Slit lamp examination in the cooperative patient may show associated injuries such as iris transillumination defect (red reflex obscured by vitreous hemorrhage); corneal lacerations; iris prolapse;hyphemafrom ciliary body disruption; and lens injuries, including dislocation or subluxation. A shallow anterior chamber may be the only sign of occult globe rupture and is associated with a worse prognosis. A posterior rupture may present with a deeper anterior chamber due to extrusion of vitreous from the posterior segment.

PhysicalIn peripheral iris prolapse, the iris appears as a knuckle of colored tissue, resulting in a partial peripheral synechia. When the prolapse is central, the entire pupillary margin may prolapse, resulting in a total anterior synechia. In patients with a perforated cornea, the prolapsed iris is exposed.Depending on the duration of prolapse, the appearance of the iris may vary. In cases of recent prolapse, the iris appears viable. With time, the iris appears dry and nonviable. In patients who have undergone corneal transplant surgery or cataract surgery with a clear corneal incision, the appearance of the iris is the same as in a perforated cornea. When the iris prolapses through a scleral wound, it appears as a colored mass beneath the overlying conjunctiva. In this case, the iris remains viable for a long time. The pupil appears peaked in the region of the iris prolapse. The anterior chamber is formed as the prolapsed iris seals the wound. Minimal or no wound leakage occurs. Wound leak is verified using the Seidel test. A drop of 2% fluorescein sodium is instilled in the conjunctival sac. The wound is examined under the slit lamp with cobalt blue light. The fluorescein appears greenish. Wound leak can be easily identified when the fluorescein is diluted by the aqueous humor. Gentle pressure on the eye may be needed to induce leakage. Intraocular pressure is lower than normal, but hypotony is uncommon after iris prolapse. In long-standing iris prolapse, chronic iridocyclitis, cystoid macular edema, or glaucoma may be seen. The prolapsed iris may act as a scaffold for infection, epithelial downgrowth, or fibrous ingrowth. Rarely, sympathetic ophthalmia may occur. Carefully examining the fellow eye for cells and flare is important3.5 Traumatic IritisTraumatic IritisSymptomsDull, aching/throbbing pain, photophobia, tearing, onset of symptoms within 3 days of trauma.SignsCritical. White blood cells and flare in the AC (seen under high-power magnification by focusing into the AC with a small, bright beam from the slit lamp).Other. Pain in the traumatized eye when light enters either eye; lower (although sometimes higher) IOP; smaller pupil (which dilates poorly) or larger pupil (caused by iris sphincter tears) in the traumatized eye; perilimbal conjunctival injection; occasionally, decreased vision.Differential Diagnosis Nongranulomatous anterior uveitis (NGAU): No history of trauma, or the degree of trauma is not consistent with the level of inflammation. See 12.1, Anterior Uveitis. Traumatic microhyphema: RBCs suspended in the AC. See 3.6, Hyphema and Microhyphema. Traumatic corneal abrasion: May have an accompanying AC reaction. See 3.2, Corneal Abrasion. Traumatic retinal detachment: May produce an AC reaction or may see pigment in the anterior vitreous. See 11.3, Retinal Detachment.Work-UpComplete ophthalmic examination, including IOP measurement and dilated fundus examination.TreatmentCycloplegic agent (e.g., cyclopentolate 2% t.i.d. or scopolamine 0.25% t.i.d.). If the patient is very symptomatic, 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 Recheck in 5 to 7 days. If resolved, the cycloplegic agent is discontinued and the steroid is tapered. One 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 MicrohyphemaTraumatic HyphemaSymptomsPain, blurred vision, history of blunt trauma.Signs(See Figure 3.6.1.)Blood or clot or both in the AC, usually visible without a slit lamp. A total (100%) P.20

hyphema may be black or red. When black, it is called an 8-ball or black ball hyphema; when red, the circulating blood cells may settle with time to become less than a 100% hyphema.

Figure 3.6.1. Hyphema.

