Ruptured Globe and Penetrating Ocular Injury). Evaluate for other traumatic injuries. Document the extent (e.g., measure hyphema height) and location of any clot and blood. Measure the IOP. Perform a dilated retinal evaluation without scleral depression. Consider gentle B-scan ultrasound if the fundus view is poor. Avoid gonioscopy unless intractable increased IOP develops, but if necessary, perform gently. If the view is poor, consider UBM to better evaluate the anterior segment and look for possible lens capsule rupture, IOFB, or other anterior-segment abnormalities.

3. Consider a CT scan of the orbits and brain (axial, coronal, and parasagittal views, 1-mm sections through the orbits) when indicated (e.g., suspected orbital fracture or IOFB, loss of consciousness).

4. Patients should be screened for sickle cell trait or disease (order Sickledex screen; if necessary, may check hemoglobin electrophoresis) as clinically appropriate.

Treatment

Many aspects remain controversial, including whether hospitalization and absolute bed rest are necessary, but an atraumatic upright environment is essential. Consider hospitalization for noncompliant patients, patients with bleeding diathesis or blood dyscrasia, other severe ocular or orbital injuries, and/or concomitant significant IOP elevation and sickle cell trait or disease. Additionally, consider hospitalization and aggressive treatment for children, especially those at risk for amblyopia (e.g., those younger than 7 to 10 years), when a thorough clinical examination is difficult, or when child abuse is suspected.

1. Confine either to bed rest with bathroom privileges or to limited activity. Elevate the head of the bed to allow blood to settle. Discourage strenuous activity, bending, or heavy lifting.

2. Place a rigid shield (metal or clear plastic) over the involved eye at all times. Do not patch because this prevents recognition of sudden visual change in the event of a rebleed.

3. Cycloplege the affected eye (e.g., cyclopentolate 1% or 2% b.i.d. to t.i.d., homatropine 5% b.i.d. to t.i.d., or atropine 1% daily to b.i.d.).

4. Avoid antiplatelet/anticoagulant medications (i.e., aspirincontaining products and NSAIDs) unless otherwise medically necessary. Do not abruptly stop daily aspirin regimen without consulting with prescribing physicians.

5. Mild analgesics only (e.g., acetaminophen). Avoid sedatives.

6. Use topical steroids (e.g., prednisolone acetate 1% q.i.d. to q1h) if any suggestion of iritis (e.g., photophobia, deep ache, ciliary flush), evidence of lens capsule rupture, any protein (e.g., fibrin), or definitive WBCs in AC. Taper steroids quickly as soon as signs and symptoms resolve to reduce the likelihood of steroid-induced glaucoma.

NOTE: No definitive evidence exists regarding steroid use in improving outcomes for hyphemas. Use must be balanced with the risks of topical steroids (increased infection potential, increased IOP, cataract). In children, particular caution must be used regarding topical steroids. Children may get rapid rises in IOP, and with prolonged use, there is a risk for cataract. As outlined above, in certain cases, steroids may be beneficial, but steroids should be prescribed in an individualized manner. Children must be monitored closely for increased IOP and should be tapered off steroids as soon as possible.

7. For increased IOP:

• Non-sickle cell disease or trait (>30 mm Hg):

 Start with a beta-blocker (e.g., timolol or levobunolol 0.5% b.i.d.).

 If IOP is still high, add topical alpha-agonist (e.g., apraclonidine 0.5% or brimonidine 0.1% or 0.2% t.i.d.) or topical carbonic anhydrase inhibitor (e.g., dorzolamide 2% or brinzolamide 1% t.i.d.). Avoid prostaglandin analogues and miotics (may increase inflammation). In children younger than 2 years, topical alpha-agonists are contraindicated.

NOTE: Increased IOP, especially soon after trauma, may be transient, secondary to acute mechanical plugging of the trabecular meshwork. Elevating the patient’s head may decrease IOP by causing RBCs to settle inferiorly and clot.

 If topical therapy fails, add acetazolamide (up to 500 mg p.o. q12h for adults, 20 mg/kg/d divided three times per day for children) or mannitol (1 to 2 g/kg i.v. over 45 minutes q24h). If mannitol is necessary to control the IOP, surgical evacuation may be imminent.

• Sickle cell disease or trait (>24 mm Hg):

 Start with a beta-blocker (e.g., timolol or levobunolol 0.5% b.i.d.).

 All other agents must be used with extreme caution: Topical dorzolamide and brinzolamide may reduce aqueous pH and induce increased sickling; topical alpha-agonists (e.g., brimonidine or apraclonidine) may affect iris vasculature; miotics and prostaglandins may promote inflammation.

 If possible, avoid systemic diuretics because they promote sickling by inducing systemic acidosis and volume contraction. If a carbonic anhydrase inhibitor is necessary, use methazolamide (50 or 100 mg p.o. b.i.d. to t.i.d.) instead of acetazolamide (controversial). If mannitol is necessary to control the IOP, surgical evacuation may be imminent.

• AC paracentesis may be considered if IOP cannot be safely lowered medically (see Appendix 13, Anterior Chamber Paracentesis). This procedure is typically a temporizing measure when the need for urgent surgical evacuation is anticipated.

8. If hospitalized, use antiemetics p.r.n. for severe nausea or vomiting (e.g., ondansetron 4 or 8 mg q4-8h p.r.n.; if ≤12 years of age, please refer to the appropriate dosing instructions). Indications for surgical evacuation of hyphema:

 Corneal stromal blood staining, especially in children.

 Significant visual deterioration.

 Hyphema that does not decrease to ≤50% by 8 days (to prevent peripheral anterior synechiae).

 IOP ≥60 mm Hg for ≥48 hours, despite maximal medical therapy (to prevent optic atrophy).

 IOP ≥25 mm Hg with total hyphema for ≥5 days (to prevent corneal stromal blood staining).

 IOP ≥24 mm Hg for ≥24 hours (or any transient increase in IOP ≥30 mm Hg) in sickle cell trait or disease patients.

 Consider early surgical intervention for children at risk for amblyopia.

NOTE: Previously, systemic aminocaproic acid was used in hospitalized patients to stabilize the clot and to prevent rebleeding. This therapy is rarely used nowadays. Evidence supporting the use of topical antifibrinolytic agents such as aminocaproic acid and tranexamic acid is inconclusive. Some studies suggest that topical antifibrinolytic agents may be useful in reducing the risk of rebleeding but might prolong resolution time. Additionally, aminocaproic acid has been reported to have several adverse side effects; the benefits and risks of antifibrinolytic therapy remain controversial.

Follow Up

1. The patient should be seen daily after initial trauma to check visual acuity, IOP, and for a slit lamp examination. Look for new bleeding (most commonly occurs within the first 5 to 10 days), increased IOP, corneal blood staining, and other intraocular injuries as the blood clears (e.g., iridodialysis; subluxated or dislocated lens, or cataract). Hemolysis, which may appear as bright red fluid, should be distinguished from a rebleed, which forms a new, bright red clot. Rebleeding occurs in 0.4% to 35% of patients, usually 2 to 7 days after trauma. If the IOP is increased, treat as described earlier. Time between visits may be increased once consistent improvement in clinical examination is documented.

2. The patient should be instructed to return immediately if a sudden increase in pain or decrease in vision is noted (which may be symptoms of a rebleed or increased IOP).

3. If a significant rebleed or an intractable IOP increase occurs, hospitalization or surgical evacuation of the blood may be considered.

4. After the initial close follow-up period, the patient may be maintained on a long-acting cycloplegic agent (e.g., atropine 1% daily to b.i.d.) depending on the severity of the condition. Topical steroids may be tapered as the blood, fibrin, and WBCs resolve.

5. Protective glasses or an eye shield should be worn during the day and an eye shield at night.

6. The patient must refrain from strenuous physical activities (including Valsalva maneuvers) for at least 1 week after the initial injury or rebleed. Normal activities may be resumed once the hyphema has resolved and the patient is out of the rebleed time frame.

7. Future outpatient follow up:

 If hospitalized, see 2 to 3 days after discharge. If not hospitalized, see several days to 1 week after initial daily follow-up period, depending on condition severity (amount of blood, potential for IOP increase, other ocular or orbital injuries).

 Follow up 4 weeks after trauma for gonioscopy and dilated fundus examination with scleral depression for all patients.

 Some experts suggest annual follow up because of the potential for development of angle-recession glaucoma.

 If any complications arise, more frequent follow up is required.

 If filtering surgery was performed, follow up and activity restrictions are based on the surgeon’s specific recommendations.

TRAUMATIC MICROHYPHEMA

Symptoms

See Hyphema above.

Signs

Suspended RBCs in the AC (no settled blood or clot), visible with a slit lamp. Sometimes there may be enough suspended RBCs to see a haziness of the AC (e.g., poor visualization of iris details) without a slit lamp; in these cases, the RBCs may eventually settle out as a frank hyphema.

Workup

See Hyphema above.

Treatment

1. Most microhyphemas can be treated on an outpatient basis.

2. See treatment for Hyphema above.

Follow Up

1. The patient should return on the third day after the initial trauma and again at 1 week. If the IOP is >25 mm Hg at presentation, the patient should be followed daily for 3 consecutive days for pressure monitoring and again at 1 week. Sickle cell patients with initial IOP of >24 mm Hg should also be followed daily for 3 consecutive days.

2. Otherwise, see follow up for Hyphema above.

NONTRAUMATIC (SPONTANEOUS) AND POSTSURGICAL HYPHEMA OR MICROHYPHEMA

Symptoms

May present with decreased vision or with transient visual loss (intermittent bleeding may cloud vision temporarily).

Etiology of Spontaneous Hyphema or Microhyphema

 Occult trauma: must be excluded; evaluate for child or elder abuse.

 Neovascularization of the iris or angle (e.g., from diabetes, old central retinal vascular occlusion, ocular ischemic syndrome, chronic uveitis).

 Blood dyscrasias and coagulopathies.

 Iris-intraocular lens chafing.

 Herpetic keratouveitis.

 Use of anticoagulants (e.g., ethanol, aspirin, warfarin).

 Other (e.g., Fuchs heterochromic iridocyclitis, iris microaneurysm, leukemia, iris or ciliary body melanoma, retinoblastoma, juvenile xanthogranuloma).

Workup

As for traumatic hyphemas, plus:

1. Gentle gonioscopy initially to evaluate for neovascularization or masses in the angle.

2. Consider the following studies:

 Prothrombin time (PT)/international normalized ratio (INR), partial thromboplastin time (PTT), complete blood count (CBC) with platelet count, bleeding time, and proteins C and S.

 UBM to evaluate for possible malpositioning of intraocular lens haptics, ciliary body masses, or other anterior-segment pathology.

 Fluorescein angiogram of iris.

Treatment

Cycloplegia (see Hyphema), limited activity, elevation of head of bed, and avoidance of medically unnecessary antiplatelet/anticoagulant medications (e.g., aspirin and NSAIDs). Recommend protective rigid metal or plastic shield if etiology is unclear. Monitor IOP. Postsurgical hyphemas and microhyphemas are usually self-limited and often require observation only, with close attention to IOP.

REFERENCE

Bansal S, Gunasekeran DV, Ang B, et al. Controversies in the pathophysiology and management of hyphema. Surv Ophthalmol. 2016;61(3):297-308.

3.7 Iridodialysis/Cyclodialysis

Definitions

Iridodialysis: Disinsertion of the iris from the scleral spur. Elevated IOP can result from trabecular meshwork damage and/or formation of peripheral anterior synechiae.

Cyclodialysis: Disinsertion of the ciliary body from the scleral spur. Increased uveoscleral outflow occurs initially resulting in hypotony. IOP elevation can later result from closure of a cyclodialysis cleft, leading to glaucoma.

Symptoms

Usually asymptomatic unless glaucoma or hypotony/hypotony maculopathy develop. Large iridodialyses may be associated with monocular diplopia, glare, and photophobia. Both are associated with blunt trauma or penetrating globe injuries. Typically, unilateral.

