Ординатура / Офтальмология / Английские материалы / Clinical Pathways in Glaucoma_Zimmerman, Kooner_2001

290 Traumatic Glaucoma

GLAUCOMA SECONDARY TO LENS DISLOCATION

Definition

What Is Meant by Glaucoma Secondary to Lens Dislocation?

This is glaucoma caused by traumatic lens displacement as a result of nonpenetrating trauma. Lens displacement is caused by zonular disruption. Partial zonular disruption leads to subluxation of the lens, where the lens is displaced but remains partially or completely within the pupillary area. Total zonular disruption leads to lens dislocation, where the lens comes to lie completely in the anterior chamber (anterior dislocation), or falls back into the vitreous cavity (posterior dislocation).

What are the Mechanisms of Glaucoma Secondary to Lens Dislocation?

With lens subluxation, forward displacement of the lens or herniation of vitreous through the ruptured zonules may cause pupillary block and angle-closure glaucoma. With total anterior dislocation, angle-closure glaucoma may occur due to pupillary block, and open-angle glaucoma may occur from direct obstruction of the iridocorneal angle by the lens or lens fragments. Posterior lens dislocation is less likely to cause glaucoma than anterior dislocation. In such cases, glaucoma may occur due to herniation of vitreous through the pupil with pupillary block. If a posteriorly dislocated lens develops hypermature cataract, phakolytic glaucoma may occur.

Epidemiology and Importance

What Is the Incidence of Lens Dislocation

Following Nonpenetrating Trauma?

Lens dislocation, whether subluxation or complete dislocation, is a very common sequela of nonpenetrating ocular injury and should be suspected in every case. Mieler et al81 found that out of four golf-related nonpenetrating eye injuries, three were associated with lens dislocation. Chorich et al82 also reported four eye injuries caused by bungee cords, in which two were associated with lens subluxation.

What Is the Incidence of Glaucoma

Following Lens Dislocation?

Lens dislocation is a significant risk factor for traumatic glaucoma. In a retrospective review of 73 cases of glaucoma following nonpenetrating trauma, Sihota et al83 found that 38.4% had some form of lens displacement. Rodman84 reported a 77.5% incidence of glaucoma with anterior lens dislocation and 87.5% with subluxated or posteriorly dislocated lenses in a histopathologic review of 120 cases.

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relieve pupillary block and to prevent corneal endothelial decompensation. If the lens is soft, it may be removed by vitrectomy instrumentation. If the lens is hard, intracapsular extraction is more appropriate. In both cases, the procedure should include an anterior vitrectomy.

Pupillary block by vitreous may be relieved by Nd:YAG laser iridotomy. If lens extraction is indicated, anterior vitrectomy is performed at the time of lens extraction. A posteriorly dislocated lens usually does not cause problems. If the lens is hypermature and inducing phakolytic glaucoma, the lens is removed by pars plana vitrectomy techniques.

GLAUCOMA SECONDARY TO FORWARD DISPLACEMENT

OF THE IRIS-LENS DIAPHRAGM

Definition

What Is Meant by Glaucoma Secondary to Forward Displacement of the Iris-Lens Diaphragm?

This a form of traumatic angle-closure glaucoma secondary to forward movement of the iris-lens diaphragm.

What Is the Cause of Forward Displacement of the

Iris-Lens Diaphragm Following Nonpenetrating Trauma?

This may result either from forward rotation of the ciliary body due to posttraumatic choroidal or ciliary body edema,85 or from malignant glaucoma (aqueous misdirection syndrome).86

Epidemiology and Importance

What Is the Risk of Glaucoma After Forward

Displacement of the Iris-Lens Diaphragm?

The incidence of forward displacement of the iris-lens diaphragm after blunt trauma is very low.85 However, when it does occur, the risk of glaucoma is high.

DIAGNOSIS AND DIFFERENTIAL DIAGNOSIS

How Is Forward Displacement of the Iris-Lens Diaphragm

Diagnosed?

The condition is diagnosed when there is elevated IOP together with a shallow anterior chamber (see Fig. 13–5). The iris appears draped over an anteriorly displaced lens, as opposed to other causes of pupillary block where the anterior chamber appears relatively deep centrally with anterior bowing of the peripheral iris. Gonioscopy reveals angle closure due to iridocorneal apposition.

