16 Anterior Chamber

165 EPITHELIAL INGROWTH 379.8

(Epithelial Downgrowth)

F. Hampton Roy, MD, FACS

●Photocoagulation can confirm the diagnosis, but surgery should follow promptly because photocoagulation causes moderate anterior chamber inflammation.

●Iris biopsy or corneal endothelial curettage provides histologic confirmation.

Little Rock, Arkansas

ETIOLOGY/INCIDENCE

Epithelial ingrowth in a sheet-like fashion is a rare and problematic complication of ocular trauma or anterior segment surgery. Factors contributing to its presence include postoperative wound leak, hypotony, prolonged inflammation, and the presence of any external ‘wick’ into the eye. Fortunately, the incidence of epithelial ingrowth after surgery has decreased from 1% around 1960 to less than 0.1%.

Differential diagnosis

●Anteriorly shelved cataract incision, seen as a diagonal intrastromal line on slit-lamp examination.

●Fibrous ingrowth, distinguished by its slow growth and vascularity.

●Vitreocorneal adhesions, which can have a grayish color and cause overlying corneal edema.

●Detachment of Descemet’s layer.

●Peripheral corneal edema due to endothelial cell loss from surgery or trauma.

●Reduplication of Descemet’s layer, which can grow to involve the posterior cornea, angle, and iris; however, the photocoagulation test is negative.

The diagnosis of epithelial ingrowth, which is often delayed, is based on a constellation of signs and symptoms, together with awareness of the importance of early diagnosis; suspicion of the disease allows earlier diagnosis and attempt at surgical treatment.

Clinical signs and symptoms

●The onset is insidious, usually occurring within 3 years after surgery or trauma.

●The patient has tearing; dull, aching pain; photophobia; and blurred vision.

●Wound gape, bleb, or fistula may be revealed with 2% fluorescein and light pressure on the eye.

●On the posterior cornea, a translucent membrane is demarcated by a grayish, often scalloped edge, with focal pearly areas of thickening.

●Diminished corneal sensation, corneal vascularization, edema, or a combination may be present.

●Anterior chamber cells (‘flaky’) and flare often are present.

●Glaucoma is present in half of cases.

●Iris involvement, as indicated by areas of immobility, distor-

tion, and obliteration of detail, can be delineated using argon laser (500-μm spot, 100 mW, 0.1 second); normal iris sustains a slight burn, whereas an epithelial sheet overlying the iris shows fluffy white lesions.

●Festoons of epithelial sheets over the pupil, lens implant, and vitreous face can be seen in advanced cases.

Before surgery, the site of incision, any fistula or bleb, and the exent of iris involvement are determined.

●Local excision consists of fistula repair, vitrector excision of involved iris and vitreous, and removal of the intraocular lens and capsular bag, if present. With an air bubble in the anterior chamber, a single freeze-thaw procedure is applied to areas of involved cornea, sufficient to form ice crystals on the posterior surface. Areas of ciliary body involvement are treated similarly.

●En bloc excision of epithelial sheets has been reported with variable success. A tectonic corneoscleral graft is necessary after this surgical approach.

COMPLICATIONS

●Closure of a leaking fistula in an otherwise inoperable eye can lead to intractable glaucoma.

●Corneal transplantation may be needed after cryotherapy to an extensively involved cornea.

●Epithelial involvement of the angle, iris, and ciliary body may progress while the extent of corneal involvement seems stable; therefore, observation alone with medical treatment is not advocated.

●Vitreous hemorrhage, retinal detachment, glaucoma, and recurrence may complicate excision of ingrowth.

Chamber Anterior • 16 SECTION

REFERENCES

Ghaiy R, Meyer DR, Farber MA: Epithelial downgrowth complicating evisceration with orbital implant exposure. Arch Ophthalmol 123(9):1268– 1270, 2005.

Giaconi JA, Coleman AL, Aldave AJ: Epithelial downgrowth following surgery for congenital glaucoma. Am J Ophthalmol 138(6):1075–1077, 2004.

