Ординатура / Офтальмология / Английские материалы / Clinical Pathways in Glaucoma_Zimmerman, Kooner_2001
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280 Traumatic Glaucoma
Epidemiology and Importance
What Are the Risk Factors for Ghost Cell Glaucoma?
The main risk factor is vitreous hemorrhage that persists long enough to allow erythrocyte degeneration. The second is disruption of the anterior hyaloid, which allows the degenerated cells to pass forward to the anterior chamber. Both of the above events may occur as a result of ocular trauma, or from nontraumatic causes, as discussed above.
A small hyphema is unlikely to produce ghost cell glaucoma. However, in the setting of an eight-ball or near-total hyphema, ghost cells may form, which may contribute to a prolonged IOP elevation seen even after removal of the blood. Aspirates from eight-ball hyphema show a significant number of ghost cells hidden within the clot.50
Diagnosis and Differential Diagnosis
How Is Ghost Cell Glaucoma Diagnosed?
As mentioned above, the degree of IOP elevation is variable. If the IOP is in the 50 to 60 mm Hg range, there may be severe ocular pain.
With the slit lamp, using high magnification and a narrow slit beam, ghost cells are seen in the anterior chamber as tiny khaki-colored cells. If the cornea is edematous from marked pressure elevation, a drop of topical glycerol may be needed to clear the cornea and permit a clearer view of the aqueous. Occasionally, these cells may collect inferiorly in the anterior chamber, forming a khaki-colored layer. If fresher erythrocytes have also reached the anterior chamber, they too may form a layer.51
Gonioscopy may be normal. If there are enough ghost cells, they may deposit on the trabecular meshwork, giving it a khaki hue, especially in the inferior angle. The lens may be subluxated or dislocated. Ophthalmoscopy usually will reveal vitreous hemorrhage. If the lens is cataractous, ultrasonography may be needed to confirm the presence of vitreous hemorrhage.
In doubtful cases, an aqueous sample may be obtained for cytologic diagnosis. After topical anesthesia, a 30-gauge needle is used to aspirate aqueous through a temporal paracentesis.52 The aqueous sample is then spread on a slide and examined by phase contrast microscopy.53,54 Ghost cells appear as spherical cells with a thin membrane. Clumps of degenerated hemoglobin (Heinz bodies) are seen adhering to the internal aspect of the cell membrane. Unlike hemolytic glaucoma, there are few, if any macrophages. Methyl violet 1% staining may aid in the diagnosis,55 and the aspirate can be subjected to scanning and transmission electron microscopy, where available.54
What Is the Differential Diagnosis
of Ghost Cell Glaucoma?
Ghost cell glaucoma does not necessarily have to occur in the setting of trauma. Originally, ghost cell glaucoma was described following pars plana vitrectomy.56
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This is particularly liable to occur if only core vitrectomy is performed, leaving a large peripheral skirt of vitreous containing hemorrhagic debris. Because pars plana vitrectomy often disrupts the anterior hyaloid, it provides a route for ghost cells to reach the vitreous.
Ghost cell glaucoma can also occur after cataract extraction if the anterior hyaloid is disrupted. Two scenarios are possible. The first possibility is that the vitreous hemorrhage existed preoperatively. In such a case, ghost cells are released from an existing reservoir, and pressure elevation may occur only a few days after surgery. In the second scenario, the surgery is complicated by hyphema, and the erythrocytes pass backward into the vitreous cavity through a disrupted anterior hyaloid face. The hyphema may produce a transient IOP rise in the early postoperative period, and then weeks later the IOP may rise again as a result of ghost cells reaching the anterior chamber.57 It is worth noting that the presence of an intraocular lens does not preclude the occurrence of ghost cell glaucoma.58
It is also possible that ghost cell glaucoma occurs without prior surgery or trauma, for example in long-standing diabetic vitreous hemorrhage when a defect in the anterior hyaloid develops, presumably spontaneously, as the vitreous liquefies.59
Similar to ghost cell glaucoma, neovascular glaucoma can also cause a sudden and high IOP elevation, together with corneal edema. There may also be an associated vitreous hemorrhage. To differentiate the two conditions, a drop of glycerol is used to clear the cornea. In neovascular glaucoma, rubeosis may be seen at the pupillary margin or the angle, together with synechial angle closure, neither of which is seen in ghost cell glaucoma. In neovascular glaucoma, there are no ghost cells in the anterior chamber.51
The combination of cells in the anterior chamber with elevated IOP is also seen in hemolytic glaucoma and glaucoma complicating uveitis. In hemolytic glaucoma, the cells are reddish-brown rather than khaki brown. In glaucoma complicating uveitis, the cells are leukocytes, not khaki-colored ghost cells. Typical signs of uveitis are circumcorneal ciliary injection, keratic precipitates, and anterior and posterior synechiae. In ghost cell glaucoma, the conjunctiva is usually white and quiet despite the presence of corneal edema, the ghost cells show no tendency to adhere to the cornea, and there are no synechiae. Questionable cases may require anterior chamber aspiration for resolution of the diagnosis.51 Figure 13–4 summarizes the differential diagnosis of posttraumatic IOP elevation associated with cells in the anterior chamber.