Ciliary body rotation is distinguished from malignant glaucoma by the presence of choroidal and/or ciliary body effusion. Choroidal effusion may be seen

ophthalmoscopically if the media are clear. Peripheral annular choroidal effusion and ciliary body effusion are best detected by ultrasonography. The absence of uveal effusion is highly suggestive of malignant glaucoma.13

What Is the Differential Diagnosis of Glaucoma Secondary to Forward Displacement of the Iris-Lens Diaphragm?

This includes all causes of elevated IOP associated with a shallow anterior chamber, namely forward rotation of the ciliary body, malignant glaucoma, pupillary block due to traumatic cataract (with lens swelling), pupillary block due to forward displacement of a subluxated lens, and pupillary block in association with traumatic uveitis. This has been discussed above (see Glaucoma Secondary to Traumatic Cataract).

Treatment and Management

How Is Glaucoma Secondary to Forward Displacement of the Iris-Lens Diaphragm Managed?

Forward rotation of the ciliary body is usually self-limited and is best treated by antiinflammatory agents such as corticosteroids and cycloplegics. Aqueous suppressants (beta-blockers, 2-agonists, and CAIs) and hyperosmotic agents are used as necessary to control the IOP. Unless there is an associated pupillary block mechanism, iridotomy is neither necessary nor helpful.

Malignant glaucoma is treated initially with vigorous cycloplegia. If the condition fails to respond, posterior vitrectomy, often with lens extraction, is needed to relieve the aqueous misdirection.13

GLAUCOMA SECONDARY TO TRAUMATIC UVEITIS

Definition

How Is Glaucoma Secondary to Traumatic Uveitis

Defined?

This is an IOP elevation associated with uveitis secondary to nonpenetrating ocular trauma.

What Is the Mechanism of Glaucoma

Secondary to Traumatic Uveitis?

There are several mechanisms by which traumatic uveitis can cause pressure elevation. The outflow pathways may become obstructed by inflammatory cells, debris, protein, or other serum components that are liberated because of vascular incompetence.87 The trabecular endothelial cells may swell as a result of inflammation, compromising outflow. More severe inflammation may completely damage the trabecular endothelial cells. Chronic inflammation may

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induce sclerosis of the trabecular meshwork. The trabecular meshwork may also become obstructed by a hyaline membrane. If posterior synechiae occur, this may lead to pupillary block and secondary angle closure.88

Epidemiology and Importance

How Often Is Uveitis Caused

by Nonpenetrating Ocular Trauma?

Rosenbaum et al89 studied a series of 496 patients with uveitis, and found 24 patients (4.8%) who had uveitis attributable to nonpenetrating trauma. In a series of 230 cases of anterior uveitis in children, Giles90 reported that the incidence of traumatic uveitis was 1.3% (60% were idiopathic).

Diagnosis and Differential Diagnosis

How Is Glaucoma Secondary

to Traumatic Uveitis Diagnosed?

Uveitis is diagnosed by the presence of flare and cells in the anterior chamber. There may also be posterior synechiae, with or without pupillary block and iris bombé. Gonioscopy may be normal or may show a hyaline membrane over the trabecular meshwork. If there is pupillary block, iridocorneal apposition may be seen on gonioscopy. Other effects of nonpenetrating trauma may be seen, such as lens subluxation, cataract, angle recession, and so on.

After the uveitis has resolved, the IOP may remain elevated as a result of permanent trabecular endothelial cell damage. Gonioscopy may be normal, so that the diagnosis can only be made by careful history taking, and the finding of other signs of nonpenetrating trauma.

What Is the Differential Diagnosis

of Glaucoma Secondary to Traumatic Uveitis?

This includes other causes of traumatic glaucoma associated with cells in the anterior chamber. Inflammatory cells may be difficult to distinguish from red blood cells. Inflammation should be suspected if the IOP is elevated with a small number of cells in the anterior chamber, because a similar quantity of fresh erythrocytes would not be expected to induce ocular hypertension in eyes with normal facility of outflow. However, if IOP returns to normal after resolution of hyphema, only to rise later in association with fine tan-colored cells in the anterior chamber, ghost cell glaucoma rather than uveitic glaucoma should be suspected. Hemolytic glaucoma is associated with reddish brown cells in the anterior chamber, which represent macrophages engulfing hemolytic debris.