Kim SK, Ibarra MS, Syed NA, et al: Development of epithelial downgrowth several decades after intraocular surgery. Cornea 24(1):108–109, 2005.

Kuchle M, Green WR: Epithelial ingrowth: a study of 207 histopathologically proven cases. Ger J Ophthalmol 5:211–223, 1996.

Rummelt V, Naumann GO: Block excision with tectonic corneoscleroplasty for cystic and/or diffuse epithelial invasion of the anterior eye segment. Report of 51 consecutive patients. Klin Monatsbl Augenheilkd 211:312– 323, 1997.

Schaeffer AR, Nalbandian RW, Brigham DW, O’Donnell FE, Jr: Epithelial downgrowth following wound dehiscence after extracapsular cataract extraction and posterior chamber lens implantation: surgical management. J Cat Refr Surg 15:437–441, 1989.

Smith PW, Stark WJ, Maumenee AE: Epithelial, fibrous, and endothelial proliferation. In: Ritch R, Krupin T, Shields MB, eds: The glaucomas. 2nd edn. St Louis, CV Mosby, 1996:1325–1361.

Yu CS, Chiu SI, Tse RK: Treatment of cystic epithelial downgrowth with intralesional administration of mitomycin C. Cornea 24(7):884–886, 2005.

166 INTRAOCULAR EPITHELIAL

CYSTS 379.8

Wen-Hsiang Lee, MD, PhD

Baltimore, Maryland

Julia A. Haller, MD

Baltimore, Maryland

Patricia W. Smith, MD

Raleigh, North Carolina

Walter J. Stark, MD

Baltimore, Maryland

ETIOLOGY

Anterior chamber epithelial cysts develop when implanted epithelial cells proliferate centripetally. Cysts have been reported after penetrating trauma, cataract surgery, penetrating keratoplasty, and perforating corneal ulcer, and they may be congenital in origin. Delayed or inadequate wound closure, especially with vitreous or iris incarceration, also contributes to epithelial cyst formation.

COURSE/PROGNOSIS

●Some cysts remain small and stable, others may grow and enlarge rapidly.

●Intervention is indicated if pupillary obstruction, iridocyclitis, secondary glaucoma, corneal decompensation, loss of vision, and intractable pain develop. Prognosis of cysts requiring surgical intervention is variable, depending on how much tissue is affected, choice of surgical technique,

associated complications, and presence or absence of recurrence.

DIAGNOSIS

●A translucent, white or gray cyst in the anterior chamber that often connects at one end with the wound.

●The cyst transilluminates, trembles with eye movement, lacks vascularity, and may demonstrate a meniscus of epithelial cells.

●The epithelial cyst typically indents the iris surface, in contrast to the primary iris stromal cysts that arise from the iris stroma.

TREATMENT

● Small cysts may be observed, often for years, if they are stable and asymptomatic. Surgical intervention is required if complications such as visual axis obstruction, glaucoma, uveitis, and corneal edema arise. Numerous surgical approaches have been reported, including aspiration, radiation, electrolysis, diathermy, injection of sclerosing agents, laser photocoagulation, vitrectomy-assisted cyst excision combined with cryodestruction, and en bloc excision.

●Argon laser photocoagulation has been applied to the pigmented base or the surface of the cyst to shrink the cyst. Limitations of photocoagulation include recurrences requiring repeat treatment, difficulty with anterior cyst wall visualization and treatment, problem with treating some large cysts, and risk of cyst rupture, converting the cyst into sheet-like epithelial ingrowth.

●En bloc excision of large cysts followed by tectonic corneoscleral grafts has been reported and can be successful. However, a more conservative, tissue-preserving, surgical approach may avoid destruction of ocular structures and may lead to better visual outcome.

●A conservative surgical strategy consists of viscodissection of the cyst wall from adjacent ocular structures, aspiration of fluid-filled cyst contents, and endolaser photocoagulation of the collapsed cyst wall and base (Figure 166.1). This may be particularly useful in children in the amblyopia age group, where preservation of the crystalline lens is important.

