Ординатура / Офтальмология / Английские материалы / Clinical Pathways in Glaucoma_Zimmerman, Kooner_2001
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300 Traumatic Glaucoma
usual signs of uveitis, there may be characteristic nodules occurring in the choroid, known as Dalen-Fuchs’ nodules, representing foci of granulomatous inflammation.112
What Is the Differential Diagnosis
of Glaucoma Complicating Inflammation?
Glaucoma complicating inflammation is to be differentiated from other types of traumatic glaucoma associated with cells in the anterior chamber. Pupillary block glaucoma is to be differentiated from other causes of traumatic glaucoma associated with a flat anterior chamber. This has been discussed above (see Glaucoma Secondary to Traumatic Uveitis). Examination of the fellow uninjured eye is essential to exclude sympathetic ophthalmia.
Sympathetic ophthalmia does not necessarily occur in the setting of unilateral accidental trauma. It may be induced by surgery in one eye, including cataract, glaucoma, and retinal detachment surgery, all of which may presumably result in uveal incarceration in the wall of the globe. Sympathetic ophthalmia should be differentiated from other causes of granulomatous panuveitis, such as the Vogt-Koyanagi-Harada syndrome.
How Is Lens-Induced Glaucoma Diagnosed?
Lens particle glaucoma glaucoma and glaucoma secondary to phakoanaphylactic uveitis are diagnosed by the presence of a corneal or corneoscleral laceration, violation of the lens capsule, and free lens matter and cells in the anterior chamber.
Relative pupillary block is diagnosed when there is a shallow anterior chamber with the iris appearing to be draped over a cataractous lens.
What Is the Differential Diagnosis
of Lens-Induced Glaucoma?
Lens particle glaucoma and glaucoma secondary to phakoanaphylactic uveitis may be confused with other types of traumatic cataract associated with cells in the anterior chamber. This includes glaucoma complicating hyphema, hemolytic glaucoma, ghost cell glaucoma (all of which are associated with intraocular hemorrhage), and glaucoma complicating traumatic uveitis. In all these entities, the lens is intact, and there is no free lens matter in the anterior chamber.
Pupillary block due to a swollen cataractous lens may occur in association with nonpenetrating ocular trauma. In such a case, there is no evidence of corneoscleral lacerations, and there may be other signs of nonpenetrating trauma, such as pupillary sphincter tears and angle recession.
How Are Epithelial Down-Growth
and Fibrous Ingrowth Diagnosed?
Epithelial down-growth may present as a cyst or sheet-like growth. The time interval between injury and the occurrence of epithelial down-growth is variable, ranging from a few days to 10 years.94
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An epithelial cyst may be either translucent or gray in color, usually appearing connected at one point with the traumatic wound. Rarely, the cyst will appear disconnected from the wound. Occasionally, a cyst will present in the posterior chamber, and grow into the anterior chamber through a peripheral iridectomy, or erode through the iris. The appearance and rate of growth of these cysts is variable, and they usually stabilize after a period of continued growth. There may be associated glaucoma, iridocyclitis, and pupillary distortion, and if large enough, the cyst may occlude the visual axis.94
Sheet-like epithelial down-growth is more irritating to the eye, so that the patient usually complains of tearing and dull-aching pain. Photophobia and blurred vision are less frequent complaints. There is usually ciliary injection, and often wound gape, an inadvertent filtering bleb, or a fistula demonstrable by Seidel testing. Band keratopathy is occasionally present.113 The cornea may or may not demonstrate edema overlying a posterior corneal membrane demarcated by a gray line, best seen on retroillumination. The gray line represents the edge of the advancing epithelial sheet, and may be scalloped, with focal pearllike areas of thickening. Aqueous flare and cells may be present and indicate iridocyclitis; flare may be disproportionate to ciliary flush or symptoms.114
The epithelial membrane grows rapidly over the iris, often obscuring iris details. In brown irides, the advancing edge of the membrane may appear as an indentation in the iris. The pupil may be distorted.
