19 Cornea

on a case-by-case basis. If there is no growth or growth of commensals only in the presence of a worsening condition, further investigations for nonbacterial pathogens must be considered.

Antimicrobial susceptibility testing

Susceptibility testing against particular antibiotics is normally performed on all significant bacterial isolates from the cornea.

Differential diagnosis

Subconjunctival injections are usually reserved for scleral and/or intraocular extension of the infection, or in cases with questionable compliance with the treatment regimen.

Initial topical broad-spectrum therapy is recommended until the microorganism is identified in culture. A combination of fortified antibiotic solutions effective against gram-positive and gram-negative bacteria is administered each hour, or even more frequently, for the first 24 hours: a first-generation cephalosporin (cefazolin 50 mg/mL) and gentamicin or tobramycin (9– 14 mg/mL). The antibiotics chosen as initial therapy may be

coccal blepharitis or acute conjunctivitis.

●Toxic keratopathy associated with chemical injury or overuse of topical drugs.

PROPHYLAXIS

Prophylaxis with topical antibiotics is routinely given after traumatic injury to the cornea. An agent with a wide antimicrobial spectrum, such as a fluoroquinolone or chloramphenicol, is recommended. Antibiotic prophylaxis is also given before and/or after corneal surgery, such as transplantation or refractive procedures, but its value in reducing postoperative infection remains controversial.

TREATMENT

Systemic

Systemic administration of antibiotics is not indicated for bacterial keratitis unless structures beyond the cornea are directly involved.

Ocular

The principles of the treatment of bacterial keratitis are to eliminate the replicating etiologic agent with specific antibiotics, to suppress destructive inflammation, and then to withdraw therapy so as not to hinder repair of the cornea.

toxicity and were as effective as a combination of fortified antibiotics. They have excellent activity against most strains of staphylococci, P. aeruginosa, and enteric gram-negative bacilli. S. pneumoniae and other streptococci are less sensitive, and based on in vitro susceptibility, cefazolin may be a better choice for these infections. Although quinolones are effective for most corneal infections in most parts of the world, it is unwise to assume that all keratitis is bacterial and will respond to these agents. Emerging resistance of various strains has been reported. The fourth-generation fluoroquinolones (gatifloxacin and moxifloxacin) possess an expanded spectrum of activity, greater potency, and resistance-thwarting capabilities.

Alternative agents according to culture result or the in vitro susceptibility profile are considered only if there is no favorable clinical response, or toxicity signs from the initial antibiotics (Table 186.1). If no organisms are cultured but the clinical picture suggests an active infection, the concomitant use of a cephalosporin and an aminoglycoside should be continued.

In addition, cycloplegic agents may be used to decrease synechiae formation, and reduce pain and ciliary spasm.

Surgical

Penetrating keratoplasty is indicated if corneal perforation occurs during the course of the disease and the area of necrosis is resectable, or the keratitis is unresponsive to antimicrobial therapy. The infected area should be included in the removed button. The success rate of corneal transplants made under these circumstances is low. When extensive peripheral corneal

necrosis occurs a conjunctival flap after a period of intensive chemotherapy often is the safest course of treatment.

Supportive

Close observation is mandatory. Progression of the condition may be rapid and blinding. Punctilious attention must be paid to treatment schedules. For these reasons, either hospital admission may be necessary or close follow-up is performed.

Wilhelmus KR: Bacterial keratitis. In: Pepose JS, Holland GN, Wilhelmus KR, eds: Ocular infection and immunity. St Louis, Mosby, 1996: 970–1031.

Williams KA, Muehlberg SM, Lewis RF, et al, eds: The Australian Corneal Graft Registry 1996 report. Adelaide, Mercury, 1997.

PRECAUTIONS

The use of topical corticosteroids in bacterial keratitis is controversial. Topical corticosteroids can suppress the inflammation and may reduce subsequent corneal scarring. Studies in animal models suggest that inflammation is inhibited without impairing the clearance of organisms provided an appropriate antibiotic is administered concurrently However, potential specific adverse effects include enhancement of bacterial growth by local immunosuppression, impairment of phagocytosis, or inhibition of collagen synthesis. It is probably safe to suppress anterior segment inflammation with topical steroids after the effectiveness of the antimicrobial therapy has been suggested by a nonprogressive clinical course.