COMPLICATIONS

●Recurrence of cystic ingrowth, or conversion to sheet-like form of ingrowth.

●Corneas treated with cryotherapy may opacify and require keratoplasty.

●Cataract, hemorrhage, retinal detachment, loss of vision, and loss of eye (especially with more extensive eye wall excisions).

Chamber167AnteriorCHAPTERFlat Postoperative •

Chamber Anterior • 16 SECTION

than 5 mm Hg), even with small choroidal detachment, nearly always resolves spontaneously within 7 to 10 days with no definitive intervention. Most important, activity and strain must be minimized to prevent suprachoroidal hemorrhage in the soft eye. On the other hand, flat anterior chamber associated with hypotony and a leaking conjunctiva or, alternatively, a high intraocular pressure with pupillary block or a massive hemorrhagic choroidal detachment or aqueous misdirection mandates intervention.

DIAGNOSIS

Identification of the pathogenesis is essential to plan the safest and most effective therapy. Occasionally, the appropriate etiologic diagnosis becomes clear only during surgical intervention, so the surgeon must be prepared to follow a logical series of surgical steps to do the least necessary to correct the problem and prevent its recurrence.

The wound should be examined carefully to identify any possible leak. In an eye that does not appear to be extremely soft, the intraocular pressure can be carefully measured with a sterilized applanation tonometer. A hypotonus eye suggests a wound leak or choroidal detachment, whereas a normotensive or firm eye is more suggestive of pupillary block or posterior aqueous misdirection. Pupillary block may also occur with a soft eye if wound leak or choroidal detachment coexists. Prolonged shallow or flat anterior chamber, initially arising from a wound leak or excess filtration, may eventually develop posterior aqueous misdirection as the associated inflammation blocks the access of aqueous humor to the anterior chamber.

Excess aqueous runoff through the filtration site most commonly occurs during the first few days after filtering procedures, resulting in shallowing of the anterior chamber and choroidal detachment, which in turn lead to further flattening of the anterior chamber. With the contemporary practice of ‘no-stitch’ cataract surgery, postoperative wound leaks, inadvertent filtering blebs, and their attendant flat anterior chambers occasionally occur. Pupillary block rarely follows filtration surgery if an adequate iridectomy has been performed. This condition occurs more commonly after cataract surgery, especially with anterior chamber intraocular lenses, when vitreous or lens material can block one or more iridectomies. In some cases, particularly when pupillary block has been allowed to persist, the aqueous humor may be misdirected into the vitreous cavity, driving the vitreous forward and blocking access to both the anterior and posterior chambers, leading to ‘malignant glaucoma.’

Hemorrhagic choroidal detachment also occasionally follows any intraocular procedure, but it is more common in eyes that have had multiple intraocular procedures, especially vitrectomy. Such hemorrhages may occur intraoperatively and be heralded by rapid shallowing of the anterior chamber and prolapse of ocular contents into the wound site. Even patients under local and retrobulbar anesthesia will sometimes have pain. After filtration surgery, hemorrhagic choroidal detachment more commonly occurs during the early postoperative period rather than during surgery, and again it is heralded by severe pain and loss of vision with flattening of the anterior chamber. These postoperative suprachoroidal hemorrhages occur more frequently than in previous decades because with the availability of adjunctive chemotherapy or tube implants, more high-risk eyes are being subjected to filtration surgery.

Aphakic eyes that have undergone vitrectomy are especially prone to suprachoroidal hemorrhage after filtration surgery. Although most suprachoroidal hemorrhages will absorb spontaneously, prompt diagnosis will permit the institution of appropriate therapy that can save vision.

Differential diagnosis

●Low intraocular pressure.

●Wound or bleb leak.

●Excess aqueous humor runoff.

●Serous choroidal hemorrhage.

●High/normal intraocular pressure.

●Massive serous or hemorrhagic choroidal detachment.

●Aqueous humor misdirection.