On gonioscopy the epithelium may be seen as a sheet obscuring details of the trabecular meshwork. Peripheral anterior synechiae are often present. Gonioscopy can be used to assess the extent of epithelialization of the angle, through an iridectomy, and sometimes over the ciliary body and retina.94
Fibrous ingrowth is most commonly recognized as a retrocorneal membrane. Usually, the condition does not make the eye uncomfortable. The membrane may resemble an epithelial sheet, appearing as a translucent membrane with a fairly distinct border. More commonly, the membrane appears gray and feltlike with a frayed leading margin. The overlying cornea is usually edematous. Extension of the membrane over the iris, angle, and vitreous is easily recognized as a thick enveloping membrane. The pupil may be drawn into the fibrous scar.
The condition may be fairly quiescent with minimal accompanying inflammation, or there may be massive fibrous intraocular proliferation, and later retraction, resulting in retinal detachment, hypotony, and phthisis bulbi.94
What Is the Differential Diagnosis of Epithelial
Down-Growth and Fibrous Ingrowth?
Epithelial cysts should be differentiated from congenital cysts of the iris stroma, which may be pigmented, arising from the pigment epithelium, or nonpigmented, arising from the iris stroma.115 Pigmented cysts are easy to differentiate from epithelial cysts, which are nonpigmented. On the other hand, congenital stromal cysts may be confused with epithelial cysts, but usually present at an earlier age, without a history of trauma or evidence of a penetrating wound.
Sheet-like epithelial down-growth is to be differentiated from other causes of retrocorneal membranes, such as a reduplicated Descemet’s membrane (as
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occurs in chronic iridocyclitis), detachment of Descemet’s membrane, peripheral corneal edema (usually from operative endothelial trauma), and vitreocorneal adhesion, which may cause corneal edema and have a grayish appearance.116 The posterior lip of a shelved corneal incision (as is commonly used for phacoemulsification) may also be confused with epithelial downgrowth, but is nonprogressive as opposed to an epithelial sheet.94
Fibrous ingrowth has essentially the same differential diagnosis as sheet-like epithelial down-growth. Fibrous ingrowth is distinguished from epithelial down-growth by its slow growth and vascularity.
How Is Glaucoma Secondary to Siderosis Diagnosed?
The pressure elevation associated with siderosis bulbi is asymptomatic. If there is associated cataract, the vision may be affected, even in the absence of significant retinal damage. If the lens is clear, vision may be impaired by advanced retinal damage.
In addition to pressure elevation, there is a constellation of signs due to iron deposition in the various ocular tissues. Iron deposition in the iris produces heterochromia, and mydriasis results from toxic damage to the iris sphincter. The deep cornea and anterior subcapsular portion of the lens have a rustbrown color. Advanced retinal damage produces a retinitis pigmentosa-like picture. Gonioscopy reveals rust-brown discoloration of the angle. There may also be signs of previous perforation of the globe by the foreign body, such as a sealed corneal wound, a hole, or a transillumination defect in the iris. Occasionally, a foreign body may be directly visualized in the angle by gonioscopy, or in the posterior segment by ophthalmoscopy.13
To confirm the clinical suspicion of an intraocular foreign body, appropriate radiography, ultrasonography, and CT may be of help. Magnetic resonance imaging (MRI) should be avoided as the associated magnetic field may produce movement of the foreign body, which may result in intraocular damage.117 Electrophysiologic testing may be used to assess retinal function; a depressed electroretinogram (ERG) indicates siderotic retinal damage.118
What Is the Differential Diagnosis
of Glaucoma Complicating Siderosis Bulbi?
IOP elevation, a history of ocular trauma, rust-brown discoloration of the angle, and possibly mydriasis from traumatic iris sphincter rupture are also seen in hemosiderotic glaucoma (see above). However, the other signs of iron deposition seen in siderosis are absent. Angle recession glaucoma is another form of traumatic secondary open-angle glaucoma associated with traumatic mydriasis but is differentiated from siderotic glaucoma by its characteristic gonioscopic picture and the absence of other signs of siderosis.
How Is Glaucoma Secondary to Chalcosis Diagnosed?