COMMENTS

Continuation of the inflammation or the prolonged use of topical antibiotics can inhibit epithelial closure; thus, intensive medication should be maintained only until the clinical course suggests that bacterial growth is suppressed. Usually, only 2 or 3 days of intensive therapy are necessary, with careful reduction of medication over the next week. It often is possible for patients with a healing epithelial and stromal defect to be off the medication and under close supervision within 10 days.

Positive clinical response includes blunting of the perimeter of the infiltrate and reduction of its density, reduction of the anterior chamber inflammation, stabilization of the stromal thinning and re-epithelialization.

REFERENCES

Badenoch PR, Hay GJ, McDonald PJ, Coster DJ: A rat model of bacterial keratitis: effects of antibiotics and corticosteroid. Arch Ophthalmol 103:718–722, 1985.

Christy NE, Sommer A: Antibiotic prophylaxis of postoperative endophthalmitis. Ann Ophthalmol 11:1261–1265, 1979.

Huang AJW, Wichiensin P, Yang MC: Bacterial keratitis. In: Krachmer JH, Mannis MJ, Holland EJ, eds: Cornea. 2nd edn. Elevier Mosby, 2005:1005–1033.

Hyndiuk RA, Eiferman RA, Caldwell DR, et al: Comparison of ciprofloxacin ophthalmic solution 0.3% to fortified tobramycin-cefazolin in treating bacterial corneal ulcers: Ciprofloxacin Bacterial Keratitis Study Group. Ophthalmology 103:1854–1862, 1996.

McDonnell PJ: Empirical or culture-guided therapy for microbial keratitis? A plea for data. Arch Ophthalmol 114:84–87, 1996.

O’Brien TP, Maguire MG, Fink NE, et al: Efficacy of ofloxacin vs cefazolin and tobramycin in the therapy for bacterial keratitis: report from the Bacterial Keratitis Study Research Group. Arch Ophthalmol 113:1257– 1265, 1995.

Stern GA, Schemmer GB, Farber RD, Gorovoy MS: Effect of topical antibiotic solutions on corneal epithelial wound healing. Arch Ophthalmol 101:644–647, 1983.

187 CONJUNCTIVAL, CORNEAL, OR SCLERAL CYSTS 371.23

(Epithelial Inclusion Cysts, Intrastromal

Corneal Cysts)

James C. Liu, MD, MBA

San Jose, California

ETIOLOGY/INCIDENCE

Intracorneal cysts are rare lesions that have been described after trauma and congenitally. This is a slowly progressive condition in young patients. The eyes are usually quiet and uninflamed. Individual cases were presumed to be congenital in origin, but recent reports have overwhelmingly documented trauma as the most likely cause of corneal cysts. They usually appear after trauma to the cornea or sclera and probably develop from surface epithelium that was implanted in the stroma during the injury. The ectopic epithelium proliferates and enlarges to form a corneal or sclerocorneal cyst, depending on the location of trauma. The desquamated material within the cyst settles and gives the cyst its typical appearance, that of a pseudohypopyon. Therapeutic success and the procedure largely depend on the location of the cyst and the patient’s visual impairment from the cystic lesion. Current discussion does not include epithelial cyst under the corneal flap following laser in situ keratomileusis (LASIK), reader should refer to a LASIK text for its treatment and management.

●The age of the patient at which the cyst is discovered varies significantly because the time of trauma varies.

●Most patients are young, in their first two decades of life. This finding may be attributed to the greater metabolic activity of corneal epithelial cells of young individuals. This enables the epithelium to survive and proliferate when implanted intrastromally.

●There is no gender predilection.

●Although in some cases there is no history of trauma, even minor corneal epithelial injury can cause implantation of epithelium in the stroma with subsequent development of intrastromal cyst, and these minor injuries can be easily forgotten or overlooked.

DIAGNOSIS

Clinical signs and symptoms

●Most patients present with a history of trauma or a previous surgical procedure.

●The vision of the affected eye varies widely on presentation from 20/20 to light perception, depending on the size and location of the cyst.

●The appearance of the cyst depends on the stage of development. In the early stages, the cyst may look like a small

nebulous opacity. In the advanced stages, the cyst becomes oval to round.

●The cyst may be single and round, or multiloculated. The color ranges from clear to opalescent; however, the majority of cysts have a hypopyon-like feature in which cloudy debris settles inferiorly and the top of the cyst is filled with clear fluid.

inflamed or there are signs of corneal edema from endothelial cell damage.