TREATMENT

Ocular

Appropriate therapy for the flat anterior chamber depends entirely on correct determination of its pathogenesis. Wound leaks usually require surgical repair, but very tiny wound leaks sometimes heal spontaneously with a pressure dressing and the administration of aqueous suppressants to reduce aqueous flow. Absorbable collagen shields or large-diameter soft contact lenses may also successfully tamponade a slowly leaking bleb until it heals with endogenous fibrosis.

When a flat anterior chamber results from excess filtration, tamponade with a Simmons scleral shell or hydrogel largediameter contact lens applied with or without a pressure dressing often is useful if applied before extensive choroidal detachment is well established (see Surgical for management of choroidal detachment). The anterior chamber usually deepens within 2 to 3 hours, but the tamponade should then be left in place for at least 48 hours. Mydriasis and cycloplegia are also helpful to retrodisplace the lens-iris diaphragm and prevent complicating pupillary block.

Pupillary block rarely follows filtration surgery if an adequate iridectomy has been performed; it more commonly occurs after cataract surgery or after filtration in aphakic or pseudophakic eyes. These eyes invariably require a laser or surgical iridectomy, but the attack should initially be broken medically to reduce the intraocular pressure and to allow clearing of the cornea. Mydriasis should be achieved with 1% cyclopentolate plus 2.5% phenylephrine. Vitreous dehydration with osmotic agents, such as oral glycerin, oral isosorbide, or intravenous mannitol, is also useful in combination with ocular mydriatic/ cycloplegic agents to reverse some cases of pupillary block and posterior entrapment of aqueous humor.

A flat anterior chamber, associated with visible patent iridectomy, a high intraocular pressure, and a visible red fundus reflex, should raise the specter of posteriorly entrapped aqueous humor (aqueous misdirection) or malignant glaucoma. In previous years, these cases required surgical intervention, and the diagnosis often was made with the patient on the operating table. Currently, eyes with malignant glaucoma, which are aphakic or pseudophakic, are more typically treated in the office with the neodymium-YAG laser. The vitreous face appears to be tightly adherent to the entire posterior surface of the posterior capsule, the intraocular lens, and the iris, and the vitreous appears to be bulging forward through a patent iridectomy. Careful slit-lamp examination of the vitreous cavity reveals vitreous fibrils pressed densely against the posterior capsule or anterior hyaloid face, with clear fluid-containing space entrapped

posteriorly. In some cases, these findings can be confirmed by ultrasonic examination. Disruption of the anterior and posterior vitreous surface with the YAG laser allows a pathway for posteriorly entrapped aqueous humor to enter the anterior chamber and exit the eye. This neodymium-YAG laser ‘vitrotomy’ results in dramatic deepening of the anterior chamber and lowering of intraocular pressure. Malignant glaucoma in the phakic eye is more difficult to treat with YAG vitrotomy because of poor visibility; it usually requires surgical intervention with vitrectomy.

Vitreous dehydration with osmotic agents, such as oral glycerin, oral isosorbide, or intravenous mannitol, is useful in combination with ocular mydriatic/cycloplegic agents to reverse some cases of pupillary block and posterior aqueous entrapment.

Surgical

Wound leaks usually should be repaired surgically. Small focal or diffusely oozing leaks from filtering blebs may be tamponaded temporarily with the large soft contact lenses while natural wound-healing mechanisms fill in the offending defects. Filtration blebs leaking substantially associated with a flat anterior chamber usually must be repaired surgically. Tapered noncutting needles with 10-0 suture material permit surgical closure with minimal further disruption of delicate conjunctiva. Leaking cystic blebs at the limbus may be excised locally, sliding adjacent conjunctiva over to cover the resultant defect. To provide a smooth limbal area and to firmly anchor the new conjunctiva, a very small corneal-scleral groove can be prepared to recess the conjunctival flap edge for suturing.