Work-Up History: Mechanism (including force, velocity, type, and direction) of injury? Protective eyewear? Time of injury? Time of visual loss? Usually the visual compromise occurs at the time of injury; decreasing vision over time suggests a rebleed or continued bleed. Use of medications with anticoagulant properties [aspirin, NSAIDs, warfarin (e.g., Coumadin), or clopidogrel (e.g., Plavix)]? Personal or family history of sickle cell disease/trait? Symptoms of coagulopathy (e.g., bloody nose-blowing, bleeding gums with tooth brushing, easy bruising)? Ocular examination, first ruling out a ruptured globe (see 3.14, Ruptured Globe and Penetrating Ocular Injury). Evaluate for other traumatic injuries. Document the extent (e.g., measure the hyphema height) and location of any clot and blood. Measure the IOP. Perform a dilated retinal evaluation without scleral depression. Consider a gentle UBM if the view of the fundus is poor. Avoid gonioscopy unless intractable increased IOP develops. If gonioscopy is necessary, gently use a Zeiss 4 mirror lens. Consider UBM to evaluate the anterior segment if the view is poor and lens capsule rupture, IOFB, or other anterior segment abnormalities are suspected. Consider a CT scan of the orbits and brain (axial and coronal views, with 1- to 3-mm sections through the orbits) when indicated (e.g., suspected orbital fracture or IOFB, loss of consciousness). Black and Mediterranean patients should be screened for sickle cell trait or disease (order Sickledex screen; if necessary, may check hemoglobin electrophoresis).TreatmentMany 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, patients with other severe ocular or orbital injuries, and patients with concomitant significant IOP elevation and sickle cell. In addition, consider hospitalization and aggressive treatment for children, especially those at risk for amblyopia (e.g., those under age 7 to 8) or when child abuse is suspected. Confine either to bed rest with bathroom privileges or to limited activity. Elevate head of bed to allow blood to settle. Place a shield (metal or clear plastic) over the involved eye at all times. Do not patch because this prevents recognition of sudden visual loss in the event of a rebleed. Atropine 1% solution b.i.d. to t.i.d. or scopolamine 0.25% b.i.d. to t.i.d. No aspirin-containing products or NSAIDs. Mild analgesics only (e.g., acetaminophen). Avoid sedatives. Use topical steroids (e.g., prednisolone acetate 1% four to eight times per day) if any suggestion of iritis (e.g., photophobia, deep ache, ciliary flush), evidence of lens capsule rupture, any protein (e.g., fibrin), or definitive white blood cells in anterior P.21

chamber. Reduce the frequency of steroids as soon as signs and symptoms resolve to reduce the likelihood of steroid-induced glaucoma. For increased IOP: Nonsickle cell disease/trait (>30 mm Hg): Start with a beta-blocker (e.g., timolol or levobunolol 0.5% b.i.d.). If IOP still high, add topical alphaagonist (e.g., apraclonidine 0.5%, or brimonidine 0.2% t.i.d.) or topical carbonic anhydrase inhibitor (e.g., dorzolamide 2%, or brinzolamide 1% t.i.d.). Avoid prostaglandin analogs and miotics (may increase inflammation). In children under 5, topical alphaagonists are contraindicated. If topical therapy fails, add acetazolamide (500 mg p.o., q12h for adults, 20 mg/kg/day divided three times per day for children) or mannitol [1 to 2 g/kg intravenously (i.v.) over 45 minutes q24h]. If mannitol is necessary to control the IOP, surgical evacuation may be imminent. Sickle cell disease/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 alphaagonists (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 mg p.o., q8h instead of acetazolamide (controversial). If mannitol is necessary to control the IOP, surgical evacuation may be imminent. AC paracentesis is safe and effective if IOP cannot be safely lowered medically (see Appendix 13, Anterior Chamber Paracentesis). This procedure is often only a temporizing measure when the need for surgical evacuation is anticipated. If hospitalized, use antiemetics p.r.n. for severe nausea or vomiting [e.g., prochlorperazine 10 mg intramuscularly (i.m.) q8h or 25 mg q12h p.r.n.; 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 trait/disease patients.NoteIn children, particular caution must be used regarding topical steroids. Children often get rapid rises in IOP and with prolonged use there is a significant 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 the steroids as soon as possible.NoteIncreased IOP, especially soon after trauma, may be transient, secondary to acute mechanical plugging of the trabecular meshwork. Elevating the patient's head may decrease the IOP by causing RBCs to settle inferiorly.NotePreviously, systemic aminocaproic acid was used in hospitalized patients to stabilize the clot and to prevent rebleeding. This therapy is rarely used now. Topical aminocaproic acid (e.g., Caprogel) is currently under research and development. Preliminary studies suggest it may be useful in reducing risk of rebleeding. Further research is needed before the role for topical aminocaproic acid in the management of hyphemas can be determined.P.22