Light microscopic examination of the cysts has been carried out by numerous authors, and the findings have been similar. The surface epithelium and Bowman’s layer were normal. The stroma typically was nonvascularized and noninflamed. Occa-

mal location appears most frequently in reports. It could extend horizontally into the limbus or sclera and posteriorly into the anterior chamber. Rarely, communication with the anterior chamber is formed.

●Isolated intrastromal cysts with no communication with anterior chamber is the hallmark.

●The size varies dramatically from a few millimeters in diameter to covering the entire cornea. The cysts tend to progressively enlarge at a slow pace, usually taking months to years to become noticeable.

●The surrounding tissue of the eye appears white and noninflamed.

●There may or may not be blood vessels around the cyst.

●The epithelial layer of the cornea above the cyst could be normal without fluorescein staining. In other patients, previous trauma may leave an obvious corneal scar over the cyst.

●The cysts typically do not cause significant pain or discomfort.

●Corneal cysts are usually unilateral, although Fox reported a bilateral corneal cyst in one patient.

Laboratory findings

The development of intrastromal corneal cysts represents an aberration of the normal wound-healing process. After the penetrating or perforating laceration to the cornea, edema of the corneal stroma and fibrin plug formation usually occur. Later, fibroplastic proliferation into the clot begins with the adjacent stromal cells. This fibrous reaction forms a linear scar, and posteriorly to the endothelium it extends across the wound and lays down a thin membrane. On the anterior surface, as the wound heals, the initial epithelial downgrowth between the wound edges is gradually pushed toward the surface by the fibrous scar. Occasionally, epithelium becomes sequestered and isolated within the corneal stroma. Early authors speculated on different congenital and embryonic causes of the development of these cysts. When more recent reports are examined, the concept of congenital origin appears doubtful. These cysts are usually unilateral and are not associated with other congenital anomalies. They are not inherited, and they have a similar appearance to cysts of known traumatic cause. Therefore, the congenital origin of corneal cysts is very unlikely. The inciting trauma in these cases may be relatively minor, such as a pencil, a pen, scissors, or other sharp objects. Minor injuries heal quickly, cause minimal symptoms, and may go unnoticed until the cysts reach a clinically significant size.

●In most recent reported cases, a history of corneal trauma is well documented, ranging from minor corneal ulceration to severe trauma causing hyphema and cataracts.

cells lining the cysts varied in morphology, ranging from squamous to columnar and from one cell thick to multilaminar. The anterior cystic cells tend to be flattened or squamous, whereas the posterior cells are rounder or columnar. The epithelial cells were quiet without any signs of inflammation or malignant transformation. Desquamated cells were present in the cyst. There were no glandular structures or hair follicles.

TREATMENT

The treatment of intracorneal cysts depends on the depth, size, and location of the cyst at the time of diagnosis.

●The conservative approach is advised if the cyst does not involve the pupil or central cornea and if the patient still has good vision.

●Simple observation is prudent. These cysts are indolent and enlarge slowly or not at all over the years. Spontaneous reabsorption of the cysts has been reported; however, in these cases, the cysts most likely rupture into the anterior chamber. Others have reported very slow enlargement or no change in the size of the cyst for as long as 6 years.

●When the cyst has achieved a significant size or if it is near the pupillary axis and affects visual acuity, a definitive procedure should be considered.

●A simple incision and drainage procedure or needle aspiration has no permanent effect. These procedures have been tried repeatedly, and the result has been the same; the cysts invariably refill over time.

●Marsupialization through removal of a portion of the anterior wall of the cyst followed by destruction of the epithelial cell with chemical cautery is highly successful. Different chemical solutions have been used for the destruction of epithelial cells, including 10% acetic acid, 1% trichloroacetic acid, 1% iodine and cocaine.

●After chemical cauterization of the cavity, fine temporary sutures, such as 10-0 nylon, may be used to hold the walls of the cavity together until they have sealed. This suture is tied on the corneal surface and the knots are rotated into the stroma. This suture can be removed after 3 weeks with the marsupialization technique.

The marsupialization technique usually provides a high rate of success; in reported cases, the cysts either were destroyed completely or decreased significantly in size. Marsupialization could be difficult if the cyst is deep and centrally located; to provide visual rehabilitation in these cases, penetrating keratoplasty is the best procedure. During penetrating keratoplasty, the surgeon must avoid spilling the cyst contents into the ante-

REFERENCES

Al-Rajhi A, Al-Kharashi S: Epithelial inclusion cyst following epikeratoplasty. J Refract Surg 12:516–519, 1996.