Signs

(See Figure 3.7.1.)

FIGURE 3.7.1 Iridodialysis.

Critical. Characteristic gonioscopic findings as described above.

Other. Decreased or elevated IOP, glaucomatous optic nerve changes (see 9.1, Primary Open Angle Glaucoma), angle recession, and hypotony syndrome (see 13.11, Hypotony Syndrome). Other signs of trauma include hyphema, cataract, and pupillary irregularities.

Differential Diagnosis

In setting of glaucoma, see 9.1, Primary Open Angle Glaucoma.

Workup

See 9.6, Angle-Recession Glaucoma.

Treatment

1. Sunglasses, contact lenses with an artificial pupil, or surgical correction if large iridodialysis and patient symptomatic.

2. If glaucoma develops, treatment is similar to that for primary open angle glaucoma (see 9.1, Primary Open Angle Glaucoma). Aqueous suppressants are usually first-line therapy. Miotics are generally avoided because they may reopen cyclodialysis clefts, causing hypotony. Strong mydriatics may close clefts, resulting in pressure spikes. Often these spikes are transient and easily controlled with topical therapy, as the meshwork resumes aqueous filtration after several hours.

3. If hypotony syndrome develops due to cyclodialysis clefts, first- line treatment is usually atropine b.i.d. to reapproximate the ciliary body to the sclera and steroids to decrease inflammation. Further surgical treatment is described in Section 13.11, Hypotony Syndrome.

Follow Up

1. See 9.1, Primary Open Angle Glaucoma.

2. Carefully monitor both eyes due to the high incidence of delayed open-angle and steroid-response glaucoma in the traumatized eye and an approximately 50% risk of open-angle glaucoma in the uninvolved eye.

REFERENCES

Gonzalez-Martin-Moro J, Contreras-Martin I, Munoz-Negrete FJ, et al. Cyclodialysis: an update. Int Ophthalmol. 2017;37:441-457.

Tesluk GC, Spaeth GL. The occurrence of primary open-angle glaucoma in the fellow eye of patients with unilateral angle-cleavage glaucoma. Ophthalmology. 1985;92:904-911.

3.8 Eyelid Laceration

Symptoms

Periorbital pain, tearing, bleeding, and history of facial trauma.

Signs

(See Figure 3.8.1.)

FIGURE 3.8.1 Marginal eyelid laceration.

Partial- or full-thickness eyelid defect involving the skin and subcutaneous tissues. Superficial lacerations/abrasions may mask a deep laceration, foreign body, or penetrating/perforating injury to the lacrimal drainage system (e.g., punctum, canaliculus, common canaliculus, lacrimal sac), globe, orbit, or cranial vault.

Workup

FIGURE 3.8.2 Canalicular laceration.

FIGURE 3.8.3 Canalicular laceration showing exposed tip after probing the punctum.

1. History: Determine the mechanism and timing of injury: bite, foreign body potential, etc.

2. Complete ocular evaluation, including bilateral dilated fundus examination. Ensure there is no injury to the globe, orbital soft tissue (including the optic nerve), or intracranial compartment before attempting eyelid repair.

3. Carefully evert the eyelids and use toothed forceps or cottontipped applicators to gently pull open one edge of the wound to determine the depth of penetration. (If foreign body suspected, get imaging described below before extensive wound exploration.)

4. CT scan of brain, orbits, and midface (axial, coronal, and parasagittal views, 1- to 2-mm sections) should be obtained with any history suggestive of penetrating injury or severe blunt trauma to rule out fracture, retained foreign body, ruptured globe, or intracranial injury. If there is any suspicion of deeper injury, obtain imaging before eyelid laceration repair. Loss of consciousness mandates a CT of the brain. Depending on the mechanism of injury, the cervical spine may need to be cleared.

5. If laceration is nasal to the punctum, even if not obviously through the canalicular system, punctal dilation and probing with irrigation of the canalicular system should be considered to exclude canalicular involvement (see Figures 3.8.2 and 3.8.3; Appendix 7, Technique for Diagnostic Probing and Irrigation of the Lacrimal System). High suspicion should be maintained for unnoticed canalicular lacerations in the pediatric population, particularly with dog bite injuries.

6. Be suspicious in glancing blunt trauma to the lateral cheek (zygoma). A lateral glancing mechanism may abruptly stretch the medial canthal anatomy, resulting in avulsion of the medial canthal tendon with concomitant canalicular laceration. Canalicular lacerations are often missed with this mechanism because clinical attention is directed laterally to the zygoma and the medial canthal soft tissues often reappose into a normal position, camouflaging the extent of the injury.

 NOTE: Dogbites are notorious for causing canalicular lacerations and predominantly occur in young children. Probing should be performed in all such cases, even with lacerations that appear to be superficial. Uncooperative patients should undergo conscious sedation or an examination under anesthesia to thoroughly examine the eyelids, lacrimal drainage system, and globes.

Treatment

1. Consider tetanus prophylaxis (see Appendix 2, Tetanus Prophylaxis, for indications).

2. Consider systemic antibiotics for 7 to 10 days if contamination or foreign body is suspected (e.g., amoxicillin/clavulanate [500/125 mg p.o. b.i.d. to t.i.d. or 875/125 mg p.o. b.i.d.], doxycycline [100 mg p.o. b.i.d.], trimethoprim/sulfamethoxazole [80/400 mg or 160/800 mg p.o. daily to b.i.d.], or cephalexin [250 to 500 mg p.o. q.i.d.] [adults]; 25 to 50 mg/kg/d divided into four doses [children]). For human or animal bites, consider penicillin V. If indicated, consider rabies prophylaxis.

NOTE: In most states, animal bites must be reported to the local Department of Health.

3. Repair eyelid laceration.

3A.Determine appropriate setting for repair. Indications for operating room repair include the following:

 Association with ocular or deep adnexal trauma that requires surgery (e.g., ruptured globe or intraorbital foreign body).

 Involvement of the lacrimal drainage apparatus except when uncomplicated and close to the punctum in a cooperative patient. Note that canalicular laceration repair is not an ophthalmic emergency and can be delayed up to 4 days with no negative effects.

 Involvement of the levator aponeurosis of the upper eyelid or the superior rectus muscle.

 Visible orbital fat in an eyelid laceration, indicating penetration of the orbital septum. All such patients require CT imaging and careful documentation of levator and extraocular muscle (EOM) function. Exploration of deeper tissue planes may be necessary.

 Medial canthal tendon avulsion (exhibits displacement, excessive rounding, or abnormal laxity of the medial canthus).

 Extensive tissue loss (especially more than one-third of the eyelid) or severe distortion of anatomy.

3B.Procedure for eyelid laceration repair at the bedside:

NOTE: Eye protection should be worn by all healthcare providers.

 Place a drop of topical anesthetic in each eye. Place a protective scleral shell over the affected eye, and cover the uninvolved eye with a moistened, folded gauze sponge. Clean the area of injury and surrounding skin with copious irrigation and 10% povidone-iodine solution (avoid povidone soap because this irritates the cornea). Isolate the area with surgical drapes.

NOTE: Lacerations from human or animal bites or those with significant contamination risk may require minimal debridement of necrotic tissue. Because of the excellent blood supply to the eyelids, primary repair is usually performed. Alternatively, contaminated wounds may be left open for delayed repair. All attempts should be made to preserve the eyelid skin. However, skin grafting should be considered if significant portions of the skin are necrotic or lost in the initial injury. For primary repair, proceed to the subsequent steps.

 Administer local subcutaneous anesthetic (e.g., 2% lidocaine with epinephrine). Since direct injection of local anesthetic causes tissue distortion and bleeding, use the minimal amount of anesthetic needed or perform field blocks (e.g., supraorbital, infraorbital, and/or anterior ethmoidal nerve blocks).

 If foreign bodies are encountered unexpectedly and appear to penetrate the globe or orbital tissues, do NOT remove. Involvement of the orbit, cavernous sinus, or brain requires an extensive preoperative evaluation and a multidisciplinary approach (e.g., otolaryngology or neurosurgery) and ancillary testing (e.g., angiography).

 Close the laceration as follows.

NONMARGINAL EYELID LACERATION

See bullets above. Then close the skin with interrupted 6-0 absorbable (e.g., plain gut, chromic gut) sutures. Some surgeons prefer using monofilament nonabsorbable material (e.g., nylon, polypropylene) to potentially decrease scarring. Nonabsorbable sutures should be avoided in patients who may not follow up compliantly. Avoid deep sutures within the confines of the orbital rim and never suture the orbital septum. Skin and dermis thickens markedly beyond the orbital rim; in these areas, a layered closure may be indicated to minimize skin tension.

MARGINAL EYELID LACERATION

Key Points

FIGURE 3.8.4 Marginal eyelid laceration repair, traditional method. A: Reapproximate the gray line with a 6-0 silk suture. B: The most important step is to realign the tarsal edges with multiple interrupted 5-0 or 6-0 absorbable (e.g., Vicryl) sutures. Take partial-thickness bites. C: Failure to realign the tarsus will compromise the integrity of the eyelid, resulting in splaying and notching. D: Tie the tarsal and gray line sutures. E: Place another marginal 6-0 silk suture. F: Suture the skin with interrupted 6-0 plain gut, securing the tails of the marginal sutures.

• There are many ways to approach marginal eyelid laceration repair, and we will describe a traditional method. The most important step is reapproximation of the tarsus along its vertical axis to allow for proper eyelid alignment and healing. Reapproximation of the tarsus at the margin alone will not provide structural integrity to the eyelid; the injured tarsus will splay apart, resulting in eyelid notching (see Figure 3.8.4C).

NOTE: If patient reliability is questionable, use absorbable 6-0 polyglactin sutures (e.g., Vicryl) for every step.

 Be careful to avoid deeper, buried subcutaneous sutures that can incorporate the orbital septum, resulting in eyelid tethering. In general, deep sutures should be avoided in the zone between the tarsus and orbital rim (the vertical lengths of the upper and lower tarsi are approximately 10 mm and 5 mm, respectively).

 Deep tarsal sutures should be lamellar (partial thickness), especially in the upper eyelid, to avoid penetration through the underlying conjunctiva and subsequent corneal irritation/injury.

 If unsure about patient reliability or in patients who will not cooperate for suture removal (e.g., young children, patients with advanced dementia, etc.), use absorbable 6-0 polyglactin suture (e.g., Vicryl) in the eyelid margin instead of nonabsorbable material (e.g., silk).

Procedure Steps

(See Figure 3.8.4.)

a. Place a 6-0 silk suture from gray line to gray line, entering and exiting the gray line 2 mm from the laceration edge. (As already noted, in difficult or unreliable patients, use absorbable suture material only.) Put the suture on traction with a hemostat to ensure good reapproximation of the splayed tarsus and gray line. Leave the suture untied.

NOTE: This marginal suture provides no structural integrity to the eyelid; its main function is to align the eyelid margin anatomy to ensure a good cosmetic repair.

b. Realign the tarsal edges with interrupted sutures placed through an anterior approach (e.g., 5-0 or 6-0 Vicryl on a spatulated needle). This is the most important structural step in marginal laceration closure. In the upper eyelid, three sutures can usually be placed. In the lower eyelid, two sutures are typically the maximum. A single tarsal suture, in addition to the marginal suture, may be adequate for appropriate tarsal realignment depending on the height of the laceration. Failure to reapproximate the tarsus along its entire vertical length will result in eyelid splaying and notching.

c. Tie down and trim the tarsal sutures. Tie down the marginal silk suture leaving long tails.

d. Place and tie another 6-0 silk marginal suture either anterior or posterior to the gray-line suture, again leaving long tails. The posterior suture is often unnecessary, and its absence may decrease the risk of postoperative corneal abrasion. When placing marginal sutures, attempt to realign the normal eyelid anatomy (lash line, meibomian glands, gray line).

e. Use interrupted 6-0 plain gut sutures to close the skin along the length of the laceration. Incorporate the tails of all eyelid margin sutures into the skin suture closest to the eyelid margin to keep tails away from the corneal surface.

f. Final steps:

 Remove the protective scleral shell.