Glaucoma due to pupillary block should be differentiated from other causes of traumatic glaucoma associated with a shallow anterior chamber (see Diagnosis and Differential Diagnosis under Glaucoma Secondary to Forward Displacement of the Iris-Lens Diaphragm, above).

After resolution of inflammation, the presence of glaucoma due to postinflammatory trabecular damage may be confused with other causes of chronic secondary open-angle glaucoma following trauma. This includes angle-recession and siderotic glaucoma, both of which have characteristic gonioscopic findings (see above). Lastly, elevated pressure secondary to medical therapy for uveitis should also be considered, such as steroid-induced and mydriatic glaucoma.

Treatment and Management

How Is Glaucoma Secondary to Traumatic Uveitis Treated?

Initial treatment should consist of antiinflammatory and antiglaucomatous medications. Antiinflammatory medications include corticosteroids, nonsteroidal antiinflammatory drugs, and cycloplegics. Antiglaucomatous medications that may be used are aqueous suppressants such as beta-blockers,2-agonists, and CAIs. Miotics should be avoided as they increase blood–- aqueous barrier breakdown.

In cases with posterior synechiae and pupillary block, vigorous cycloplegia may break the synechiae and relieve the pupillary block. If this fails, prompt laser iridotomy is needed to reestablish normal aqueous flow.

In most cases, the IOP normalizes once inflammation resolves. If IOP elevation persists, and is uncontrollable by medication, filtering surgery may be indicated.

GLAUCOMA COMPLICATING PENETRATING TRAUMA

Definition

What Is Meant by Glaucoma Complicating

Penetrating Trauma?

Penetrating (or “perforating”) trauma is an injury to the globe that results in a full-thickness laceration of the ocular wall. This may or may not be associated with a retained intraocular foreign body. Occasionally, the injurious agent may pass through the anterior portion of the globe, traverse the eye, and exit again through the posterior part of the ocular wall, producing a double penetrating injury. A penetrating injury may produce elevation of the IOP, either acutely or as a delayed effect.

What Are the Mechanisms

of Glaucoma Complicating Penetrating Trauma?

Several mechanisms may produce glaucoma in an eye that has sustained penetrating trauma. A prolonged flat anterior chamber may result in peripheral anterior synechiae. Intraocular inflammation is associated with glaucoma that results from a variety of mechanisms (see Glaucoma Secondary to Traumatic Uveitis, above). Inflammation of the uninjured fellow eye, known as sympathetic ophthalmia, may produce glaucoma in the uninjured eye. Intraocular

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hemorrhage may occur following penetrating trauma, and may induce IOP elevation by several mechanisms, namely, glaucoma complicating hyphema, ghost cell glaucoma, hemolytic glaucoma, and hemosiderotic glaucoma. All forms of glaucoma associated with intraocular hemorrhage have been discussed above (see Glaucoma Complicating Nonpenetrating Trauma). Lens injury with violation of the lens capsule may also produce glaucoma, as will be discussed below. Epithelial down-growth and fibrous ingrowth may also cause glaucoma. A retained (and often missed) metallic foreign body may remain in the eye and cause chemical effects. Iron foreign bodies cause siderosis, and copper causes chalcosis, both conditions being associated with glaucoma.

Table 13–4 lists the causes of glaucoma complicating penetrating trauma.

What Are the Mechanisms of Lens-Induced Glaucoma in Association with Penetrating Trauma?

Lens injury may induce glaucoma through one of three mechanisms. The first is lens particle glaucoma glaucoma, where the trabecular meshwork becomes obstructed with cortical material and and inflammatory cells. Another mechanism is phacoanaphylaxis, where patients becomes sensitized to their own lens proteins and develop a granulomatous reaction around the lens. If the trabecular meshwork becomes involved in the inflammatory process, glaucoma may develop.91 Alternatively, the lens may swell, causing relative pupillary block and secondary angle closure.13

What Is the Definition of Glaucoma Secondary

to Epithelial Down-Growth and Fibrous Ingrowth?