Avni I, Cahane M, Blumenthal M, Naveh N: Transformation of corneal epithelial cyst into anterior chamber implantation cyst and scleral cyst: A rare occurrence. J Pediatr Ophthalmol Strabismus 26:303–306, 1989.

Binder PS, Beale JP, Zavala EY: The histopathology of a case of keratophakia. Arch Ophthalmol 100:101–105, 1982.

Bloomfield SE, Jakobiec FA, Iwamoto T: Traumatic intrastromal corneal cyst. Ophthalmology 87:951–955, 1980.

Chan MY, Liao HR, Fong JC: Traumatic intracorneal cyst. Am J Ophthalmol 21:303–305, 1989.

Claiborne JH: Epithelial corneal cyst. Transam Ophthalmol 10:588–593, 1984.

Fox LW: Bilateral cysts of the cornea. Br J Ophthalmol 12:249–254, 1928.

Jester JV, Villasenor RA, Miyashiro J: Epithelial inclusion cysts following radial keratotomy. Arch Ophthalmol 101:611–615, 1983.

Liakos GM: Intracorneal and sclerocorneal cysts. Br J Ophthalmol 62:155– 158, 1978.

Purcell J, Brady H: Intrastromal epithelial corneal cyst. Ophthalmic Surg 14:491–499, 1983.

Reed JW, Dahlman CH: Corneal cyst: a report of 8 cases. Arch Ophthalmol 86:648–652, 1971.

Vrolijk M: Corneoscleral cyst. Acta Ophthalmol 19:44–51, 1941.

Wood T: Corneal intrastromal cyst. Ann Ophthalmol 8:967–968, 1976.

Yee RD, Hit TH: Corneal intrastromal cyst following lamellar keratoplasty. Am J Ophthalmol 7:644–646, 1975.

188 CORNEAL ABRASIONS, CONTUSIONS, LACERATIONS 918.2, AND PERFORATIONS 370.06

Guruswami Arunagiri, MD, FRCSEd

Danville, Pennsylvania

Rupan Trikha, MD

Danville, Pennsylvania

Corneal abrasions

Corneal abrasion is the loss of part or all of the corneal epithelium, from direct or indirect injury. It is one of the most common reasons for new patient visits to the ophthalmic emergency room.

ETIOLOGY

●Mechanical: fingernail, paper, foreign body, curling iron, mascara brush, plant, and contact lens.

●Chemical: hair sprays, alkali and acid exposure.

●Iatrogenic: eye patching, tonometry, ocular surgery, general anesthesia.

●Others: heat, ultraviolet light.

●Symptoms may be delayed for several hours with ultraviolet keratitis or contact lens related injury.

Clinical signs

●Visual acuity is decreased due to excessive tearing or abrasion in the visual axis.

●Conjunctival erythema, chemosis and lid edema can occur in severe cases.

●Using a slit lamp, the edges of the abrasion can be visualized with direct illumination and scleral scatter techniques.

●Corneal light reflex is blunted due to surface irregularity.

●Initially, an epithelial defect is present with clear underlying stroma. A very mild stromal infilatrate may be present with minimal anterior chamber cell and flare reaction 12 to 24 hours later.

●Fluorescein dye with a cobalt-blue light filter will enhance visualization of the abrasion.

●Topical anesthetics may be used if pain and photophobia limit examination.

●Multiple, vertical, linear corneal abrasions are usually due to an upper lid palpebral foreign body and examination by lid eversion should be performed.

●Stromal abrasions are rare and due to trauma from a sharp or abrasive object. Most commonly seen with fingernail injury in sports. Often a corneal flap of varying thickness may be seen. These injuries take longer to heal, and are often associated with edema below the involved area.

●Atypical presentations or cases not involving trauma require consideration of other causes, especially herpes simplex epithelial keratitis.

●High velocity objects can penetrate the cornea and leave minimal evidence except a small epithelial defect.

TREATMENT

●Antibiotic prophylaxis with a broad-spectrum antibiotic (e.g. fluroquinolone, polysporin, erythromycin) is recommended in all cases, and may be in the form of an ointment or solution.

●For contact lens wearers, an antibiotic with pseudomonal coverage (e.g. fluroquinolone) should be used.

●Cycloplegic agents (e.g. cyclopentolate, homatropine) reduce discomfort from traumatic iritis. Topical nonsteroidal antiinflammatory drug drops can also be used for pain control (e.g. diclofenac, ketorolac).