 Apply antibiotic ointment (e.g., bacitracin or erythromycin) to the wound t.i.d.

• Dress the wound and consider oral antibiotics if needed. For lacerations beyond the orbital rim where deeper dermis is encountered, one can apply a topical adhesive (benzoin or Mastisol) and Steri-Strips perpendicular to the axis of the laceration to reinforce the sutures and decrease skin tension. Antibiotic ointment is applied once the strips have been placed.

Follow Up

If nonabsorbable sutures are used (e.g., silk), eyelid margin sutures should be left in place for 5 to 10 days, and other superficial sutures for 4 to 7 days. The integrity of an eyelid margin repair is provided by the longer lasting tarsal sutures. Therefore, the eyelid margin sutures can be removed as soon as 5 days postoperatively. If a small notch is present, it can be followed over the ensuing 3 to 6 months to allow for scar maturation. A small eyelid notch will often soften and disappear on its own.

3.9 Orbital Blowout Fracture

Symptoms

Pain with eye movement; local tenderness; eyelid edema; binocular diplopia; crepitus (particularly after nose blowing); and numbness of the cheek, upper lip, and/or teeth. Tearing may be a symptom of nasolacrimal duct obstruction or injury seen with medial buttress, Le Fort II, or nasoethmoidal complex fractures, but this is typically a late complaint. Acute tearing is usually due to ocular irritation (e.g., chemosis, corneal abrasion, iritis).

Signs

Critical. Restricted eye movement (especially in upward gaze, lateral gaze, or both), subcutaneous or conjunctival emphysema, hypesthesia in the distribution of the infraorbital nerve (ipsilateral cheek and upper lip), point tenderness, enophthalmos (may initially be masked by orbital edema and hemorrhage), and hypoglobus.

Other. Epistaxis, eyelid edema, and ecchymosis. Superior rim and orbital roof fractures may manifest hypesthesia in the distribution of the supratrochlear or supraorbital nerve (ipsilateral forehead), ptosis, and step-off deformity along the anterior table of the frontal sinuses (superior orbital rim and glabella). Trismus, malar flattening, and a palpable step-off deformity of the inferior orbital rim are characteristic of tripod (zygomatic complex) fractures. Optic neuropathy may be present secondary to posterior indirect traumatic optic neuropathy (PI-TON) or from a direct mechanism (orbital compartment syndrome [OCS] secondary to retrobulbar hemorrhage, foreign body, etc.; see below).

Differential Diagnosis of Muscle Entrapment in Orbital Fracture

 Orbital edema and hemorrhage with or without a blowout fracture: May have limitation of ocular movement, periorbital swelling, and ecchymosis, but these will markedly improve or completely resolve over 7 to 10 days.

 Cranial nerve palsy: Limitation of ocular movement, but no restriction on forced duction testing. Will have abnormal results on active force generation testing. In cases of suspected traumatic cranial neuropathy, significant skull base and intracranial injury have occurred and CT imaging should be obtained.

 Laceration or direct contusion of EOMs: Often the site of penetrating injury is missed, especially if it occurs in the conjunctival cul-de-sacs. Look carefully for evidence of conjunctival laceration or orbital fat prolapse. Complete EOM laceration usually results in a large angle ocular deviation away from the injured muscle with no ocular movement toward the muscle. CT is often helpful in distinguishing EOM contusion from EOM laceration. On occasion, exploration of the EOM may be necessary under anesthesia.

Workup

FIGURE 3.9.1 Eyelid retraction with Desmarres retractors or clean bent paperclips.

1. Complete ophthalmic examination, including visual acuity, motility, IOP, and globe displacement. Check pupils and color vision to rule out TON (see 3.11, Traumatic Optic Neuropathy). Compare sensation of the affected cheek with that on the contralateral side; palpate the eyelids for crepitus (subcutaneous emphysema); palpate the orbital rim for step-off deformities. Evaluate the globe carefully for an apparent or occult rupture, hyphema or microhyphema, traumatic iritis, and retinal or choroidal damage. A full, dilated examination may be difficult in uncooperative patients with periocular edema but is extremely important in the management of orbital fractures. If eyelid and periocular edema limit the view, special techniques may be necessary (e.g., use of Desmarres eyelid retractors or clean bent paperclips [see Figure 3.9.1], lateral cantholysis, examination under general anesthesia).

FIGURE 3.9.2 Computed tomography (CT) of orbital blowout fracture.

FIGURE 3.9.3 Coronal and sagittal cuts of a white-eyed blowout fracture (WEBOF) in a patient with an entrapped inferior rectus. White arrow, entrapped orbital soft tissue; red arrows, orbital floor fracture.

NOTE: It is of paramount importance to rule out intraocular and optic nerve injury as quickly as possible in ALL patients presenting with suspected orbital fracture.

NOTE: Pediatric patients are particularly at risk for a unique type of blowout injury: the “trapdoor” fracture. Because pediatric bones lack complete calcification, they tend to “greenstick” rather than completely fracture. This results in an initial fracture, herniation of orbital soft tissue (including EOM) through the fracture site, and rapid snapping back of the malleable bone akin to a trapdoor on a spring. Because of the tight reapposition of the fracture edges, the soft tissue trapped within the fracture becomes ischemic. Children with this type of fracture often have a remarkably benign external periocular appearance but significant EOM restriction (usually vertical) on examination; this constellation of findings has been dubbed the “white-eyed blowout fracture” (WEBOF). Children may present with a vague history, allow only a limited ocular examination, and be misdiagnosed as having an intracranial injury (e.g., concussion) leading to delay in management of WEBOF. Be aware of the oculocardiac reflex (nausea or vomiting, bradycardia, syncope, dehydration) that can accompany entrapment. Even in cases where correct orbital imaging is performed, CT evidence of an orbital fracture may be minimal and routinely missed. Careful examination of coronal and parasagittal views is critical in such cases.

In typical (i.e., non-WEBOF) orbital fractures, forced duction testing or testing of the doll’s eye reflex may be performed if limitation of eye movement persists beyond 1 week and restriction is suspected. In the early phase, it is often difficult to distinguish soft tissue edema or contusion from soft tissue entrapment in the fracture. See Appendix 6, Forced Duction Test and Active Force Generation Test.

2. CT of the orbit and midface (axial, coronal, and parasagittal views, 1- to 1.5-mm sections, without contrast) is obtained in all cases of suspected orbital fractures. Bone windows are especially helpful in fracture evaluation (see Figures 3.9.2 and 3.9.3), including the narrow, oft-missed WEBOF. Inclusion of the midfacial skeleton is mandatory to rule out zygomatic complex or other midfacial fractures. If there is any history of loss of consciousness, brain imaging is recommended.

NOTE: In the absence of visual symptoms (subjective change in vision, diplopia, periocular pain, photophobia, floaters or flashes), patients with orbital fractures are unlikely to have an ophthalmic condition requiring intervention within 24 hours. However, all patients with orbital fractures should undergo a complete ophthalmic examination within 48 hours of injury. Any patient complaining of blurred vision, severe pain, or other significant visual symptoms should undergo more urgent ophthalmic evaluation.

Treatment

1. Consider broad-spectrum oral antibiotics (e.g., amoxicillin/clavulanate [500/125 mg p.o. b.i.d. to t.i.d. or 875/125 mg p.o. b.i.d.], doxycycline [100 mg p.o. daily to b.i.d.], trimethoprim/sulfamethoxazole [80/400 mg or 160/800 mg p.o. daily to b.i.d.], or cephalexin [250 to 500 mg p.o. q.i.d.] [adults]) for 7 to 10 days. Antibiotics may be considered if the patient has a history of chronic sinusitis or diabetes or is otherwise immunocompromised. This recommendation is based on limited, anecdotal evidence. In all other patients, the decision about antibiotic use is left to the treating physician. Prophylactic antibiotics should not be considered mandatory in patients with orbital fractures.

2. Instruct the patient to avoid nose blowing. Forced air into the orbit can lead to OCS and optic neuropathy.

3. Nasal decongestants (e.g., oxymetazoline nasal spray b.i.d.) for 3 days. Use is limited to 3 days to minimize rebound nasal congestion.

4. Apply ice packs to the eyelids for 20 minutes every 1 to 2 hours for the first 24 to 48 hours and attempt a 30-degree inclination when at rest.

5. Consider oral corticosteroids (e.g., methylprednisolone dose pack) if extensive swelling limits examination of ocular motility and globe position. Some experts advise the use of oral antibiotics if corticosteroid therapy is considered, but there are no data to support the effectiveness of such a regimen. Avoid corticosteroids in patients with concomitant traumatic brain injury (TBI).

6. Neurosurgical consultation is recommended for all fractures involving the orbital roof, frontal sinus, or cribriform plate and for all fractures associated with intracranial hemorrhage. Otolaryngology or oral maxillofacial surgery consultation may be useful for frontal sinus, midfacial, and mandibular fractures.

7. Consider surgical repair based on the following criteria.

NOTE: Orbital fracture repair should be deferred or delayed if there is any evidence of full-thickness globe injury or penetrating trauma. Presence of hyphema or microhyphema typically delays orbital fracture repair for 10 to 14 days.

Immediate Repair (Within 24 to 48 hours)

If there is clinical evidence of muscle entrapment with nonresolving bradycardia, heart block, nausea, vomiting, or syncope (most often encountered in children with WEBOF). Patients with muscle entrapment require urgent orbital exploration to release any incarcerated muscle to decrease the chance of permanent restrictive strabismus from muscle ischemia and fibrosis, as well as to alleviate systemic symptoms from the oculocardiac reflex.

Repair in 1 to 2 Weeks

 Persistent, symptomatic diplopia in primary or downgaze that has not improved over 1 to 2 weeks. CT may show muscle distortion or herniation around fractures. Forced ductions may be useful in identifying bony restriction. Note that diplopia may take more than two weeks to improve or resolve. Some surgeons will wait 6 to 8 weeks before offering surgical repair for persistent diplopia.

 Large orbital floor fractures (>50%) or large combined medial wall and orbital floor fractures that are likely to cause cosmetically unacceptable globe dystopia (enophthalmos and/or hypoglobus) over time. Globe dystopia at initial presentation is indicative of a large fracture. It is also reasonable to wait several months to see if enophthalmos develops before offering repair. There is no clear evidence that early repair is more effective in preventing or reversing globe malposition compared to delayed repair. However, many surgeons prefer early repair simply because dissection planes and abnormal (fractured) bony anatomy are more easily discernable before posttraumatic fibrosis sets in. It may be prudent to avoid early surgery for prevention of possible globe malposition in older patients, patients with significant medical comorbidities, or patients on anticoagulation therapy for significant cardiovascular conditions.

 Complex trauma involving the orbital rim or displacement of the lateral wall and/or the zygomatic arch. Complex fractures of the midface (zygomatic complex, Le Fort II) or skull base (Le Fort III).

Nasoethmoidal complex fractures. Superior or superomedial orbital rim fractures involving the frontal sinuses.

Delayed Repair

• Old fractures that have resulted in enophthalmos or hypoglobus can be repaired at any later date.

 NOTE: The role of anticoagulation in postoperative or posttrauma patients is debatable. Anecdotal reports have described orbital hemorrhage in patients with orbital and midfacial fractures who were anticoagulated for prophylaxis against deep vein thrombosis (DVT). On the other hand, multiple large studies have also demonstrated an increased risk of DVT and pulmonary embolism (PE) in postoperative patients who are obtunded or cannot ambulate. At the very least, all inpatients with orbital fractures awaiting surgery and all postoperative orbital fracture patients should be placed on intermittent pneumatic compression (IPC) therapy and encouraged to ambulate. In patients at high risk for DVT, including those who are obtunded from concomitant intracranial injury, a detailed discussion with the primary care team regarding anticoagulation should be documented, and the risks for and against such therapy should be discussed in detail with the patient and family.