There may be signs of foreign body entry such as a sealed corneal wound, a hole, or a transillumination defect in the iris. The foreign body may be seen in
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the angle by gonioscopy, or in the posterior pole by ophthalmoscopy. Imaging studies may be needed to confirm the presence of a foreign body. The iridocorneal angle is open.
Copper may be deposited in the cornea, lens, vitreous, and retina. Copper deposits in the cornea appear as a golden brown, ruby red, or green pigment ring in the peripheral Descemet’s membrane (Kayser-Fleischer ring). Lens opacities occur in the form of anterior subcapsular cataract.112 Posterior segment examination may reveal fibrillary degeneration of the vitreous, and/or maculopathy secondary to copper deposition in the retina.109 Vision may be affected by cataract, vitreous opacification, or maculopathy.
Electroretinographic (ERG) findings in chalcosis are not as striking as those seen in siderosis. If there is significant vitreous opacification, this may mildly depress the ERG; otherwise ERG is usually within the normal range.109
What Is the Differential Diagnosis of Chalcosis?
Chalcosis oculi is seen in Wilson’s disease, primary biliary cirrhosis, chronic active hepatitis, exogenous copper administration, and progressive intrahepatic cholestasis of childhood. Wilson’s disease is distinguished from other conditions by low serum ceruloplasmin and the presence of neurologic symptoms.119 In all types of chalcosis not caused by an intraocular foreign body, the condition is characteristically bilateral. Unless there are bilateral foreign bodies, posttraumatic chalcosis is unilateral.
Figures 13–6 and 13–7 outline the differential diagnosis of IOP elevation following recent and old penetrating trauma.
Treatment and Management
How Is Glaucoma Secondary
to a Flat Anterior Chamber Managed?
The best treatment for this problem is prevention, by meticulous initial closure of corneal and corneoscleral lacerations. In the early postoperative period, a flat or shallow anterior chamber, hyptony, and a positive Seidel test are indicators of wound leakage. A small leak may be initially managed with a bandage contact lens. If this fails to reform the anterior chamber, resuturing of the wound is indicated. If the wound edges are excessively friable, or if it is judged that adequate suturing would induce excessive astigmatism, cyanocrylate tissue adhesive is a useful tool.
If there is established glaucoma, initial management is by aqueous suppressants. Failure of medical treatment is an indication for filtering surgery.
How Is Glaucoma Secondary to Inflammation Treated?
Initial management consists of corticosteroids, cycloplegic agents, and aqueous suppressants. Laser iridotomy may be required for iris bombé. Persistent IOP elevation despite resolution of inflammation may be an indication for filtering surgery (see Glaucoma Secondary to Traumatic Uveitis, above).
Figure 13–6. High IOP after recent penetrating trauma.
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Figure 13–7. Differential diagnosis of high IOP with old penetrating trauma.
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Sympathetic ophthalmia warrants special mention. The condition should always be suspected in the fellow eye in cases of penetrating ocular trauma. Once the condition is recognized, it should be treated aggressively with high doses of systemic corticosteroids and/or immunosuppressive drugs, usually for a prolonged period. The exciting eye should be removed if it does not have functional visual potential.103
How Is Glaucoma Secondary to Intraocular Hemorrhage (in Association with Penetrating Trauma) Treated?
Intraocular hemorrhage may complicate penetrating trauma and lead to several types of glaucoma, including glaucoma secondary to hyphema, hemolytic glaucoma, ghost cell glaucoma, and siderotic glaucoma. The management of these discussions is discussed above (see Glaucoma Complicating Nonpenetrating Trauma).
How Is Lens-Induced Glaucoma Treated?
Both lens particle glaucoma and glaucoma secondary to phakoanaphylactic uveitis are initially treated with aqueous suppressants to decrease IOP, corticosteroids to control inflammation, and mydriatics to prevent and/or treat posterior synechiae. If the IOP remains elevated, lens removal is indicated.91.
Relative pupillary block due to a swollen lens is also treated by lens removal. Initially, pharmacologic mydriasis or a laser iridotomy may relieve the pupillary block. If this fails, aqueous suppressants are given until the lens is removed.13
How Is Glaucoma Complicating an Epithelial Cyst Managed?