Follow-Up The patient should be seen daily for 3 days after initial trauma to check visual acuity, IOP, and for a slit-lamp examination. Look for new bleeding, increased IOP, corneal blood staining, and other intraocular injuries as the blood clears (e.g., iridodialysis; subluxated, disclocated, or cataractous lens). Hemolysis, which may appear as bright red fluid, should be distinguished from a rebleed, which forms a new, bright red clot. If the IOP is increased, treat as described earlier. 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 secondary glaucoma). If a significant rebleed or an intractable IOP increase occurs, the patient should be hospitalized. After the initial close follow-up period, the patient may be maintained on a long-acting cycloplegic (e.g., atropine 1% solution q.d. to b.i.d., scopolamine 0.25% q.d. to b.i.d.), depending on the severity of the condition. Topical steroids may be tapered as the blood, fibrin, and white blood cells resolve. Glasses or eye shield during the day and eye shield at night. As with any patient, protective eyewear (polycarbonate or Trivex lenses) should be worn any time significant potential for an eye injury exists. The patient must refrain from strenuous physical activities (including bearing down or Valsalva maneuvers) for 1 week after the initial injury or rebleed. Normal activities may be resumed 1 week from the date of injury or rebleed. This period should be extended if blood remains in the anterior chamber. Future outpatient follow-up: If patient was 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 severity of condition (amount of blood, potential for IOP increase, other ocular or orbital pathologic processes). Four 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.3.13 Corneal LacerationParital-Thickness LacerationSigns(See Figure 3.13.1.)The anterior chamber is not entered and, therefore, the cornea is not perforated.Work-Up 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 the depth of the AC and compare with the fellow eye. A shallow AC indicates an actively leaking wound or a self-sealed leak (see Full-Thickness Laceration below). Deeper AC in the involved eye can be an indication of a posterior rupture. Check iris for transillumination defects (TIDs) and evaluate lens for a cataract or a foreign body tract (must have a high level of suspicion with P.39

projectile objects). Presence of TIDs and lens abnormalities are an indication of a ruptured globe. IOP should be measured only after a ruptured globe is ruled out. Use applanation only if the laceration site can be avoided. Otherwise, use a Tono-Pen to check the IOP.

Figure 3.13.1. Corneal laceration.

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 Laceration below).Treatment A cycloplegic (e.g., scopolamine 0.25%) and an antibiotic [e.g., frequent polymyxin B/ bacitracin ointment (e.g., Polysporin) or fluoroquinolone drops, depending on the nature of the wound]. 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 avoid excessive scarring and corneal irregularity, especially in the visual axis.

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

Tetanus toxoid for dirty wounds (see Appendix 2, Tetanus Prophylaxis).Follow-UpReevaluate daily until the epithelium heals.Full-Thickness Laceration(See Figure 3.13.2.)See 3.14, Ruptured Globe and Penetrating Ocular Injury. Note that small, self-sealing, or slow-leaking lacerations may be treated with aqueous suppressants, bandage soft contact lenses, fluoroquinolone drops q.i.d., and precautions as listed in 3.14. Alternatively, a pressure patch and twice-daily antibiotics may be used. Avoid topical steroids. If an IOFB is pres-ent, see 3.15, Intraocular Foreign Body.3.14 Ruptured Globe and Penetrating Ocular InjuryRuptured Globe and Penetrating Ocular InjurySymptomsPain, decreased vision, loss of fluid from eye. History of trauma, fall, or sharp object entering globe.Signs(See Figure 3.14.1.)Critical. Full-thickness scleral or corneal laceration, severe subconjunctival hemorrhage P.40

(especially involving 360 degrees of bulbar conjunctiva, often bullous), a deep or shallow AC compared to the fellow eye, peaked or irregular pupil, iris TIDs, lens material in the AC, foreign body tract in the lens, or limitation of extraocular motility (greatest in direction of rupture). Intraocular contents may be outside of the globe.

Figure 3.14.1. Ruptured globe showing flat anterior chamber, iris prolapse, and peaked pupil.

Other. Low IOP (although it may be normal or increased), iridodialysis, cyclodialysis, hyphema (i.e., clotted blood in AC), periorbital ecchymosis, vitreous hemorrhage, dislocated or subluxed lens, and traumatic optic neuropathy. Commotio retinae, choroidal rupture, and retinal breaks may be seen but are often obscured by vitreous hemorrhage.Work-Up/TreatmentOnce the diagnosis of a ruptured globe is made, 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 the intraocular contents. Diagnosis should be made by penlight, or if possible, by slit-lamp examination (with very gentle manipulation). Once the diagnosis is made, then the following measures should be taken: Protect the eye with a shield at all times. Obtain CT scan of the brain and orbits (axial and coronal views, 1-mm sections) to rule out IOFB in most cases. Gentle UBM may be needed to localize posterior rupture site(s) or to rule out intraocular foreign bodies not visible on CT scan (nonmetallic, wood, etc.). However, UBM should not be done in patients with an obvious anterior rupture for the risk of extrusion of intraocular contents. A trained ophthalmologist should evaluate the patient before UBM or other manipulation is performed on a ruptured globe suspect. Admit patient to the hospital with no food or drink (NPO). Place patient on bed rest with bathroom privileges. Avoid bending over and Valsalva maneuvers. 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. Also give ciprofloxacin 400 mg p.o./i.v. b.i.d. (fourth-generation fluoroquinolones, such as gatifloxacin 400 mg q.d. or moxifloxacin 400 mg q.d. may have better vitreous penetration). For children