Follow Up

Patients should be seen at 1 and 2 weeks after trauma to be evaluated for persistent diplopia and/or enophthalmos after the acute orbital edema has resolved. If sinusitis symptoms develop or were present prior to the injury, the patient should be seen within a few days of the injury. Patients should also be monitored for development of associated ocular injuries as indicated (e.g., orbital cellulitis, anglerecession glaucoma, retinal detachment). Gonioscopy and dilated fundus examination with scleral depression is performed about 4 weeks after trauma if a hyphema or microhyphema was present. Warning symptoms of retinal detachment and orbital cellulitis are explained to the patient.

3.10 Traumatic Retrobulbar Hemorrhage (Orbital Hemorrhage)

Symptoms

Pain, decreased vision, inability to open the eyelids due to severe swelling, recent history of trauma or surgery to the eyelids or orbit, and history of anticoagulation. Because the orbit is a bony compartment with firm anterior soft tissue tethering by the orbital septum, any process (blood, pus, air) that rapidly fills the orbit results in a compartment syndrome. As pressure builds within the orbit, ischemia to the optic nerve, globe, and retina occur, potentially resulting in devastating, permanent visual loss. OCS is an ophthalmic emergency.

 NOTE: Most iatrogenic postoperative orbital hemorrhages evolve within the first 6 hours following surgery.

Signs

(See Figure 3.10.1.)

FIGURE 3.10.1 Retrobulbar hemorrhage.

Critical. Proptosis with resistance to retropulsion, tense (“rock hard”) eyelids that are difficult to open, vision loss, afferent pupillary defect, dyschromatopsia, and increased IOP.

Other. Eyelid ecchymosis, diffuse subconjunctival hemorrhage, chemosis, congested conjunctival vessels, evidence of disc swelling from compressive optic neuropathy or retinal vascular occlusion, and limited extraocular motility in any or all fields of gaze.

Differential Diagnosis

 Orbital cellulitis: Fever, proptosis, chemosis, limitation, or pain with eye movement; also may follow trauma, but usually not as acutely. A rapidly expanding orbital abscess may result in OCS, and in such cases, the acute management is the same as that for orbital hemorrhage. See 7.3.1, Orbital Cellulitis.

 Severe orbital emphysema ("tension pneumo-orbit”): Tight orbit, tight eyelids, crepitus, and decreased extraocular motility; may follow orbital fracture with or without nose blowing. See 3.9, Orbital Blowout Fracture.

 Orbital fracture: Limited extraocular motility, enophthalmos, or proptosis may be present. See 3.9, Orbital Blowout Fracture.

 Ruptured globe: Subconjunctival edema and hemorrhage may mask a ruptured globe. See 3.14, Ruptured Globe and Penetrating Ocular Injury.

 High-flow (direct) carotid-cavernous fistula: May follow trauma either acutely or subacutely; most are spontaneous and nontraumatic. Pulsatile exophthalmos, ocular/brow bruit, corkscrew arterialized conjunctival vessels, chemosis, and increased IOP may be seen. Usually unilateral, although bilateral signs from a unilateral fistula may be seen occasionally. See 10.10, Cavernous Sinus and Associated Syndromes (Multiple Ocular Motor Nerve Palsies).

 Varix: Increased proptosis with Valsalva maneuver. Not usually seen acutely after trauma, and in the vast majority of orbital varices, there is no history of trauma or surgery.

 Lymphangioma: Usually in younger patients. May have acute proptosis, ecchymosis, and external ophthalmoplegia after minimal trauma or upper respiratory tract infection. MRI is usually diagnostic.

 Spontaneous retrobulbar hemorrhage: Signs and symptoms are identical to those of traumatic or postoperative hemorrhage. May occur in patients who are chronically anticoagulated or with an underlying coagulopathy from other systemic disease (e.g., hemophilia). Occasionally reported in pregnant women, especially during labor. Typically seen as a subperiosteal hematoma along the orbital roof and may be misdiagnosed as an orbital neoplasm. MRI is helpful in identifying blood-breakdown products (see 14.3, magnetic resonance imaging).

Workup

1. Complete ophthalmic examination; check specifically for an afferent pupillary defect, loss of color vision, the degree of tightness of the eyelids, resistance to retropulsion, increased IOP, pulsations of the central retinal artery (often precedes artery occlusion), choroidal folds (sign of globe distortion from severe optic nerve stretching), and optic nerve edema. Note that visual function may span from normal to no light perception.

2. CT scan of the orbit (axial, coronal, and parasagittal views). When vision and/or optic nerve function are threatened, CT should always be delayed until definitive treatment with canthotomy/cantholysis. CT rarely shows a discreet hematoma. Typically, retrobulbar hemorrhage manifests as a diffuse, increased reticular pattern of the intraconal orbital fat. The so- called teardrop or tenting sign may be seen: the optic nerve is at maximum stretch and distorts (tents) the back of the globe into a teardrop shape. This is an ominous radiologic sign, especially if the posterior scleral angle is <130 degrees. The presence of an orbital fracture may help to decompress the orbit and decrease, but not rule out, the possibility of OCS. It is important to remember that patients can still develop OCS and optic neuropathy even with large orbital fractures, as blood may simply fill the adjacent paranasal sinus and then cause an OCS.

NOTE: Retrobulbar hemorrhage with OCS is a clinical diagnosis and does not require imaging. A delay while CT is being obtained may cause further visual compromise. Imaging can be obtained once the OCS has been decompressed and visual function stabilized.

Treatment

The key to effective management of clinically significant retrobulbar hemorrhage with OCS is timely and aggressive soft tissue decompression. The initial goal is to decrease the compression on critical soft tissues, mainly the optic nerve. All patients should be treated utilizing the same guidelines, even if the hemorrhage is thought to have occurred hours or days ago, since it is often impossible to know at what point along the clinical timeline optic neuropathy manifested.

FIGURE 3.10.2 Lateral canthotomy and cantholysis. A: Lateral canthotomy. B: Grasp the lateral lower eyelid with toothed forceps. C: Pull the eyelid anteriorly. Point the scissors toward the patient’s nose, strum the lateral canthal tendon, and cut.

1. If optic neuropathy is present, immediately release orbital pressure with lateral canthotomy and inferior cantholysis (see Figure 3.10.2 below). The procedure can be performed in an office or ER setting with basic instrumentation and local anesthetic injection if possible. Conscious sedation can be used in the ER setting if this does not delay treatment, but is usually unnecessary.

2. If there are no orbital signs and no evidence of ocular ischemia or compressive optic neuropathy but the IOP is increased (e.g., >35 mm Hg in a patient with a normal optic nerve, or >20 mm Hg in a patient with glaucoma who normally has a lower IOP), the patient is treated in a more stepwise fashion in an effort to reduce the IOP (see below and 9.1, Primary Open Angle Glaucoma).

Canthotomy and Cantholysis

(See Figure 3.10.2.)

The goal of canthotomy and cantholysis is to perform an adequate soft tissue decompression of the orbit by disinserting the lower eyelid from its periosteal attachments. A nonperfused retina infarcts irreversibly in approximately 90 minutes, and a delay of definitive treatment of longer duration may lead to retinal nerve fiber death and permanent vision loss.

NOTE: A canthotomy alone is inadequate treatment. A cantholysis must be performed.

a. Consider subdermal injection of lidocaine 2% with epinephrine (inject away from the eye). Because of the eyelid edema and acidotic local environment, local anesthesia may not be effective. A field block may be used. The patient should be warned that the procedure may be painful, but fortunately in most cases, canthotomy and cantholysis can be performed quickly.

b. Consider placing a hemostat horizontally at the lateral canthus and clamp for 1 minute to compress the tissue and reduce bleeding (an optional step that should not be performed without good local anesthesia).

c. Only two instruments are needed for canthotomy and cantholysis: A pair of blunt-tipped scissors (e.g., Westcott or Stevens) and forceps with heavy teeth (e.g., Bishop Harmon or Adson). Avoid sharp-tipped scissors to minimize the chance of globe injury. Delicate forceps (e.g., 0.12-mm Castroviejo) will not provide enough traction to effectively disinsert the eyelid and should not be used.

d. Perform the canthotomy. Place the scissors across the lateral canthus and incise the canthus for about 1-cm full thickness (from conjunctiva to skin). Forceps are not needed for this step. This step simply gains access to the inferior crux of the lateral canthal tendon. It provides little soft tissue decompression.

e. Perform inferior cantholysis. With the toothed forceps, grasp the lower eyelid at the inner edge of the incised canthus. With the patient supine, traction should be directed upward, toward the ceiling. Place the scissors in an open position just beneath the skin, with the tips pointing toward the tip of the nose, and begin to cut. Some advocate “strumming” of the lateral canthal tendon, but this is not essential and sometimes difficult to assess because of tissue edema. As the canthal tendon is released, the eyelid should come completely away from the globe.

NOTE: The cantholysis is critical to decompress the orbit and is done exclusively by feel. Do not visually search for a specific tendon or anatomic landmark.

f. There are several clues to a successful cantholysis. The eyelid should release completely away from the globe. Once the forceps are released, the lateral portion of the eyelid margin should move medially, usually to the lateral aspect of the limbus of the globe. If any eyelid margin still remains in its normal position lateral to the temporal limbus, the cantholysis is incomplete: keep cutting!

g. The incision will bleed; however, cautery is usually unnecessary. Pressure over the bone of the lateral orbital rim (but not on the globe and orbit) for several minutes usually results in good control. However, with the widespread use of anticoagulant and antiplatelet medications (e.g., warfarin, aspirin, clopidogrel) as well as increasing prescription of irreversible anticoagulants (e.g., rivaroxaban, dabigatran, etc.), excessive bleeding can be encountered. In these cases, manual pressure is often inadequate and applying hemostatic aids (e.g., biologic agents such as thrombin and fibrinogen or physical agents such as gelatin, collagen, cellulose) may be necessary. Cautery is effective if available.

h. The results of a successful cantholysis are usually evident within the first 15 minutes. IOP should decrease, and the retina should reperfuse. Cadaver studies have shown a reliable correlation between IOP and intraorbital pressure. A significant decrease in IOP after cantholysis is indicative of a successful orbital soft tissue decompression. Depending on the timing of the cantholysis in relation to the hemorrhage, vision may dramatically improve. Superior cantholysis is usually unnecessary: cadaver studies have not shown a dramatic decrease in intraorbital pressure with superior cantholysis. In addition, superior cantholysis may result in lacrimal gland incision, which can bleed profusely. By far the most common reason for persistent signs of OCS following inferior cantholysis is inadequate cantholysis. Make sure the cantholysis is performed effectively.

3. Close observation is indicated in all cases of retrobulbar hemorrhage, including those that have not yet affected visual function. It is therefore dangerous to assume that a patient with recent injury/surgery, retrobulbar hemorrhage, and normal optic nerve function is stable enough for discharge. In such cases, it is best to follow the patient for 4 to 6 hours with serial examinations in the ER or hospital. If a patient presents with no evidence of OCS 6 or more hours after the initial insult, it is reasonable to discharge the patient with specific instructions (see follow up). For patients presenting with OCS, see NOTE below.

 NOTE: The efficacy of inferior cantholysis for OCS is based on the assumption that at the time of the procedure, all active orbital bleeding has tamponaded; this is indeed the case in the majority of retrobulbar hemorrhages. However, if active bleeding persists, the OCS will recur as the blood fills the decompressed orbit. For this reason, it is prudent to monitor patients who present with OCS and optic neuropathy for 12 to 24 hours following cantholysis.

4. Anticoagulants (e.g., warfarin) and antiplatelet agents (e.g., aspirin) are often discontinued, if possible, to prevent rebleeding. This decision must be made in conjunction with an internist or cardiologist. Intravenous corticosteroids may be indicated to further decrease soft tissue edema when no TBI is present. Antibiotics may be indicated, depending on the etiology of the hemorrhage. Frequent ice compresses (20 minutes on, 20 minutes off) are important, and their compliant use should be emphasized to the patient and the nursing staff.