An epithelial cyst that is causing glaucoma should be widely excised, if possible intact. Large cysts that are adherent to the cornea, iris, or vitreous face are first collapsed using a 25-gauge needle. If the collapsed cyst is small, it is frozen through the cornea after an insulating air bubble is placed in the anterior chamber. Larger cysts may require vitrectomy instruments to remove adherent vitreous and iris, whereas epithelial remnants are frozen as described above. If surgical excision and freezing result in persistent corneal edema, penetrating keratoplasty may be subsequently performed to improve vision.120
How Is Glaucoma Complicating Sheet-Like Epithelial
Down-Growth Managed?
Management has two aims: removing epithelial tissue and controlling glaucoma. If there is a Seidel-positive fistula (where the epithelial cells have entered), this should be closed, if necessary with the use of patch grafts.121 Preoperatively, the involved iris is marked with photocoagulation spots. The iris and vitreous with adherent epithelium are removed with vitrectomy instruments through the pars plana. Generous anterior vitrectomy is performed followed by air/fluid exchange. Epithelial tissue on the corneal endothelium, iridocorneal angle, ciliary body, and peripheral retina are treated with transcorneal and transscleral cryotherapy. If there is extensive involve-
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ment of the cornea, penetrating keratoplasty may be needed. Despite significant advances in microsurgery, epithelial down-growth remains a highly challenging problem with a high rate of recurrence.94,120
Regarding pressure control, initial management is by aqueous suppressants. Medical treatment usually fails to control pressure, and surgery is required. Conventional filtration surgery has a high rate of failure. A trial of 5-FU as an adjunct to trabeculectomy did not significantly improve pressure control.122 Some authors have reported good results with seton procedures.123
How Is Glaucoma Complicating Fibrous Ingrowth
Managed?
Many eyes with fibrous ingrowth remain quiescent, and periodic observation often reveals maturation of the fibrous scar without progressive damage to the globe. However, if glaucoma does occur, the condition is initially managed with aqueous suppressants. If this fails, filtering surgery is attempted. Blind eyes are best treated with cyclodestructive procedures.94
How Is Glaucoma Complicating Siderosis Bulbi
Managed?
The pressure elevation is initially managed with aqueous suppressants. If this fails, filtering surgery may be needed. If there is poor visual potential, evidenced by a subnormal or extinguished ERG, cyclodestructive procedures may be more appropriate. In the presence of good visual potential, and decreasing ERG amplitudes on serial testing, removal of the foreign body is needed to limit further retinal damage. However, this may be difficult if the foreign body is encapsulated.
How Is Glaucoma Secondary to Chalcosis Managed?
The pressure elevation is initially managed with aqueous suppressants. If this fails, filtering surgery may be needed. The foreign body is removed by vitrectomy techniques. Cataract extraction and/or vitrectomy may be needed to improve vision.
GLAUCOMA SECONDARY TO CHEMICAL INJURY
Definition
What Is Meant by Glaucoma Secondary to Chemical Injury?
Chemical injury to the eye may be caused by acids or alkalis. Alkaline chemicals, which may penetrate into the anterior chamber within seconds of contact, usually cause more severe anterior segment damage, including anterior segment ischemia. In contrast, acidic chemicals cause coagulation of tissue proteins, which limits the penetration resulting in more superficial injuries, unless the exposure is prolonged and the acid concentration is high. Both types of injury, especially alkali-induced, may be associated with glaucoma.
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What Is the Mechanism
of Glaucoma Secondary to Chemical Injury?
Immediately after injury, glaucoma may occur due to anterior segment shrinkage124 and increased uveal blood flow, which may be prostaglandinmediated.125 Anterior chamber inflammation, with hypopyon in more severe cases, may develop and contribute to the pressure rise. However, in some cases damage may be so severe as to cause ciliary shutdown, which may result in hypotony.126
In the next few weeks to months, there is ongoing repair and scarring, associated with some degree of inflammation. In this phase, pressure elevation may be a result of trabecular meshwork damage that occurred at the time of injury. Glaucoma may also occur as a result of peripheral anterior synechiae formation from inflammation or pupillary block associated with posterior synechiae to the lens. The lens may become cataractous and contribute to the pressure rise by producing pupillary block or by a phacolytic mechanism when lens materials are released.127
In later phases, when the repair processes are complete, glaucoma is usually due to trabecular damage and/or the formation of peripheral anterior synechiae.128
Epidemiology and Importance
What Are the Settings In Which Chemical Injury Occurs?