●Oral non-narcotic or narcotic analgesia is rarely required.

●Steroid use for iritis in this setting is not recommended as it can hinder epithelial healing and increase risk of infection.

●Eye patch use is controversial and should not be used in patients with history of contact lens use or injury involving vegetable matter.

●Bandage soft contact lenses (BSCL) are very effective in reducing pain, but should only be used with topical antibiotic coverage. BSCL use is contraindicated in cases involving vegetable matter or artificial fingernails.

●Follow up examination should be performed at every 2–5 days, and sooner for high-risk cases, until the epithelial defect has healed.

●Infection.

●Corneal scaring.

●Recurrent corneal erosions:

●Occur due to poor adhesion of epithelium to underlying basement membrane;

●Treatment is the same as for any corneal abrasion;

●Prevention involves long-term lubrication with ointment at bedtime;

●In persistent cases, superficial keratectomy or micropuncture may be necessary for resolution.

Corneal contusions

Corneal contusion results from blunt trauma to the cornea without penetration of the ocular surface.

ETIOLOGY

Common causes include injury with rubber bands, bungee cords, automobile airbags and BB gun pellets.

DIAGNOSIS

●Symptoms: pain, photophobia, and decreased vision.

●Signs:

●Focal edema at the site of impact, or rarely diffuse corneal edema with severe endothelial damage;

●Breaks in Descemet’s membrane can occur from severe stretching and bending of the cornea;

●Rarely, endothelial rings composed of damaged endothelial cells, fibrin, and leukocytes, surrounded by normal endothelium may be present. These resolve within a few days;

DIAGNOSIS

History is crucial in the diagnosis and for medical-legal reasons.

Information should be obtained of the time and place of injury, as well as the activity being done, uses of safety glasses, first aid measures undertaken, and additional injuries that occurred.

●Symptoms: eye pain, tearing, bleeding, foreign body sensation, photophobia, and decreased vision.

●Evaluation:

●Visual acuity should be measured with pinhole or corrective lens when possible;

●A wire lid speculum is useful when there is significant chemosis and ecchymosis;

●External pressure or manipulation of foreign bodies at the site of laceration should be avoided;

●Location, size, depth of the laceration, and prolapse of intraocular tissue should be noted. With prolapse of intraocular tissues, further examination is deferred until surgery;

●Seidel test using fluorescein with cobalt blue light may be necessary to identify occult leakage of aqueous;

●Further examination for lid laceration, hyphema, iritis, iridodialysis, disruption of the lens capsule and cataract, vitreous hemorrhage, intra-ocular foreign body must be done;

●In suspected cases of intra-ocular foreign body, CT scan or ultrasound in expert hands is recommended.

TREATMENT

sis, angle recession, traumatic cataract, vitreous hemorrhage, choroidal rupture, retinal detachment, and commotio retina.

TREATMENT

Treatment of corneal contusions is initially conservative. In most cases the cornea regains its clarity in a few days, in spite of permanent endothelial cell loss.

●Topical steroid drops (e.g. Prednisolone Acetate) and hypertonic saline solutions (e.g. Hypertonic sodium chloride drops) have been used with little benefit.

●Penetrating keratoplasty is indicated for persistent corneal edema or stromal scar.

●Associated ocular injuries such as listed above should be managed appropriately.

Corneal laceration 918.2

ETIOLOGY

Corneal lacerations result from a sharp object that cuts through corneal tissue. A common cause includes high-speed pieces of material released when grinding or cutting metal, wood, glass, or plastic.

full thickness.

●All patients require prophylaxis with broad-spectrum topical antibiotic (e.g. fluroquinolone) and a cycloplegic agent (e.g. homatropine, cyclopentolate).

●Partial thickness laceration:

●Medically treated with topical broad-spectrum antibiotics with or without a cycloplegic agent;

●Deep partial thickness lacerations may be sutured to reduce scaring, and risk of rupture.

●Full thickness lacerations:

●For lacerations less than 2 mm and with minimal tissue loss, a bandage contact lens with or without cyanoacrylate glue (not FDA approved) may be used;

●Lacerations larger than 2 mm or with tissue loss are repaired surgically. A shield is placed over the injured eye to prevent further damage, and the patient kept NPO.

●Use of systemic antibiotics is controversial. We give systemic antibiotics (ceftazidime and vancomycin) in the setting all full thickness corneal lacerations. Most agree with use of systemic prophylaxis in the presence of an intraocular foreign body.