In the absence of a wound leak, surgical anterior chamber reformation after filtering surgery almost always includes drainage of suprachoroidal fluid from a choroidal detachment. Most moderately shallow anterior chambers after filtering surgery will reform spontaneously without any intervention. Deepening the chamber at the slit-lamp examination is rarely necessary and subjects the patient to the risk of infection and lens injury.

If surgical intervention must be undertaken for suprachoroidal detachment, it is best performed with good anesthetic control and visibility in an operating room. After the anterior chamber is surgically reformed through a corneal paracentesis wound, suprachoroidal fluid should be drained completely from two inferior posterior sclerotomies. If no suprachoroidal fluid is present and the anterior chamber remains flat, especially with increased intraocular pressure, pupillary block or posterior misdirection of aqueous humor is likely to be present. In this case, an additional peripheral iridectomy should be performed. If the anterior chamber remains shallow even after peripheral iridectomy, malignant glaucoma from posterior diversion of aqueous humor is the most likely diagnosis. In this case, liquid vitreous may be aspirated through the pars plana as described by Chandler in 1949 and Simmons in 1972 or, even better, through a vitrectomy, performed via the pars plana in phakic eyes if visibility permits or through the limbus in the aphakic eye.

If pupillary block is strongly suspected, the safest procedure probably is laser iridotomy. An incomplete iridectomy is readily opened with an argon laser applied to the underlying intact iris pigment epithelium. An occluded iridectomy requires additional laser iridectomies to be placed. Two iridotomies, one on each side of the intraocular lens, should be performed in patients with pupillary block associated with anterior chamber intraocular lenses.

COMPLICATIONS

●Anterior synechia.

●Angle-closure glaucoma.

●Corneal decompensation.

●Cataract.

●Tractional retinal detachment.

●Hypotony.

●Cystoid macular edema.

REFERENCES

Arevalo JF, Garcia RA, Fernandez CF: Anterior segment inflammation and hypotony after posterior segment surgery. Ophthalmol Clin North Am 17(4):527–537, 2004.

Azuara-Blanco A, Dua HS: Malignant glaucoma after diode laser cyclophotocoagulation. Am J Ophthalmol 127(4):467–469, 1999.

Beigi B, O’Keefe M, Algawi K, et al: Sulphur hexafluoride in the treatment of flat anterior chamber following trabeculectomy. Eye 11(Pt 5):672–676, 1997.

Gressel MG, Parrish RK, II, Heurer DK: Delayed nonexpulsive suprachoroidal hemorrhage. Arch Ophthalmol 102:1757–1760, 1984.

Shields MB: Trabeculectomy vs. full-thickness filtering operation for control of glaucoma. Ophthalmic Surg 11:498–505, 1980.

168 TRAUMATIC HYPHEMA 921.3

Bahram Rahmani, MD, MPH

Chicago, Illinois

ETIOLOGY/EPIDEMIOLOGY

Hyphema is an accumulation of blood in the anterior chamber of the eye. Trauma is the most common cause of hyphema, although bleeding may occur spontaneously in conditions such as rubeosis iridis, leukemia, hemophilia, anticoagulation therapy, retinoblastoma or juvenile xanthogranuloma of the iris. Presence of hyphema can be a sign of associated damage to other intraocular tissues which is usually the cause of poor vision after the resolution of the hyphema.

Mean annual incidence of traumatic hyphema is about 17 per 100,000 population. Patients with traumatic hyphema are predominantly male with a median age below 20 years of age. The majority of traumatic hyphema occurs in the pediatric population. Direct injury resulting in traumatic hyphema in adults usually consists of a high-energy blow to the orbit or blunt trauma to the cornea and eyeball from a finger or a fist, while a low velocity missile such as a rock, a ball or a stick is commonly responsible for hyphema in children. Lack of protective eyewear in sports is a predisposing factor and the current literature suggests that further education of workers, athletes and parents, along with an increase in the use of polycarbonate safety lenses, may decrease the incidence rate of traumatic hyphema. Hyphema may also occur with penetrating injuries of the globe, but here we consider the management of hyphema that occurs after closed globe trauma.