Treatment and Management
How Is Ghost Cell Glaucoma Managed?
Initial management consists of medically lowering the IOP by aqueous suppressants such as beta-blockers, 2-agonists, and CAIs. Miotics are of doubtful value.
If the pressure does not respond to medical management, anterior chamber washout is performed using a blunt cannula inserted into the anterior chamber through a temporal paracentesis. Balanced salt solution is injected into the
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Figure 13–4. High IOP and anterior chamber cells after recent blunt trauma.
angle, and the paracentesis should be wide enough to allow egress of fluid. Approximately 10 mL of fluid are usually needed to wash out the ghost cells from the angle. Before the procedure, an aqueous sample may be obtained for cytologic examination.51
If the IOP remains elevated despite repeated anterior chamber washouts, this indicates that there is still a reservoir of ghost cells in the vitreous. In such a case, pars plana vitrectomy is required to resolve the condition.58,60,61 Special attention must be given to the removal of all ghost cells, including those in the vitreous base. If the offending ghost cells are not completely removed, the remaining cells are released by the vitrectomy procedure, actually worsening the condition.61
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ANGLE RECESSION GLAUCOMA
Definition
How Is Angle Recession Glaucoma Defined?
This is a chronic open-angle glaucoma that occurs secondary to posttraumatic angle recession.
What Is the Mechanism of IOP Elevation in
Angle Recession Glaucoma?
Angle recession is a deepening of the anterior chamber angle resulting from a tear in the face of the ciliary body between the scleral spur and the iris root, frequently occurring between the circular and longitudinal muscles of the ciliary body. In most cases, at least 180 degrees of the angle needs to be affected for IOP elevation to develop. Characteristically, the IOP elevation occurs years after the initial trauma that caused angle recession. In a series of 18 patients with angle recession, Herschler62 reported that the mean duration between initial trauma and the discovery of IOP elevation was 16 years.62 Mermoud et al63 studied 65 patients with angle recession and found that the latency period between injury and diagnosis of glaucoma averaged 7.6 ± 9.5 years.
The exact mechanism of IOP elevation in association with angle recession is controversial. It has been suggested that angle recession provides evidence of past injury but is not the actual cause of the glaucoma. It is believed, rather, that the initial trauma causes degeneration or proliferative changes in the trabecular tissue, which decrease outflow facility.64 Another theory is that the cause of glaucoma is the formation of a Descemet-like membrane that grows from the cornea over the anterior chamber angle.64–66
Epidemiology and Importance
What Is the Incidence of Angle Recession
Following Blunt Trauma?
The incidence of angle recession following blunt trauma varies in different reports from 60 to 94%.2,15,67–69 Therefore, it should be suspected in every case of blunt ocular trauma, regardless of IOP level. Bilateral angle recession has been reported in 55 to 59% of South African patients with angle recession.63,70
What Are the Risk Factors For IOP Elevation
Following Angle Recession?
The risk of IOP elevation after angle recession appears to be correlated with the extent of angle recession. Studies have shown that all patients who developed IOP elevation had greater than 180 degrees of angle recession.67,71 Similarly, Salmon et al70 reported that the prevalence of glaucoma in 146 eyes with angle recession of any degree was 5%, whereas in eyes with 360-degree angle recessions, the prevalence of glaucoma was 8%.