●Antiemetic agents (e.g. promethazine, metaclopramide) should be used as needed to prevent Valsalva.

●Tetanus toxoid is recommended for all full thickness wounds.

●Postoperatively, patients are prescribed polycarbonate safety glasses for constant use to avoid injuries to either eye.

Surgical technique

Surgical repair in penetrating wounds should be performed in the operating room with general anesthesia. Depolarizing agents like succinylcholine, and retrobulbar anesthesia is avoided to prevent co-contraction of extraocular muscles and extrusion of intraocular contents.

A detailed description of surgical technique is beyond the scope of this chapter. The primary goal of surgery is to restore the anatomic integrity of the globe. Visual restoration is only secondary.

General principles for repair

●Use 10-0 nylon for suturing.

●Sutures are placed at 90% depth on both sides of the wound.

●Suturing should be watertight, and induce minimal scarring or astigmatism.

●Limbal or peripheral sutures are placed first. Wider spaced, long compressive sutures are applied peripherally to maintain flatter curvature.

●Suturing in the visual axis should be avoided, but if needed, short, minimally compressive sutures are applied to maintain steeper curvature.

●Knots should be trimmed and buried away from the visual axis.

●For perpendicular wounds, the length of each suture pass should be symmetrical from the anterior surface of the cornea.

●For oblique wounds, length of suture pass should be symmetrical from the posterior surface of the cornea. For combination wounds the perpendicular wounds are closed first.

●Watertight closure of the wound may be difficult in cases of tissue loss, puncture wounds, or unusual lacerations. In these cases, a X-shaped suture may be placed. Corneal patch or lamellar graft, or primary penetrating keratoplasty can be considered in severe or difficult cases.

●In traumas that are less than 24 to 36 hours with no signs of infection, viable uvea and retina are reposited through a paracentesis incision with viscoelastic device or cyclodialysis spatula. Nonviable tissue is excised.

●Vitreous prolapse is treated by vitrectomy with Wekcels and Wescott scissors or with automated vitrector. Surgery for cataract with an intact lens capsule is deferred for a later date.

●Cataract surgery is indicated for intumescent lens, anterior capsular rupture with release of lens material, but is performed after the corneal laceration is sutured. Intra ocular lens implantation is controversial.

●Vitreous hemorrhage, intraocular foreign body, retinal detachment should be managed by a retinal surgeon.

●Vitreous involvement predisposes to retinal detachment from direct traction or vitreal-fibrous proliferation and contraction.

●Direct damage to angle structures, or obstruction from inflammatory debris or cells can lead to glaucoma.

Corneal perforations 370.06

In addition to traumatic corneal injuries, corneal perforations can result from:

●Trauma;

●Corneal ulcers;

●Inflammatory diseases — connective tissue diseases, Mooren’s ulcer;

●Exposure keratopathy, neurotrophic disease;

●Ectatic disorders — kerataconus, keratoglobus, pellucid marginal degeneration;

●Xerosis (vitamin A deficiency, cicatricial ocular surface diseases);

●Degenerative disease — Terrien’s;

●Postsurgical.

●Symptoms: pain, decreased vision, tearing, photophobia.

●Signs:

●Shallow or flat anterior chamber;

●Radiating Descemet’s folds;

●Uveal tissue prolapse;

●Seidel test positive for aqueous leak;

●Central clear zone in area of infiltrate;

●Hypotony.

TREATMENT

Treatment is guided by the etiology of the corneal perforation.

●Small, non-traumatic perforations can be treated with cyanoacrylate glue and a bandage contact lens.

●Larger perforations require patch grafting or penetrating keratoplasty (PKP) to restore ocular integrity.

●Infectious perforations have a better outcome with PKP instead of glue.

●Ocular surface or immunologic disorders are more effectively treated with glue to delay or prevent PKP.

●Amniotic membrane transplant can also be used for treating perforations. This is a multi-step procedure and involves wound debridement, filling of wound with pieces of amniotic membrane tissue, followed by suturing two layers of amniotic membrane over the effected area.

●Intravitreal or subtenon’s antibiotics are highly recommended at the time of surgery in the setting of infectious causes.

●Treatment of the underlying medical condition, such as connective tissue disease or vitamin A deficiency, has to be addressed simultaneously.