5. Medical IOP control as needed (see 9.1, Primary Open Angle Glaucoma and 9.4, Acute Angle Closure Glaucoma for treatment indications/contraindications):

 Topical IOP-lowering agents such as beta-blockers, alphaagonists, or carbonic anhydrase inhibitors.

 Oral carbonic anhydrase inhibitor (e.g., acetazolamide).

 Hyperosmotic agent (e.g., mannitol).

NOTE: When an OCS exists in a situation where canthotomy/cantholysis cannot immediately be completed, the use of IV mannitol may serve as a temporizing measure and assist in lowering intraocular and intraorbital pressure based on a recent study in which primates were subjected to experimental orbital hemorrhage. However, there should be no systemic or intracranial contraindications to mannitol before administration. Note that IV mannitol is not a substitute for definitive management of OCS by canthotomy/cantholysis!

Follow Up

In cases where vision is threatened, monitor the patient closely until stable, with frequent vision and IOP checks.

Any patient with a posttraumatic orbital hemorrhage older than 6 to 8 hours with normal visual function should be instructed in detail on how to serially measure visual function, especially over the first 24 hours, and to return immediately if vision deteriorates. Cantholysis wounds may be left open with application of antibiotic ointment t.i.d. to spontaneously heal, or closed with a secondary canthoplasty 1 to 3 weeks later. If reconstruction of the lateral canthus is indicated, it may be performed as an outpatient procedure under local anesthesia. The inferior canthal tendon is sutured back to the inner aspect of the lateral orbital rim. Interestingly, a significant percentage of eyelids will heal adequately without any surgery. If a residual optic neuropathy is present, the patient should be followed with serial examinations and visual fields. It is not uncommon for visual function to continue to improve over the first 6 months.

REFERENCES

Johnson D , Winterborn A , Kratky V . Efficacy of intravenous mannitol in the management of orbital compartment syndrome: a nonhuman primate model. Ophthal Plast Reconstr Surg. 2016;32:187-190.

Murchison AP , Bilyk JR , Savino PJ . Traumatic cranial neuropathies. In: Black EV , Nesi FA , Calvano CJ , Gladstone GJ , Levine MR , eds. Smith and Nesi’s Ophthalmic Plastic and Reconstructive Surgery. C.V. Mosby; 2021.

3.11 Traumatic Optic Neuropathy

Symptoms

Decreased visual acuity, dyschromatopsia, or visual field defect after a traumatic injury to the eye or periocular area; other trauma symptoms (e.g., pain, periocular edema).

Signs

Critical. A new afferent pupillary defect in a traumatized orbit that cannot be accounted for by previously existing or concomitant ocular pathology.

Other. Decreased color vision in the affected eye, a visual field defect, and other signs of trauma. Acutely, the optic disc appears normal in most cases of posterior indirect TON. In cases of anterior TON, optic disc avulsion may be obvious on funduscopic examination unless obscured by vitreous hemorrhage (VH). Extraocular motility may be compromised in these cases because of associated EOM avulsion or contusion. TON may be associated with intracranial injury.

NOTE: Optic disc pallor usually does not appear for weeks after a traumatic optic nerve injury. If pallor is present immediately after trauma, a preexisting optic neuropathy should be suspected.

Differential Diagnosis of a Traumatic Afferent Pupillary Defect

• Bilateral, asymmetric TON.

 Severe retinal trauma: Retinal abnormality is evident on examination.

 Traumatic, diffuse VH: Obscured view of retina, relative afferent pupillary defect (RAPD) is mild if present.

 Intracranial trauma with asymmetric damage to the prechiasmal optic nerves.

Etiology

TON is typically categorized based on location of injury (anterior or posterior) and mechanism of injury (direct or indirect). Anterior TON is arbitrarily defined as occurring anterior to the entrance of the central retinal artery into the optic nerve. Direct TON is usually due to compression, contusion, and/or laceration of the optic nerve. Indirect TON is typically due to deceleration injury with shearing of the nerve and vascular supply in the optic canal, and much less commonly due to rapid rotation of the globe leading to optic nerve head avulsion.

FIGURE 3.11.1 Computed tomography (CT) of bony impingement of the optic nerve. Red arrow and circle, bone fractures impinging on optic nerve.

 Compressive optic neuropathy from orbital hemorrhage: Most common TON. (See 3.10, Traumatic Retrobulbar Hemorrhage.)

 Compressive optic neuropathy from orbital foreign body: A subcategory of direct TON. (See 3.12, Intraorbital Foreign Body.)

 Bony impingement: A posterior direct TON that results from impingement of the apical or intracanalicular optic nerve from a fracture at the orbital apex and/or optic canal. Mechanisms vary widely. Direct bony impingement on the optic canal may result from a skull base fracture that also involves adjacent structures, including the cavernous sinus, with resultant cranial neuropathy (see Figure 3.11.1).

 Optic nerve sheath hematoma: An extremely rare and difficult to diagnose direct or indirect TON. Imaging may show perineural blood in the optic nerve sheath. Often a presumptive diagnosis requiring an abnormal fundus appearance, typically a combination of retinal venous and arterial occlusions (e.g., central retinal artery occlusion, central retinal vein occlusion). Progressive visual loss may occur as the hematoma expands. In most cases, optic nerve sheath hematoma is seen in conjunction with retinal hemorrhages and a subarachnoid intracranial bleed (Terson syndrome).

 Deceleration injury: The second most common form of TON, specifically known as posterior indirect TON, but often simply referred to as TON. The skull (usually the forehead, but can be the midface) hits a static object (e.g., steering wheel, bicycle handlebars, pavement) while the soft tissue within the orbit continues to move forward. Since the optic nerve is tethered at the optic canal, shearing of the nutrient pial vessels may occur with subsequent optic nerve edema within the confined space of the optic canal. A second “shock wave” mechanism may also occur. Cadaver studies have shown that a blow to the frontal bone is transmitted to the optic canal. Visual loss from posterior indirect TON is typically immediate and progresses in fewer than 10% of cases.

 Others (e.g., optic nerve laceration, prechiasmal optic nerve avulsion).

Workup

1. History: Mechanism of injury (e.g., deceleration, blow to the forehead)? Loss of consciousness, nausea and/or vomiting, headache, clear nasal discharge (suggestive of cerebrospinal fluid leakage)? Past ocular history including history of amblyopia, strabismus surgery, previous optic neuropathy, retinal detachment, glaucoma, etc.?

2. Complete ocular examination including an assessment of visual acuity and pupils. This may be difficult depending on the patient’s mental status, use of sedatives, narcotics, etc.

NOTE: If a bilateral, symmetric TON is present, an RAPD may be absent. Also remember that if an RAPD is present, the patient may have either a unilateral TON or a bilateral asymmetric TON. Do not assume that vision is not compromised in the fellow eye, especially in comatose or sedated patients.

3. Color vision testing in each eye. Checking red desaturation is a useful alternative if Ishihara color plates are not available.

4. Visual fields by confrontation. Formal visual field testing is helpful if available.

5. CT scan of the head and orbit (axial, coronal, and parasagittal views) with thin (i.e., 1 mm) sections through the optic canal and skull base to rule out an intraorbital foreign body or bony impingement on the optic nerve. There may be fractures along the cribriform plate, the sphenoid sinus, and the medial wall of the cavernous sinus. A normal CT in no way rules out posterior indirect TON. Similarly, an optic canal fracture does not mean TON is present.

6. B-scan ultrasound if optic nerve head avulsion is suspected but is obscured clinically by a hyphema, VH, or other media opacity.

Treatment

Depends on the type of TON:

1. Compressive optic neuropathy from orbital hemorrhage: See 3.10, Traumatic Retrobulbar Hemorrhage.

2. Compressive optic neuropathy from orbital foreign body: See 3.12, Intraorbital Foreign Body.

3. Optic nerve sheath hematoma: Optic nerve sheath fenestration may be helpful in the acute stage if optic neuropathy is progressing and no other cause is evident.

4. Optic nerve laceration: No effective treatment.

5. Optic nerve head avulsion: No effective treatment. If external ophthalmoplegia is present, surgical exploration for avulsed EOM may be necessary.

6. Deceleration injury: Effective treatment of posterior indirect TON is, at best, extremely limited. Given the results of the Corticosteroid Randomization After Significant Head Injury (CRASH) study, high-dose corticosteroids should never be offered by ophthalmologists to patients with concomitant TBI or if the TON is older than 8 hours. In the vast majority of cases, we recommend observation alone. If corticosteroids are considered (no evidence of TBI, injury within 8-hour window, no medical comorbidities), the lack of definitive therapeutic evidence and significant side effects must be discussed with the patient and/or family and the primary care team; as a practical matter, this scenario is not frequently encountered. Dosing of methylprednisolone includes a loading dose of 30 mg/kg and then 5.4 mg/kg q6h for 48 hours. Proton-pump inhibitors (e.g., omeprazole) should be given concomitantly. More recently, erythropoietin (EPO) and transcorneal electrical stimulation (TES) have been studied as potential treatments for TON. To date, the evidence is limited by study design, low study power, and lack of randomization and masking. At present, neither modality should be considered standard of care for TON.

7. Bone impingement of the optic canal: Endoscopic optic canal and orbital apex decompression may be offered in select cases, especially if the optic neuropathy is progressive. However, this option should be approached with extreme caution because of the proximity to the cavernous sinus and carotid siphon and possible bony instability of the skull base. The procedure should only be performed by an otolaryngologist and/or neurosurgeon experienced in stereotactic endoscopic sinus and skull base surgery. The patient and/or family should also be informed that there are no definitive data that prove the efficacy of this procedure in TON and that optic canal decompression may result in additional damage to the intracanalicular optic nerve. On occasion, a transcranial approach for optic canal decompression is indicated, depending on the location of the bone fragments.

Follow Up

Vision, pupillary reaction, and color vision should be evaluated daily for 1 to 2 days in cases of indirect TON where progression is suspected. With a nonprogressive TON, the patient can follow up in weeks to months to assess for spontaneous improvement. If a secondary etiology is causing a TON, follow up depends on the intervention offered and may be more frequent and prolonged. If facial and orbital fracture repair is indicated, it is crucial to document the preoperative visual acuity and visual fields (if possible) and to explain to the patient and family that TON is already present in order to avoid later claims of iatrogenic optic nerve injury. In comatose patients with suspected TON who require facial or orbital fracture repair, the family should be informed that only limited assessment of visual function is possible preoperatively, but significant traumatic visual compromise may have occurred. Always remember that an RAPD may indicate asymmetric, bilateral TON; resist any reassurances to the patient’s family of normal contralateral visual function in obtunded or uncooperative patients with an RAPD.

Anecdotally, mild to moderate posterior indirect TON may show significant spontaneous improvement over 3 to 6 months in 30% to 60% of patients, while severe initial visual loss seems to carry a worse prognosis.

REFERENCES

Edwards P , Arango M , Balica L , et al. Final results of MRC CRASH, a randomised placebo- controlled trial of intravenous corticosteroid in adults with head injury-outcomes at 6 months. Lancet. 2005;365:1957-1959.

Murchison AP , Bilyk JR , Savino PJ . Traumatic cranial neuropathies. In: Black EV , Nesi FA , Calvano CJ , Gladstone GJ , Levine MR , eds. Smith and Nesi’s Ophthalmic Plastic and Reconstructive Surgery. C.V. Mosby; 2021.

3.12 Intraorbital Foreign Body

Symptoms

Decreased vision, pain, diplopia, or may be asymptomatic. History of trauma, may be remote.

Signs

(See Figures 3.12.1 and 3.12.2.)

FIGURE 3.12.1 Intraorbital foreign body.

FIGURE 3.12.2 Computed tomography (CT) of intraorbital foreign body.

Critical. Orbital foreign body identified by clinical examination, radiograph, CT scan, and/or orbital ultrasonography.

Other. A palpable orbital mass, limitation of ocular motility, proptosis, eyelid or conjunctival laceration, erythema, edema, or ecchymosis of eyelids. Presence of an afferent pupillary defect may indicate TON.