Chemical injuries are relatively common. They may occur in the home, most commonly from detergents, disinfectants, solvents, cosmetics, drain cleaners, oven cleaners, ammonia, bleach, and other common household alkaline agents. In an agricultural setting, fertilizer and pesticides tend to be the offending agent. Chemical injuries occurring in industry are usually caused by caustic chemicals and solvents. When strong alkalis and acids are used as an assaultive weapon, the injuries are usually severe. Ocular alkaline injuries are slightly more common than acid injuries.129
Diagnosis and Differential Diagnosis
How Is Glaucoma Secondary to Chemical Injury Evaluated?
The following classification is a useful guide for assessment of severity and prognosis of the ocular injury:129–131
Grade 1 (good prognosis): Corneal epithelial damage; no ischemia.
Grade 2 (good prognosis): Cornea hazy but iris details seen; ischemia involving at least one-third of the limbus.
Grade 3 (guarded prognosis): Total loss of corneal epithelium; stromal haze blurring iris details; ischemia involving one-third to one-half of the limbus.
Grade 4 (poor prognosis): Cornea opaque, obscuring view of iris and pupil; ischemia involving more than half the limbus.
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The depth of penetration is determined clinically by the degree of initial scleral injury, and the subsequent development of cataract and/or hypotony.
The corneal changes due to chemical injury make it difficult to measure the IOP by Goldmann applanation tonometry or Shiøtz tonometry. A Tono-pen or pneumatonometer may be more useful to assess IOP. If the ocular injury is unilateral, these instruments may be calibrated against a Goldmann applanation tonometer in the other eye.13
After healing is complete, patients usually have variable degrees of corneal scarring with vascularization, usually associated with conjunctival scarring in the form of symblepharon. This makes it difficult to evaluate the optic disc and visual fields. The consensual reaction of the fellow eye may indicate optic disc damage (or coexisting extensive retinal disease). Ultrasound examination may detect advanced optic disc cupping, although normal ultrasound does not exclude glaucomatous cupping. Visual fields may be evaluated by confrontation, or formal perimetry (static or kinetic) using larger stimuli.13
What Is the Differential Diagnosis
of Glaucoma Secondary to Chemical Injury?
The differentiation between acidic and alkaline injuries is very important, as the latter tend to be more detrimental to the eye. History taking may reveal the nature of the offending agent. Testing the conjunctival cul-de-sac with litmus paper may be informative.
The combination of high IOP, corneal epithelial ulceration, corneal stromal haze and ulceration, and variable degrees of uveitis up to hypopyon may be caused by microbial keratitis, as well as by chemical injury. In most cases, adequate history taking will immediately differentiate between the two conditions. Furthermore, chemical injury that is severe enough to cause iritis is typically associated with limbal ischemia, which is not usual in the setting of microbial keratitis.
In the late phases, the corneal scarring caused by chemical injury should be differentiated from other causes of corneal scarring such as corneal infection (viral, bacterial, fungal, protozoal) and autoimmune disease such as ocular cicatricial pemphigoid and the Stevens-Johnson syndrome.
Treatment and Management
How Is Glaucoma Secondary to Chemical Burns Managed?
The immediate management of an acute chemical injury is copious irrigation of the eye, together with removal of any material retained in the cul-de-sac. Irrigation is continued until pH testing of the conjunctiva reveals a normal pH. Topical steroids (with antibiotic cover) and cycloplegics are given to treat inflammation. However, topical steroids are used with caution, as they are liable to increase the risk of corneal melting, particularly in the second and third week following injury.132 Topical citrate, ascorbate and tetracycline may be used to limit collagenolysis.133 A bandage contact lens is useful to promote reepithelialization.