COURSE/COMPLICATIONS

Sudden contusion and posterior displacement of the iris/lens complex results in a tear and bleeding from the iris and/or

168 CHAPTERHyphema Traumatic •

Chamber Anterior • 16 SECTION

child abuse or are noncompliant or unable to make frequent office visits.

Cycloplegia/NSAID

Most studies have shown that cycloplegia has no effect on the rate of rebleeding, but it dilates the pupil, relaxes the ciliary body and iris and prevents stress on their injured blood vessels. Cycloplegia decreases the inflammation and patient’s discomfort from associated traumatic iritis. Instillation of one drop of atropine at the time of first encounter provides adequate cycoplegia while avoids the manipulation and trauma of regular application of short acting cycloplegics.

Numerous studies have suggested the deleterious effect of aspirin in increasing the rate of rebleeding and most practitioners discontinue aspirin and other nonsteroidal anti-inflamma- tory agents in the face of a hyphema.

Antiglaucoma drugs

Elevated IOP is common in post traumatic period and may lead to optic atrophy and corneal blood staining. The main cause is thought to be the blockage of the inflamed trabecular meshwork by the red blood cells and inflammatory debris. Sickled cells block the meshwork and elevate the pressure more than normal erythrocytes.

Topical beta-adrenergic antagonists are usually the first choice for controlling the IOP. Topical and oral carbonic anhydrase inhibitors (CAI), hyperosmotic agents and topical alpha adrenergic agonists are also used with caution. One should avoid systemic acidosis or excessive hemoconcentration in sickle cell disease. Prostaglandin analogs and miotics may worsen the inflammation and caution should be exercised in using them in patients with traumatic hyphema.

Corticosteroids

By stabilizing the blood–ocular barrier and inhibiting fibrinolysis, corticosteroids might reduce the risk of secondary hemorrhage. Some studies, many of them not randomized, have demonstrated the effectiveness of the oral prednisone in the reduction of the rate of rebleeding in traumatic hyphema using the Yasuna’s protocol. This protocol uses 40 mg/day of oral prednisone for adults and corresponding 0.6 mg/kg/day in divided doses for children. However, the randomized clinical trials using oral prednisone have shown variable results. Although in most of the studies, the rate of rebleeding was less in the group treated with oral prednisone compared to the control; this difference has failed to reach a statistically significant level in some reports.

Topical corticosteroids have shown to reduce intraocular inflammation and may prevent the secondary hemorrhage. They may be recommended for adults with traumatic hyphema to reduce the associated iritis and prevent posterior synechiae, but in children, it is better to start them only on the fifth day of a retained hyphema or persistant iridocyclitis.

Antifibrinolytics

Topical and systemic antifibrinolytic agents such as aminocaproic acid (ACA) and tranexamic acid may be used in traumatic hyphema to reduce rebleeding. They inhibit fibrinolysis and stabilize the blood clot and allow the injured bleeding vessel more time to heal and prevent further bleeding. The current recommended dose for oral ACA is 50 mg/kg every 4 hours, up to 30 gm/day for 5 days. Topical ACA ointment is also applied to the affected eye every 4 hours for 5 days. Patient receiving oral ACA is usually admitted to the hospital, owing to the

potential side effects which include nausea, muscle weakness, abdominal cramps and hypotension. Topical ACA does not appear to have the systemic side effects and seems as effective as the oral form in lowering secondary hemorrhage risk and may be appropriate for the outpatient management. Oral dosage of tranexamic acid is 75 mg/kg per day divided into 3 doses. Tranexamic acid is more potent and has less systemic side effects compared to the ACA but has not yet been approved for ophthalmic use in the United States. Both ACA and tranexamic acid should be avoided in pregnant patients, patients with renal or hepatic dysfunction, or those at risk of thromboembolic disease.