Types of Foreign Bodies

FIGURE 3.12.3 Axial and coronal computed tomography (CT) of an orbital wooden foreign body, read initially as orbital emphysema. Note the squared-off scleral edge (arrow) on the axial image and the “stag horn” appearance (arrow) on the coronal image, both suggestive of retained orbital wood.

1. Poorly tolerated (often lead to inflammation or infection): Organic (e.g., wood or vegetable matter; see Figure 3.12.3), chemical (e.g., diesel fuel), and certain retinotoxic metallic foreign bodies (especially copper).

2. Fairly well tolerated (typically produce a chronic low-grade inflammatory reaction): Alloys that are <85% copper (e.g., brass, bronze).

3. Well tolerated (inert materials): Stone, glass, plastic, iron, lead, steel, aluminum, and most other metals and alloys, assuming that they were relatively clean on entry and have a low potential for microbial inoculation.

Workup

1. History: Determine the nature of the injury and the foreign body. Must have high index of suspicion in all trauma. Remember that children are notoriously poor historians.

2. Complete ocular and periorbital examination with special attention to pupillary reaction, IOP, and posterior segment evaluation. Carefully examine for an entry wound: at least 50% of conjunctival entry wounds are missed on clinical examination. Rule out occult globe rupture. Gentle gonioscopy may be needed.

3. CT scan of the orbit and brain (axial, coronal, and parasagittal views, with no larger than 1-mm sections of the orbit) is the initial study of choice regardless of foreign body material to rule out possible metallic foreign body. CT may miss certain materials (e.g., wood may look like air). If wood or vegetative matter is suspected, it is helpful to inform the radiologist in advance. Any lucency within the orbit can then be measured in Hounsfield units to differentiate wood from air. MRI is never the initial study in suspected foreign body and is contraindicated if a metallic foreign body is suspected or cannot be excluded, but may be a helpful adjunct to CT (especially if a wooden foreign body is suspected) once metallic foreign bodies are ruled out.

4. Based on imaging studies, determine the location of the intraorbital foreign body and rule out optic nerve or central nervous system involvement (frontal lobe, cavernous sinus, carotid artery).

5. Perform orbital B-scan ultrasonography if a foreign body is suspected, but not detected, by CT scan. B-scan is only helpful in the anterior orbit.

6. Culture any drainage sites or foreign material as appropriate.

Treatment

1. NEVER remove an intraorbital foreign body at the slit lamp without first obtaining imaging to evaluate the depth and direction of penetration. Premature removal may result in intracranial bleeding, cerebrospinal fluid leakage, worsening of intraocular injury, etc.

2. Surgical exploration, irrigation, and extraction, based on the following indications:

 Signs of infection or inflammation (e.g., fever, proptosis, restricted motility, severe chemosis, a palpable orbital mass, abscess on CT scan).

 Any organic or wooden foreign body (because of the high risk for infection and sight-threatening complications). Many copper foreign bodies require removal because of a marked inflammatory reaction.

 Infectious fistula formation.

 Signs of optic nerve compression or gaze-evoked amaurosis (decreased vision in a specific gaze).

 A large or sharp-edged foreign body (independent of composition) that can be easily extracted.

 In the setting of a ruptured globe, the globe must be repaired first. The orbital foreign body may be removed as necessary thereafter.

NOTE: Posteriorly located, inorganic foreign bodies are often simply observed if inert and not causing optic nerve compression because of the risk of iatrogenic optic neuropathy or diplopia if surgical removal is attempted. Alternatively, even an inert and otherwise asymptomatic metallic foreign body that is anterior and easily accessed may be removed with relatively low morbidity.

NOTE: If the foreign body is located in the posteromedial orbit, removal may be best achieved from an endonasal approach. Consider ENT and/or neurosurgical consultation and CT protocols for image-guided surgery when appropriate.

3. Tetanus toxoid as indicated (see Appendix 2, Tetanus Prophylaxis).

4. Consider hospitalization:

 Administer systemic antibiotics promptly (e.g., cefazolin, 1 g i.v. q8h, for clean, inert objects). If the object is contaminated or organic, treat as orbital cellulitis (see 7.3.1, Orbital Cellulitis).

 Follow vision, degree (if any) of afferent pupillary defect, extraocular motility, proptosis, and eye discomfort daily.

 Surgical exploration and removal of the foreign body when indicated (as above). Discuss with the patient and family preoperatively that successful retrieval may be impossible. Wood often splinters, and multiple procedures may be necessary to entirely remove it. Organic foreign bodies frequently cause recurrent or smoldering infection that may require months of antibiotic therapy and additional surgical exploration. This may result in progressive orbital soft tissue fibrosis and restrictive strabismus.

 If the decision is made to leave the orbital foreign body in place, discharge when stable with oral antibiotics (e.g., amoxicillin-clavulanate 250/125 to 500/125 mg p.o. q8h or 875/125 mg p.o. b.i.d.) to complete a 10- to 14-day course.

5. Patients with small inorganic foreign bodies not requiring surgical intervention may be discharged without hospitalization with oral antibiotics for a 10- to 14-day course.

Follow Up

The patient should return within 1 week of discharge (or immediately if the condition worsens). Close follow up is indicated for several weeks after the antibiotic is stopped to assure that there is no clinical evidence of infection or migration of the orbital foreign body toward a critical orbital structure (e.g., the optic nerve, EOM, globe). Reimage patient as clinically necessary. See 3.14, Ruptured Globe and Penetrating Ocular Injury; 3.11, Traumatic Optic Neuropathy; and 7.3.1, Orbital Cellulitis.

3.13 Corneal Laceration

PARTIAL-THICKNESS LACERATION

Signs

(See Figure 3.13.1.)

FIGURE 3.13.1 Corneal laceration.

The AC is not entered, and therefore, the cornea is not perforated.

Workup

1. Careful slit lamp examination should be performed to exclude ocular penetration. Carefully evaluate the conjunctiva, sclera, and cornea, checking for extension beyond the limbus in cases involving the corneal periphery. Evaluate AC depth and compare with the fellow eye. A shallow AC indicates an actively leaking wound or a self-sealed leak (see Full-Thickness Corneal Laceration below). Check for iris TIDs and evaluate the lens for a cataract or a foreign body tract (must have a high level of suspicion with projectile objects). The presence of TIDs and lens abnormalities indicates a ruptured globe.

2. Seidel test (see Appendix 5, Seidel Test to Detect a Wound Leak). If the Seidel test is positive, a full-thickness laceration is present (see Full-Thickness Corneal Laceration below). A negative Seidel test indicates either a partial-thickness laceration or a self-sealed fullthickness laceration.

3. Avoid IOP measurement if the Seidel test is positive. Measure IOP with caution if the Seidel test is negative to avoid opening a previously self-sealed full-thickness laceration.

Treatment

1. A cycloplegic (e.g., cyclopentolate 1% to 2%) and frequent application of an antibiotic (e.g., polymyxin B/bacitracin ointment or fluoroquinolone drops) depending on the nature of the wound.

2. When a moderate to deep corneal laceration is accompanied by wound gape, it is often best to suture the wound closed in the operating room to provide structural stability and to avoid excessive scarring with corneal irregularity, especially when in the visual axis.

3. If corneal foreign bodies are present and superficial, treat per Sections 3.3, Corneal and Conjunctival Foreign Bodies. If foreign bodies are in the deeper cornea, there are no signs of infection or inflammation, and are well tolerated (see 3.15, Intraocular Foreign Body, for inert foreign bodies), they may be left and watched closely. If the patient is symptomatic or if signs of infection/inflammation occur, deeper corneal foreign bodies should be removed in the operating room.

4. Tetanus toxoid for dirty wounds (see Appendix 2, Tetanus Prophylaxis).

Follow Up

Reevaluate daily until the epithelium heals.

FULL-THICKNESS CORNEAL LACERATION

(See Figure 3.13.2.)

FIGURE 3.13.2 Full-thickness corneal laceration with positive Seidel test.

See 3.14, Ruptured Globe and Penetrating Ocular Injury. Note that small, self-sealing, or slow-leaking lacerations with formed ACs may be treated with aqueous suppressants, bandage soft contact lenses, fluoroquinolone drops q.i.d., and precautions as listed in Sections 3.14, Ruptured Globe and Penetrating Ocular Injury. Avoid topical steroids. If an IOFB is present, see 3.15, Intraocular Foreign Body.

3.14 Ruptured Globe and Penetrating Ocular Injury

Symptoms

Pain, decreased vision, and loss of fluid from eye. History of trauma, fall, or sharp object entering globe.

Signs

(See Figure 3.14.1.)

FIGURE 3.14.1 Ruptured globe showing flat anterior chamber (AC), iris prolapse, and peaked pupil.

Critical. Full-thickness scleral or corneal laceration, severe subconjunctival hemorrhage (especially involving 360 degrees of bulbar conjunctiva, often bullous), a deep or shallow AC compared to the fellow eye, a peaked or irregular pupil, iris TIDs, lens material or vitreous in the AC, foreign body tract or new opacity in the lens, or extraocular motility limitation (greatest in the direction of rupture). Intraocular contents may be outside of the globe.

Other. Low IOP (may also be normal or rarely increased), iridodialysis, cyclodialysis, hyphema, periorbital ecchymosis, VH, and dislocated or subluxed lens. Commotio retinae, choroidal rupture, and retinal breaks may be seen but are often obscured by VH.

Workup/Treatment

Once a ruptured globe is diagnosed, further examination should be deferred until the time of surgical repair in the operating room. This is to avoid placing any pressure on the globe and risking extrusion of intraocular contents. Diagnosis should be made by penlight, indirect ophthalmoscope, or, if possible, slit lamp examination (with minimal manipulation). Once the diagnosis is made, the following measures should be taken:

1. Protect the eye with a hard shield at all times. Do not patch the eye.

2. CT scan of the brain and orbits (axial, coronal, and parasagittal views with 1-mm sections) to rule out IOFB.

3. Gentle B-scan ultrasound may be needed to localize posterior rupture site(s) or to rule out IOFBs not visible on CT scan (nonmetallic, wood, etc.). However, B-scan should not be done in patients with an obvious anterior rupture due to the risk of extruding intraocular contents. A trained ophthalmologist should evaluate the patient before B-scan or any other manipulation is performed on a ruptured globe suspect.

4. Admit the patient to the hospital with no food or drink (NPO).

5. Place the patient on bed rest with bathroom privileges. Avoid strenuous activities, bending, and Valsalva maneuvers.

6. Systemic antibiotics should be administered within 6 hours of injury. For adults, give cefazolin 1 g i.v. q8h or vancomycin 1 g i.v. q12h, and moxifloxacin 400 mg i.v. daily (or an equivalent fluoroquinolone). For children <12 years, give cefazolin 25 to 50 mg/kg/d i.v. in three divided doses and gentamicin 2 mg/kg i.v. q8h. Some groups recommend 48 hours of intravenous antibiotics perioperatively. A 1-week antibiotic course is typically completed postoperatively with a broad-spectrum fluoroquinolone (e.g., levofloxacin 750 mg p.o. daily).

NOTE: Antibiotic doses may need to be reduced if renal function is impaired. Gentamicin peak and trough levels are obtained 1/2 hour before and after the fifth dose, and blood urea nitrogen and creatinine levels are evaluated every other day.

7. Administer tetanus toxoid p.r.n. (see Appendix 2, Tetanus Prophylaxis).

8. Administer antiemetics (e.g., ondansetron 4 or 8 mg q4-8h) p.r.n. for nausea and vomiting to prevent Valsalva and possible expulsion of intraocular contents.

9. Administer pain medicine before and after surgery p.r.n. (often intravenous).

10. Determine time of the patient’s last meal. Timing of surgical repair is often influenced by this information.

11. Arrange for surgical repair to be done as soon as possible.

NOTE: In any severely traumatized eye in which there is no chance of restoring vision, potential enucleation should be discussed with the patient early on. This procedure should be performed within 7 to 14 days after the trauma to minimize the rare occurrence of sympathetic ophthalmia.