COMPLICATIONS

●The immediate injury can lead to iris prolapse, hyphema, cataract formation, lens disruption and vitreous loss.

●Secondary complications include infection, astigmatism, scarring, vascularization, chronic wound leak, epithelial ingrowth, iridocorneal adhesions and intraocular fibrous proliferation.

COMPLICATIONS

●Wound leak or dehiscence.

●Recurrent perforation due persistent underlying disease.

●Astigmatism, scarring, vascularization, epithelial ingrowth, iridocorneal adhesions and intraocular fibrous proliferation.

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Kaiser PK: The corneal abrasion patching study group. A comparison of pressure patching versus no patching for corneal abrasions due to trauma or foreign body removal. Ophthalmology 102(12):1936–1942, 1995.

Kunimoto DY, Kanitkar KD, Makar MS, eds: Corneal laceration. In: Wills eye manual. 4th edn. Pennsylvania, Lippincott Williams & Wilkins, 2004.

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189 Corneal Edema 371.20

(Bullous Keratopathy, Epithelial

Edema, Stromal Edema)

Joel Sugar, MD

Chicago, Illinois

Rashmi Kapur, MD, ECFMG

Chicago, Illinois

ETIOLOGY

Corneal edema is the condition of excess corneal hydration that is caused by altered fluid transport across the cornea. Epithelial edema is most troubling to visual acuity because it induces anterior irregular astigmatism. In epithelial edema, fluid accumulates initially within basal cells and then between epithelial cells, causing microbullae; ultimately, fluid accumulates beneath the basal cell layer, lifting up the corneal surface to form bullae.

Endothelial dysfunction, corneal hypoxia, and elevated intraocular pressure are the most common causes of corneal edema. Stromal infiltration and inflammation can also cause corneal edema. Endothelial dysfunction may be due to Fuchs’ dystrophy, other endothelial disorders such as iridocorneal endothelial (ICE) syndrome, or endothelial damage from trauma, including cataract or other intraocular surgery. Endothelial dysfunction may also occur after uveitis, angle-closure glaucoma, prolonged contact with silicone oil, or with chronic hypotony and inadequate corneal endothelial nutrition. Herpetic disciform keratitis with endothelial inflammation can also produce corneal edema. Hypoxia from prolonged wear of contact lenses with poor oxygen transmissibility can lead to corneal edema. Acute or severe elevations in intraocular pressure (IOP) in the presence of endothelial dysfunction can lead to corneal edema. With high elevations of IOP in the presence of normal endothelial function, the stroma initially remains thin and clear, but there is the development of epithelial edema. Hypotony results in isolated stromal edema.

Regardless of the inciting factor, endothelial cell loss results in migration of endothelial cells from neighboring areas to cover depleted areas. When these cells are not able to compensate, they enlarge and are irregular in shape (polymegathism and pleomorphism), resulting in stromal hydration and eventually leading to keratocyte loss, attenuation of Bowman’s membrane and the epithelial basement membrane, and a decrease in glycosaminoglycans in the stroma. In response, epithelial cells, keratocytes, and fibroblasts produce βig-h3, tenascin-C, and fibrillin-1, which may contribute to the poor adhesive characteristics of the epithelium and the resulting epithelial bullae.

COURSE/PROGNOSIS

Because the corneal endothelial cell density diminishes over time, corneal endothelial damage added to the normal attrition of endothelial cells with advancing age can lead to progressive corneal edema. Initial mild corneal edema may over months to years become chronic, visually disabling corneal edema. Prolonged corneal edema may lead to corneal vascularization and subepithelial pannus formation, which can complicate future surgical treatments.

DIAGNOSIS

Clinical signs and symptoms

Stromal edema is less disturbing to visual acuity and is manifest as thickening and hazy opacification of the corneal stroma with folding of Descemet’s membrane (Figure 189.1). Typically, the initial presentation of epithelial edema is blurred vision, which is most severe on awakening and decreases as the day progresses. As the severity increases, the visual acuity difficulty becomes persistent, and rupture of bullae may lead to recurrent pain, redness and photophobia. Anterior chamber inflammation may be seen as well, and secondary corneal infection can ensue.

Laboratory findings

●Epithelial edema and stromal edema are demonstrated at the slit-lamp examination or by pachymetry.

●Endothelial guttae or decreased endothelial cell density is demonstrated on slit-lamp evaluation, endothelial specular microscopy, or confocal microscopy.

FIGURE 189.1. Corneal edema with Descemet membrane folds.