Special considerations

Patients with sickle cell anemia or trait require a much more aggressive treatment than other patients. The red blood cells can sickle in the anterior chamber and impede the outflow of the aqueous from the trabecular meshwork. This will elevate the IOP, worsen the hypoxia and sickling and may lead to a refractory glaucoma. These patients are at risk of vaso-occlusive disease and even mild elevation of the IOP can lead to optic atrophy and permanent visual loss. Medical management of glaucoma should be aggressive and keep the IOP below 25 mm Hg, otherwise surgical intervention may be indicated. A beta-adrenergic antagonist is the drug of choice, but carbonic anhydrase inhibitors and hyperosmotic agents can be used. Caution should be applied to avoid acidosis that can predispose to sickling.

In the past, admission to the hospital was indicated for all children with traumatic hyphema. Recently patients treated as outpatient have been reported to have final visual outcome comparable to the inpatient. Still the patients who are suspected of rebleeding or child abuse or being noncompliant, have large hyphema (>50%) or sickle cell hemoglobinopathy or uncontrolled elevation of IOP, have to be admitted and managed as inpatient.

SURGICAL MANAGEMENT

Medical management of total hyphemas is preferable for the initial 4 days if one can control the IOP satisfactorily with medications and there is no corneal blood staining. Hyphema evacuation is recommended in the following situations:

●Mean IOP greater than 24 mm Hg for more than 24 hours in a patient with sickle cell disease.

●IOP greater than 50 mm Hg for 5 days (to prevent optic atrophy).

●IOP greater than 25 mm Hg with a total hyphema for 5 days (to prevent corneal blood staining).

●Any corneal blood staining.

●The hyphema that fails to resolve to less than 50% of the anterior chamber volume by 8 days (to prevent peripheral anterior synechiae).

Definitive clot evacuation is done in the operating room and different techniques may be used to remove the clot and/or control the elevated IOP. Clot expression and delivery through a limbal incision is advocated after day 4, when clot lysis and retraction is at its peak. Vitrectomy probe with or with out viscoelastics may be used in the anterior chamber to remove the clot when dealing with a subtotal hyphema. Instruments should not be introduced to the anterior chamber with out good visualization and a clot that adheres firmly to the iris should

168 CHAPTERHyphema Traumatic •

Chamber Anterior • 16 SECTION

not be removed. Intracameral tissue plasminogen activator injection may be considered as an adjuvant therapy in eyes with persistent elevated IOP and total hyphema, although it may increase the risk of bleeding.

Trabeculectomy combined with manual clot expression may be an effective alternative, particularly in patients with very high IOP and total hyphema, compromise in the view of the anterior chamber (e.g. corneal bloodstaining) and particular susceptibility to IOP-induced damage (e.g. sickle cell disease). Transcorneal oxygen therapy may reverse the sickling process and reduce the IOP in patients with sickle cell disease.

Corneal blood stain may take several months to years to clear, so penetrating keratoplasty may be considered in children who have significant staining and are at high risk of amblyopia.

SUMMARY

Initial bleeding

Initial encounter

●Complete medical and ocular history and medications; check for sickle cell disease/trait (patients with black ancestry), pregnancy, renal insufficiency, thromboembolic disease, bleeding disorder and anticoagulation history.

●Complete ocular examination; record the level and amount of hyphema, check for elevated pressure or corneal blood stain, avoid checking IOP of noncompliant children.

●Defer gonioscopy and scleral depression for 7 days.

●Outpatient daily examination for qualified patients; Patients who are noncompliant (e.g. late presentation), high risk (e.g. sickle cell disease, large hyphema or elevated IOP) or have associated ocular/systemic injuries and most of the children should be treated as inpatient.

●Elevate the patient’s head 30 degrees.

●Replace clotting factors and platelets if indicated.

●Apply patch and metal shield to the injured eye (only shield in very young patient).

●Limited activity.

●Atropine 0.5–1% 1 drop in traumatized eye (only once).

●Stop aspirin or other NSAID medicine.

●Acetaminophen and antiemetics if indicated.

●Start:

●Prednisone 40 mg/day for adults or 0.6 mg/kg/day PO for children in 2 divided doses for 5 days (not recommended in diabetes, peptic ulcer disease or systemic infection). Topical prednisolone acetate 1% Q4H for 5 days if oral prednisone is not used (not recommended in children).