Infection is more likely to occur in eyes with dirty injuries, retained IOFBs and rupture of lens capsule and in patients with a long delay until primary surgical repair. In patients at high risk of infection, some groups recommend intravitreal antibiotics at the time of surgical closure (see 12.15, Traumatic Endophthalmitis).

NOTE: Several studies have examined prognostic factors for ocular trauma and open globe injuries. One commonly used and validated system is the Ocular Trauma Score (OTS). See Tables 3.14.1 and 3.14.2.

TABLE 3.14.1

Calculating the OTS

LP/HM, light perception/hand motion; NLP, no light perception.

TABLE 3.14.2

Visual Prognosis per OTS

OTS, Ocular Trauma Score.

REFERENCE

Kuhn F , Maisiak R , Mann L , et al. The Ocular Trauma Score (OTS). Ophthalmol Clin North Am. 2002;15(2):163-165.

3.15 Intraocular Foreign Body

Symptoms

Eye pain, decreased vision, or may be asymptomatic; often suggestive history (e.g., hammering metal or sharp object entering globe).

Signs

(See Figure 3.15.1.)

FIGURE 3.15.1 Intraocular foreign body.

Critical. May have a clinically detectable corneal or scleral perforation site, hole in the iris, focal lens opacity, or an IOFB. IOFBs are often seen on CT scan (thin cuts), B-scan, and/or UBM.

Other. See 3.14, Ruptured Globe and Penetrating Ocular Injury. Also, microcystic (epithelial) edema of the peripheral cornea (a clue that a foreign body may be hidden in the AC angle in the same sector of the eye). Long-standing iron-containing IOFBs may cause siderosis, manifesting as anisocoria, heterochromia, corneal endothelial and epithelial deposits, anterior subcapsular cataracts, lens dislocation, retinopathy, and optic atrophy.

Types of Foreign Bodies

1. Frequently produce severe inflammatory reactions and may encapsulate within 24 hours if on the retina.

Magnetic: Iron, steel, and tin.

Nonmagnetic: Copper and vegetable matter (may be severe or mild).

2. Typically produce mild inflammatory reactions.

Magnetic: Nickel.

Nonmagnetic: Aluminum, mercury, zinc, and vegetable matter (may be severe or mild).

3. Inert foreign bodies: Carbon, gold, coal, glass, lead, gypsum plaster, platinum, porcelain, rubber, silver, and stone. Brass, an alloy of copper and zinc, is also relatively nontoxic. However, even inert foreign bodies can be toxic because of a coating or chemical additive. Most ball bearings (BBs) and gunshot pellets are made of 80% to 90% lead and 10% to 20% iron.

Workup

 History: Composition of foreign body? Time of last meal?

 Perform ocular examination, including visual acuity and careful evaluation of globe integrity. If there is an obvious perforation site, the remainder of the examination may be deferred until surgery. If there does not appear to be a risk of extrusion of intraocular contents, the globe is inspected gently to localize the perforation site and to detect the foreign body.

 Slit lamp examination; search the AC and iris for a foreign body and look for an iris TID. Examine the lens for disruption, cataract, or embedded foreign body. Check IOP.

 Consider careful gonioscopy of the AC angle if no wound leak can be detected and the globe appears intact.

 Dilated retinal examination using indirect ophthalmoscopy.

 Obtain a CT scan of the orbits and brain (coronal, axial, and parasagittal views with no larger than 1-mm sections through the orbits). MRI is contraindicated in the presence of a metallic foreign body. It may be difficult to visualize wood, glass, or plastic on a CT scan, especially acutely. Suspicion of a nonmetallic IOFB should specifically be mentioned to the reading radiologist.

 Gentle B-scan of the globe and orbit. Intraocular air can mimic a foreign body. Consider UBM to inspect the AC if IOFB is not visible on clinical examination (e.g., foreign body in the AC angle or sulcus). These steps should be deferred in patients with a definitive or suspected anterior rupture given the risk for extrusion of intraocular contents.

 Culture the wound site if it appears infected.

 Determine whether the foreign body is magnetic (e.g., examine material from which the foreign body came).

Treatment

1. Hospitalization with no food or drink (NPO) until repair.

2. Place a protective rigid shield over the involved eye. Do not patch the eye.

3. Tetanus prophylaxis as needed (see Appendix 2, Tetanus Prophylaxis).

4. Broad-spectrum gram-positive and gram-negative antibiotic coverage (e.g., vancomycin 1 g i.v. q12h and ceftazidime 1 g i.v. q12h or ciprofloxacin 400 mg i.v. q12h or moxifloxacin 400 mg i.v. q.d.).

NOTE: Fluoroquinolones are contraindicated in children and pregnant women.

5. Cycloplegia (e.g., atropine 1% b.i.d.) for posterior-segment foreign bodies.

6. Urgent surgical removal of any acute IOFB is advisable to reduce the risk of infection and development of proliferative vitreoretinopathy (PVR). For some metallic foreign bodies, a magnet may be useful during surgical extraction. Copper or contaminated foreign bodies require especially urgent removal. A chronic IOFB may require removal if associated with severe recurrent inflammation, if in the visual axis, or if causing siderosis.

7. If endophthalmitis is present, treat as per 12.15, Traumatic Endophthalmitis.

Follow Up

Observe the patient closely in the hospital for signs of inflammation or infection. If the surgeon is uncertain as to whether the foreign body was entirely removed, postoperative imaging should be considered with CT, B-scan, or UBM as above. Periodic follow up for years is required; watch for a delayed inflammatory reaction in both the traumatic and nontraumatic eye. When an IOFB is left in place, an electroretinogram (ERG) should be obtained as soon as it can be done safely. Serial ERGs should be followed to look for toxic retinopathy, which will often reverse if the foreign body is removed.

3.16 Firework or Shrapnel-/Bullet-Related Injuries

Symptoms

Ocular pain, decreased vision, foreign body sensation, tearing, redness, and photophobia; history of trauma with firework, weapons of warfare, or devices that result in high-velocity impact and shrapnel/particulate fragmentation (e.g., firecracker, sparkler, firearm, explosive, grenade).

Signs

Critical. Foreign bodies, usually irregular in shape and fragmented in nature, embedded in ocular or orbital tissues. Periocular damage secondary to associated surrounding high-energy release. Can result in open or closed globe injuries.

Other. Conjunctival injection, eyelid edema, corneal/conjunctival epithelial defects or lacerations, thermal and/or chemical burns of ocular tissues (e.g., eyelid, conjunctiva, cornea), AC reaction, hyphema, iridodialysis, angle recession, VH, and retina or optic nerve injury. Motility deficits and globe malposition may exist if the foreign body is embedded in or around the orbit.

Workup

1. History: Mechanism of injury (e.g., detonation of an explosive, missile, or firearm; distance of patient from the instrument of injury, etc.)? Size, weight, velocity, force, shape, and composition of the object? Concurrent tinnitus or hearing loss (often associated with explosions/firearms)?

2. Document visual acuity before any procedure is performed. Topical anesthetic may be necessary to facilitate examination, but be careful not to cause expulsion of ocular tissue if open globe exists. Also evaluate optic nerve function by examining pupillary response and testing color plates.

3. Examine for orbital signs by evaluating motility, globe malposition, and sectoral chemosis/inflammation, as this might help localize the landing site of shrapnel or bullet material that has entered without exit.

4. Look for periocular tissue burns or lacerations, which may warrant evaluation by internal medicine or dermatology.

5. Check the forniceal pH if an associated chemical injury is suspected. See 3.1, Chemical Burn.

6. Slit lamp examination: Locate and assess the depth of any foreign body. Examine closely for possible entry sites (rule out selfsealing lacerations), pupil irregularities, iris tears and TIDs, capsular perforations, lens opacities, hyphema, AC shallowing (or deepening in scleral perforations), and asymmetrically low IOP in the involved eye. Assess for any damage to the lacrimal apparatus.

7. Perform a dilated fundus examination to exclude possible IOFB, unless there is a risk of extrusion of intraocular contents (see 3.15, Intraocular Foreign Body). Dilation should typically be deferred if there is a foreign body lodged in the iris. In cases of chemical injury, dilate with cycloplegics only and avoid alpha-agonist drops (e.g., phenylephrine), which may exacerbate limbal ischemia.

8. Consider gentle B-scan ultrasound, CT scan of the orbit (axial, coronal, and parasagittal views, 1-mm sections), or UBM to exclude an intraocular or intraorbital foreign body. Avoid MRI if history concerning for possible metallic foreign body.

Treatment and Follow Up

1. Depends on the specific injuries present. Refer to appropriate sections as needed. Depending on the number or extent of injuries, consider exploration in the OR.

2. Consider tetanus prophylaxis (see Appendix 2, Tetanus Prophylaxis).

3. If evidence of penetrating or perforating trauma, see 3.13, Corneal Lacerations to 3.14, Ruptured Globe and Penetrating Trauma Injury.

4. If foreign bodies are present, but either inaccessible or associated with injuries that prohibit safe removal at the slit lamp, see 3.12, Intraorbital Foreign Body or 3.15, Intraocular Foreign Body. Many inert foreign bodies are well tolerated. The risk of iatrogenic optic neuropathy or diplopia with attempted surgical removal of foreign bodies must be weighed against the risk of delayed complications if left near vital orbital structures.

5. If evidence of pH alteration, see 3.1, Chemical burn.

6. If extensive facial or skull fractures exist, comanagement with neurosurgery, otolaryngology, or oromaxillofacial surgery may be needed. Delayed reconstructive procedures are often necessary.

7. Comanage with internal medicine or dermatology if periocular or facial burns exist. The patient may require care in a burn unit.

8. Follow up depends on the extent of injuries and the conditions being treated.

3.17 Commotio Retinae

Symptoms

Decreased vision or asymptomatic; history of recent ocular trauma.

Signs

(See Figure 3.17.1.)

FIGURE 3.17.1 Commotio retinae.

Critical. Confluent area of retinal whitening in the periphery or posterior pole (Berlin edema). Cherry-red spot may be present with Berlin edema. The retinal blood vessels are undisturbed in the area of retinal whitening.

Other. Additional signs of ocular trauma, such as retinal hemorrhages, may be noted.

NOTE: Visual acuity does not always correlate with the degree of retinal whitening.

Etiology

Blunt trauma to the globe causes shock waves which disrupt the photoreceptors. Retinal whitening is the result of fragmentation of the photoreceptor outer segments and intracellular edema of the retinal pigment epithelium (RPE). The inner retinal layers may also be involved depending on the force of injury.

Differential Diagnosis

 Retinal detachment: Retina elevated associated with retinal break or dialysis. See 11.3, Retinal Detachment.

 Retinal artery occlusion: Retinal whitening along the distribution of an artery. See 11.6, Central Retinal Artery Occlusion and 11.7, Branch Retinal Artery Occlusion.

 White without pressure: Common benign peripheral retinal finding. May be associated with a prominent vitreous base.

 Myelinated nerve fiber layer: Develops postnatally (see Figure 11.5.2).

 Chorioretinitis sclopetaria: Bare sclera visible through retinal and choroidal rupture on dilated examination. See 3.19, Chorioretinitis Sclopetaria.

Workup

Complete ophthalmic evaluation, including dilated fundus examination. Scleral depression is performed except when a ruptured globe, hyphema, microhyphema, or iritis is present. Optical coherence tomography (OCT) shows ellipsoid zone disruption.

Treatment

No treatment is required because this condition is self-limited. Some patients with foveal involvement may be left with chronic visual impairment and RPE atrophy or hyperpigmentation on fundus examination.

Follow Up

Dilated fundus examination is repeated in 1 to 2 weeks. Patients are instructed to return sooner if retinal detachment symptoms are experienced (see 11.3, Retinal Detachment).

3.18 Traumatic Choroidal Rupture

Symptoms

Decreased vision or asymptomatic. History of ocular trauma.