A poorly apposed corneal or corneoscleral laceration may allow epithelial elements or fibrous tissue to invade the eye. Epithelial down-growth may manifest as an epithelial cyst in the anterior chamber, or a sheet-like growth. Fibrous ingrowth usually appears in the form a retrocorneal membrane. All these conditions may be associated with glaucoma, which is usually intractable.

What Is the Mechanism of Glaucoma Secondary to Epithelial Down-Growth and Fibrous Ingrowth?

An enlarging epithelial cyst may induce glaucoma by preventing aqueous from reaching portions of the angle. There may also be associated iritis, which may

Table 13–4. Types of Glaucoma Associated with Penetrating Trauma

Glaucoma secondary to flat anterior chamber Glaucoma secondary to inflammation Glaucoma secondary to intraocular hemorrhage Lens-induced glaucoma

Glaucoma secondary to epithelial down-growth and fibrous ingrowth Glaucoma secondary to siderosis

Glaucoma secondary to chalcosis

elevate the IOP by several mechanisms (see Glaucoma Secondary to Traumatic Uveitis, above).

Sheet-like epithelial down-growth produces glaucoma through several mechanisms. Hypotony, inflammation, and shallowing of the anterior chamber lead to broad peripheral anterior synechiae. Proliferating epithelium covers the trabecular meshwork, as well as the false angle caused by peripheral anterior synechiae. Areas of trabecular meshwork underlying the epithelial sheet undergo sclerosis and necrosis.92 Chronic inflammation of the uvea leads to trabeculitis and decreased outflow facility. Pupillary block glaucoma is produced when the epithelial sheet occludes or secludes the pupil.93 Hemorrhagic and ghost cell glaucoma may result from repeated hemorrhage from friable neovascularization. Chronic hypotony may progress to intractable glaucoma if the fistula closes, either spontaneously or iatrogenically.94

Glaucoma in association with fibrous ingrowth occurs from obliteration of the angle structures, and peripheral anterior synechiae occur from persistent flat anterior chamber or inflammation or recurrent bleeding from friable neovascularization, often leading to hemolytic glaucoma.95,96

What Is Meant by Glaucoma Secondary to Siderosis Bulbi?

Iron released from retained metallic foreign bodies is deposited in various intraocular structures resulting in toxic damage. This condition is termed siderosis bulbi. Involvement of the trabecular meshwork may lead to secondary open-angle glaucoma. Iron is also toxic to the retina.13

What Is Meant by Glaucoma Complicating Chalcosis?

Chalcosis is a condition where copper released from a retained intraocular foreign body is oxidized within the eye, producing tissue damage. Damage to the trabecular meshwork results in glaucoma.

Epidemiology and Importance

What Is the Incidence of Penetrating Ocular Trauma?

This varies according to sex and age, the incidence being higher at younger ages and in males. Thus, in 10to 19-year-old males, the incidence of penetrating ocular trauma is 94.3 per million person-years, whereas in 60to 69-year- old females, the incidence is 3.9 per million person-years.1 Alcohol and illicit drug use increase the risk for penetrating ocular injury.3

What Are the Causes of Penetrating Ocular Trauma?

Penetrating injury may result from blunt forces (10–46%), sharp laceration (34–37%), or missiles (27–41%).3,4,97,98 Intraocular foreign bodies were present in 6% of assault-related and 35% of occupational injuries in patients registered in the National Eye Trauma System (NETS).3,4

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What Is the Incidence of Sympathetic Ophthalmia

Following Traumatic Ocular Injuries?

The incidence of sympathetic ophthalmia following traumatic ocular injuries is 0.1 to 0.3%.99–101 Jennings and Tessler102 diagnosed sympathetic ophthalmia in 1.4% (20 patients) of the total number of referred patients with uveitis seen over an 11-year period.

How Long After Trauma Does Sympathetic

Ophthalmia Occur?