Or:

●Topical 30% Aminocaproic acid gel Q6H or oral Tranexamic acid 75 mg/kg per day divided into 3 doses for 5 days are the other alternatives but are not approved by the FDA.

●Treat elevated IOP with topical timolol and/or oral/topical CAI; may add hyperosmotic agents with caution.

Subsequent encounters

●Daily examination for rebleeding; record vision, level of hyphema and corneal clarity. Check IOP if clinically indi-

cated or in high risk patients (e.g. sickle cell disease). Patients with sickle cell disease or elevated IOP may need frequent evaluation.

●Treat elevated IOP if indicated.

●Consider surgical removal of the hyphema if there is:

●Any sign of corneal blood staining or high risk of its development (large hyphema >50% of the anterior chamber with pressure >25 mm Hg for 6 days or >4 days of total hyphema);

●High risk of synechiae formation (large hyphema >50% of the anterior chamber for >8 days);

●High risk of optic atrophy (IOP > 24 mm Hg for >24 hours in sickle cell disease, IOP > 60 mm Hg for >2 days or >50 mm Hg for 5 days).

Secondary bleeding

●Admit the patient to the hospital if not already admitted.

●Consider the rebleeding as a new hyphema and continue the daily examination and treatment for at least 5 more days.

●All of the criteria for initial management of the hyphema apply to the management of the secondary bleeding.

Follow up

●Long term follow up of the hyphema patient is indicated for the detection of the late onset complications such as cataract and secondary glaucoma.

REFERENCES

Crouch ER, Jr, Frenkel M: Aminocaproic acid in the treatment of traumatic hyphema. Am J Ophthalmol 81:355–360, 1976.

Farber MD, Fiscella R, Goldberg MF: Aminocaproic acid versus prednisone for the treatment of traumatic hyphema. Ophthalmology 98:279–286, 1991.

Goldberg MF: The diagnosis and treatment of sickled erythrocytes in human hyphema. Trans Am Ophthalmol Soc 76:481–501, 1978.

Nasrullah A, Kerr NC: Sickle cell trait as a risk factor for secondary hemorrhage in children with traumatic hyphema. Am J Ophthalmol 123:783– 790, 1997.

Rahmani B, Jahadi HR: Comparison of tranexamic acid and prednisolone in the treatment of traumatic hyphema: a randomized clinical trial. Ophthalmology 106:375–379, 1999.

Rahmani B, Jahadi HR, Rajaeefard A: An analysis of risk for secondary hemorrhage in traumatic hyphema. Ophthalmology 106:380–385, 1999.

Read J: Traumatic hyphema: surgical vs medical management. Ann Ophthalmol 7(5):659–670, 1975.

Read J, Goldberg MF: Comparison of medical treatment for traumatic hyphema. Trans Am Acad Ophthalmol Otolaryngol 78:799–815, 1974.

Recchia FM, Saluja RK, Hammel K, Jeffers JB: Outpatient management of traumatic microhyphema. Ophthalmology 109:1465–1470, 2002.

Romano PE, Robinson JA: Traumatic hyphema: a comprehensive review of the past half century yields 8076 cases for which specific medical treatment reduces rebleeding 62%, from 13% to 5% (P < 0001). Binocul Vis Strabismus Q 15(2):175–186, 2000.

Rynne MV, Romano PE: Systemic corticosteroids in the treatment of traumatic hyphema. J Pediatr Ophthalmol Strabismus 17:141–143, 1980.

Sears ML: Surgical management of black ball hyphema. Trans Am Acad Ophthalmol Otolaryngol 74:820–826, 1970.

Walton W, Von Hagen S, Grigorian R, Zarbin M: Management of traumatic hyphema. Surv Ophthalmol. 47(4):297–334, 2002.

Yasuna E: Management of traumatic hyphema. Arch Ophthalmol 91:190– 191, 1974.