Signs

(See Figure 3.18.1.)

FIGURE 3.18.1 Choroidal rupture.

Critical. A yellow or white crescent-shaped subretinal streak, usually concentric to the optic disc. May be single or multiple. Often cannot be seen until several days or weeks after trauma because it may be obscured by overlying subretinal blood.

Other. Rarely, the rupture may be radially oriented. Choroidal neovascularization (CNV) may develop later. TON may be present.

Differential Diagnosis

 Lacquer cracks of high myopia: Often bilateral. A tilted disc, a scleral crescent adjacent to the disc, and a posterior staphyloma may also be seen. CNV may also develop in this condition. See 11.22, High Myopia.

 Angioid streaks: Bilateral subretinal streaks radiating from the optic disc, sometimes associated with CNV. See 11.23, Angioid Streaks.

Workup

1. Complete ocular evaluation, including dilated fundus examination to rule out retinal breaks and to detect CNV.

2. Consider OCT to characterize a choroidal rupture and evaluate potential CNV.

3. Consider fluorescein angiography to confirm the presence and location of CNV if the injury is old.

Treatment

1. Observation. There are no medical or surgical treatment options in the acute setting. Consider recommending safety eyewear. An Amsler grid may be provided, and the patient is instructed to return if any change in the appearance of the grid is noted (see Appendix 4, Amsler Grid).

2. Anti-vascular endothelial growth factor (VEGF) therapy may be used if CNV develops. See 11.17, Neovascular or Exudative (Wet) Age-Related Macular Degeneration, for more information on CNV treatment.

Follow Up

After ocular trauma, patients with hemorrhage obscuring the underlying choroid are reevaluated every 1 to 2 weeks until the choroid can be well visualized. Although CNV is rare overall, ruptures that are particularly long or closer to the fovea are at greater risk for CNV development. Fundus examinations may be performed every 6 to 12 months depending on the severity and risk of progression to CNV. Patients treated for CNV must be followed closely after treatment to watch for persistent or new CNV (see 11.17, Neovascular or Exudative (Wet) Age-Related Macular Degeneration, for further follow-up guidelines).

3.19 Chorioretinitis Sclopetaria

Symptoms

Visual loss; severity depends on the region of involvement. History of high-velocity missile injury to orbit (e.g., a BB, bullet, or shrapnel).

Signs

(See Figure 3.19.1.)

FIGURE 3.19.1 Chorioretinitis sclopetaria.

Critical. Areas of choroidal and retinal rupture leaving bare sclera visible on fundus examination, typically demonstrating a “claw-like” configuration of fundus atrophy and pigmentation.

Other. Subretinal, intraretinal, preretinal, and VH often involving the macula. Eventually blood is resorbed and the resultant defects are replaced by fibrous tissue. Intraorbital foreign body. Can have associated avulsion of vitreous base, which can cause peripheral retinal dialysis.

Etiology

Caused by a high-velocity missile passing through the orbit without perforating the globe. Resultant shock waves lead to chorioretinal rupture from the sclera.

Differential Diagnosis

• Ruptured globe: Severe subconjunctival hemorrhage and chemosis, often with deep or shallow AC; low IOP; and peaked, irregular pupil. See 3.14, Ruptured Globe and Penetrating Ocular Injury.

 Choroidal rupture: White or yellow crescent-shaped subretinal streak usually concentric to the optic nerve. No retinal break is present. Initially, retinal hemorrhage in the posterior pole may obscure a choroidal rupture, which subsequently becomes apparent as the blood clears. See 3.18, Traumatic Choroidal Rupture.

 Optic nerve avulsion: Decreased vision with RAPD on examination and hemorrhagic depression or excavation of the optic disc if partial, or retraction of entire nerve if complete. Often associated with VH. No treatment is available, and visual prognosis depends on extent of injury. See 3.11, Traumatic Optic Neuropathy.

Workup

1. History: Known injury with a projectile?

2. Complete ocular evaluation including dilated fundus examination. Look for areas of retinal and choroidal rupture with underlying bare sclera. Carefully examine the conjunctiva and sclera to rule out ruptured globe. Rule out IOFB. Carefully examine the retinal periphery for retinal tears or dialysis.

3. Protect the eye with a rigid shield.

4. CT scan of the orbit (axial, coronal, and parasagittal views, 1-mm sections) to check for intrascleral, intraocular, or intraorbital foreign bodies. Gentle B-scan or UBM may be helpful to rule out intraocular or intraorbital foreign bodies.

Treatment

Observation, as there is no effective treatment. Complications, including retinal dialysis and detachment, are treated appropriately. Surgery can be considered for nonclearing VH.

Follow Up

Sequential examinations are required every 2 to 4 weeks looking for signs of retinal detachment as blood clears. Patients should be followed until an atrophic “claw-like” scar replaces areas of hemorrhage.

3.20 Purtscher Retinopathy

Symptoms

Decreased vision, often sudden; can be severe. History of compression injury to the head, chest, or lower extremities (e.g., long bone fractures), but not a direct ocular injury.

Signs

(See Figure 3.20.1.)

FIGURE 3.20.1 Purtscher retinopathy.

Critical. Multiple cotton wool spots and/or intraretinal hemorrhages in a configuration around the optic nerve; can also have larger areas of superficial retinal whitening with perivascular clearing (Purtscher flecken). Changes are typically bilateral but may be asymmetric or unilateral.

Other. Serous macular detachment, dilated tortuous vessels, hard exudates, optic disc edema (though the disc usually appears normal), macular pseudo-cherry-red spot, RAPD, and optic atrophy when chronic.

Differential Diagnosis

1. Pseudo-Purtscher retinopathy: Several entities with the same or similar presentation but not associated with trauma (Purtscher retinopathy by definition occurs with trauma), including acute pancreatitis, malignant hypertension, thrombotic thrombocytopenic purpura (TTP), hemolytic uremic syndrome (HUS), collagen vascular diseases (e.g., systemic lupus erythematosus, scleroderma, dermatomyositis, Sjogren syndrome), chronic renal failure, amniotic fluid embolism, retrobulbar anesthesia, orbital steroid injection, and alcohol use.

2. Central retinal vein occlusion: Unilateral, multiple hemorrhages and cotton wool spots diffusely throughout the retina. See 11.8, Central Retinal Vein Occlusion.

3. Central retinal artery occlusion: Unilateral retinal whitening with a cherry-red spot; see 11.6, Central Retinal Artery Occlusion.

Etiology

Not well understood. It is felt that the findings are due to occlusion of small arterioles in the peripapillary retina by different particles depending on the associated systemic condition: complement activation, fibrin clots, platelet-leukocyte aggregates, or fat emboli.

Workup

1. History: Compression injury to the head or chest? Long bone fracture? If no trauma, any symptoms associated with causes of pseudo-Purtscher retinopathy (see above, e.g., renal failure, rheumatologic disease)?

2. Complete ocular evaluation including dilated fundus examination. Rule out direct globe injury.

3. CT of the head, chest, or long bones as indicated.

4. If characteristic findings occur in association with severe head or chest trauma, then the diagnosis is established and no further workup is required. Without trauma, the patient needs a systemic workup to investigate other causes (e.g., blood pressure measurement, basic metabolic panel [BMP], CBC, amylase, lipase, rheumatologic evaluation).

5. Fluorescein angiography: Shows patchy capillary nonperfusion in regions of retinal whitening.

Treatment

No ocular treatment available. Must treat the underlying condition if possible to prevent further damage.

Follow Up

Repeat dilated fundus examination in 2 to 4 weeks. Retinal lesions resolve over a few weeks to months. Visual acuity may remain reduced but may return to baseline in 50% of cases.

3.21 Shaken Baby Syndrome

Definition

Form of abusive head trauma characterized by intracranial hemorrhage, brain injury, multifocal fractures, and/or retinal hemorrhages due to repeated acceleration-deceleration forces with or without blunt head impact. External signs of trauma are often absent.

Symptoms

Change in mental status, new-onset seizures, poor feeding, and irritability. Child is usually <1 year of age but rarely >3 years of age. Symptoms and signs often inconsistent with history.

Signs

Critical. Retinal hemorrhages are present in ~85% of cases. Two- thirds are too numerous to count and multilayered (pre-, intra-, and subretinal), extending throughout the retina to the ora serrata. Markedly asymmetric hemorrhages in up to 20% of cases, unilateral in ~2%. Macular retinoschisis (hemorrhagic macular cysts, most often subinternal limiting membrane) may be seen with or without surrounding paramacular retinal folds. Most commonly associated brain lesions are subarachnoid and subdural hemorrhages. Characteristic fractures include the ribs and/or long bone epiphyses. Cerebral edema and death occur in ~ 20% to 30% of cases.

Other. Subretinal and VH less common. Retinal detachment, papilledema, late optic atrophy, and optic nerve avulsion are infrequent. Postmortem findings include orbital, optic nerve sheath, optic nerve sheath intradural, and posterior intrascleral hemorrhage.

Differential Diagnosis

• Severe accidental injury: Accompanied by other external injuries consistent with the history. Even in the most severe accidental injuries (e.g., motor vehicle accidents [MVA]), retinal hemorrhages are uncommon. In the usual trauma of childhood, retinal hemorrhages are typically mild and do not extend to the ora serrata. Severe retinal hemorrhages similar to shaken baby syndrome have only been reported in fatal head crush, fatal MVA, and an 11-m fall onto concrete.

 Birth trauma: Retinal hemorrhages can be extensive, but nerve fiber layer hemorrhages are gone by 2 weeks, and dot/blot hemorrhages typically disappear by 4 to 6 weeks. Foveal, preretinal, and VH may persist longer. No retinoschisis or retinal folds. Clinical history must be consistent. Most common cause of retinal hemorrhage in neonates.

 Coagulopathies, leukemia, and other blood dyscrasias. Rare, but should be ruled out. Other than leukemia, in which infiltrates are usually present, these entities do not cause extensive retinal hemorrhages.

 Hyperacute elevation of intracranial pressure (e.g., ruptured aneurysm) may cause extensive retinal hemorrhage. Easily differentiated by neuroimaging. Otherwise, increased intracranial pressure in children does NOT result in extensive retinal hemorrhage beyond the peripapillary area.

 Hypoxia, immunizations, cardiopulmonary resuscitation (CPR), meningitis, sepsis, and cortical vein thrombosis are often offered as alternate explanations in the courtroom for retinal hemorrhages, but these are not usually supported by available clinical and research evidence. Type, distribution, and number of hemorrhages is helpful in ascertaining causality.

Workup

1. History from caregiver(s) is best obtained by a child abuse pediatrician or a representative team. Be alert for history incompatible with injuries or changing versions of history.

2. Complete ophthalmic examination, including pupils (for afferent pupillary defect) and dilated fundus examination.

3. Laboratory: CBC with platelet count, PT/INR, and PTT. Consider additional evaluation based on initial screening results.

4. Imaging: CT or MRI; skeletal survey. Consider bone scan.

5. Admit patient to hospital if shaken baby syndrome is suspected. Requires coordinated care by neurosurgery, pediatrics, ophthalmology, and social services.

NOTE: Careful documentation is an integral part of the evaluation, as the medical record may be used as a legal document. Ocular photography is not the gold standard for documenting retinal hemorrhages but may be useful if available. A thorough detailed description is essential with or without a drawing, including type, number, and distribution of hemorrhages and presence/absence of retinoschisis/folds.

Treatment

Predominantly supportive. Focus is on systemic complications. Ocular manifestations are usually observed. In cases of nonabsorbing dense VH, vitrectomy may be considered due to the risk of amblyopia.

NOTE: All physicians are legally mandated to report suspected child abuse. There is legal precedence for prosecution of nonreporters.

Follow Up

Prognosis is variable and unpredictable. Survivors can suffer from significant cognitive disabilities, and severe visual loss occurs in 20% of children, usually from optic atrophy or brain injury. Even if no retinal hemorrhages exist, ophthalmologic follow up is recommended for children with brain injury.