Chan et al103 studied 32 cases of sympathetic ophthalmia and found that 18 cases (56%) occurred within 1 year of injury. Eight patients (25%) developed the condition more than 3 years following injury. Two cases (6%) occurred within 2 weeks after injury; 10 cases (31%) between 2 weeks and 3 months; six cases (19%) between 3 months and 1 year; and four patients (13%) between 1 and 3 years. In one other patient, the interval between injury and the occurrence of the condition was 64 years.

What Are the Risk Factors for the Occurrence of Epithelial Down-Gowth and Fibrous Ingrowth After Penetrating Trauma?

The basic risk factor for both epithelial down-growth and fibrous ingrowth is poor wound closure, whether from faulty surgical technique or because of the nature of the wound (excessively lacerated with friable edges). Poor wound closure results in incarceration of tissue, serving as a wick that facilitates postoperative wound gape. Apposition of iris to the wound provides a source of nutrients for the proliferating cells. Chronic inflammation contributes to poor wound healing. Recurrent bleeding from a vascularized, inflamed wound is thought to provide a fibrin scaffold for fibrous proliferation into the anterior chamber.94

What Is the Incidence of Epithelial Down-Growth

and Fibrous Ingrowth?

The incidence of these conditions is low, and decreasing over time, mainly due to advances in microsurgical techniques. Terry et al104 estimated a rate of 0.35% epithelialization after traumatic and surgical perforations based on 28 diagnostic laboratory specimens out of 8,000 cases. Although most studies pertain to cataract surgery, they show the trend for epithelial down-growth to decrease over time; in the older literature, 17 to 26% of all enucleations after cataract surgery were due to this complication, whereas recently the incidence ranges from 0.12 to 0.08%.105 Allen106 reported an 11% incidence of fibrous ingrowth in 237 eyes enucleated for trauma. In general, the incidence of fibrous down-growth in enucleated eyes tends to be lower than epithelial down-growth.107.

What Is the Incidence of Glaucoma Secondary to Siderosis and Chalcosis?

This is a relatively rare form of traumatic glaucoma. Percival108 reported a series of 153 patients with posterior segment intraocular foreign bodies (iron or otherwise), in which only eight (5%) developed glaucoma that was not attributable to lens-induced mechanisms. Glaucoma appears to be less frequently associated with chalcosis than with siderosis.109

Diagnosis and Differential Diagnosis

How Is Glaucoma Secondary

to a Flat Anterior Chamber Diagnosed?

In addition to elevated IOP, there are signs of a healed corneal or corneoscleral laceration. This laceration may have been sutured, or it may have been neglected, with the formation of anterior iris synechiae to the resultant scar. The anterior chamber may be irregular in depth. Gonioscopy will reveal a closed angle due to the presence of peripheral anterior synechiae.

What Is the Differential Diagnosis of Glaucoma Secondary to a Flat Anterior Chamber?

Other causes of a previously flat anterior chamber include corneal melting due to corneal infection (e.g., bacterial or herpetic), and sterile corneal melting as a result of collagen vascular disease (e.g., rheumatoid arhthritis). In such cases, there is no history of ocular trauma.

Peripheral anterior synechiae may form as a result of prolonged pupillary block associated with traumatic uveitis or a swollen cataractous lens, both of which may occur in the absence of penetrating trauma.

How Is Glaucoma Secondary to Inflammation Diagnosed?

Inflammation is a common sequela of penetrating trauma, and may induce pressure elevation. Inflammation may also occur in the fellow uninjured eye, presumably as a result of autosensitization of the eye to uveal pigment released into the systemic circulation at the time of trauma.110,111 The condition is termed sympathetic ophthalmia, the injured eye being the “exciting” eye, and the fellow eye being the “sympathizing” eye. This may cause IOP elevation in both eyes.

As mentioned above, inflammation is diagnosed by the presence of flare and cells in the anterior chamber, with or without posterior synechiae. The latter may induce pupillary seclusion, which leads to iris bombé and secondary angle closure. Angle closure may be confirmed by gonioscopy.

Sympathetic ophthalmia presents as bilateral granulomatous uveitis. It is therefore mandatory to examine the fellow uninjured eye if uveitis is found in the injured eye. The first symptoms of sympathetic ophthalmia are photophobia and blurring of near vision due to loss of accommodation. In addition to the