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Spaeth72 has reported that “normal” fellow eyes in patients with unilateral angle recession glaucoma are more likely to have elevated IOP and a positive response to corticosteroid-provocative testing. It has been suggested, therefore, that eyes with an underlying tendency to develop open-angle glaucoma are more likely to develop a late increase in IOP after blunt trauma.62,72
Diagnosis and Differential Diagnosis
How Is Angle Recession Glaucoma Diagnosed?
The classic presentation of angle recession glaucoma is a unilateral IOP elevation with optic disc excavation and visual field loss.73 Angle recession is suspected when the anterior chamber appears abnormally deep. The typical gonioscopic appearance of angle recession consists of a widened ciliary body band with prominence of the scleral spur. This may be present in the whole angle, or only in scattered areas. However, this appearance may change as the tear in the ciliary body begins to scar, leading to the formation of peripheral anterior synechiae with obliteration of the angle recess. Thus, the initial depth and extent of angle recession may diminish with time. In such cases, other signs of blunt trauma may provide a valuable clue for diagnosis. Such signs include tears of the trabecular meshwork, iridodialysis, cyclodialysis, pupillary sphincter tears, absent or torn iris processes, iridoschisis, iridodonesis, phacodonesis, Vossius ring (an imprint of the pupil on the anterior caspule following blunt trauma), and dark brown to black deposits (small residua of hyphema) in the angle recess inferiorly.13
As mentioned above, angle recession may be bilateral. Therefore, gonioscopy of the fellow eye is mandatory, and is very helpful for comparison purposes. When angle recession is found, the IOP does not necessarily have to be elevated. There may be coincidental pathology decreasing the IOP (e.g., cyclodialysis), effectively “neutralizing” the IOP-elevating effect of angle recession. The other possibility is that the causative injury was relatively recent, and that the pressure elevation has not yet set in. There is usually a latent period of several years following trauma before glaucoma manifests itself. Finally, not every case of angle recession will be associated with IOP elevation.
What Is the Differential Diagnosis
of Angle Recession Glaucoma?
The IOP elevation associated with angle recession is insidious in onset, asymptomatic, and typically unilateral. Therefore, the differential diagnosis of angle recession glaucoma includes all causes of chronic unilateral glaucoma, such as glaucoma associated with the pseudoexfoliation syndrome, uveitic glaucoma, glaucoma complicating intraocular tumors, neovascular glaucoma, and other causes of traumatic glaucoma. Furthermore, the condition may be superimposed on primary open-angle glaucoma, in which case examination of the fellow eye may reveal IOP elevation, an open angle, optic disc changes, and visual field loss.
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Treatment and Management
How Is Angle Recession Glaucoma Managed?
Angle recession is fairly resistant to treatment. Initially, aqueous suppressants are tried, namely beta-blockers, 2-agonists, and CAIs. Pilocarpine was reported to cause a paradoxical increase in IOP in one eye.74 It is probable that the primary mechanism of aqueous drainage in that eye was uveoscleral outflow, because of damage to the trabecular meshwork. Pilocarpine is known to inhibit uveoscleral outflow in humans.
If medical treatment fails, some form of surgery is required. The average success rate of argon laser trabeculoplasty (ALT) in angle recession glaucoma is approximately 25%.75,76 Argon laser trabeculopuncture is an alternative to ALT that has a variable success rate in the literature, ranging from 42% 77 to 91%.76 Filtering procedures are less frequently successful in angle recession glaucoma than in primary open-angle glaucoma (POAG). Mermoud et al78 reported that the success rate of filtering surgery in angle recession glaucoma was 52% versus 89% for POAG at 1 year after surgery, 32% versus 84% at 2 years, and 8% versus 76% at 3 years. The main reason for failure was fibrosis
of the fistula or filtering bleb.78
Given the relatively poor success rate of filtering surgery and the propensity to fibrosis, it is probably worthwhile in these eyes to perform primary filtering surgery with antimetabolites such as 5-fluorouracil (5-FU) or mitomycin C (MMC). In another study, Mermoud et al63 compared trabeculectomy alone to trabeculectomy with MMC or 5-FU, and demonstrated a significantly higher success rate with MMC at 1 and 2 years after surgery.63 Finally, if filtering surgery with antimetabolites fails, a seton procedure is required.
GLAUCOMA SECONDARY TO TRABECULAR INJURY
Definition
What Is Meant by Glaucoma Secondary to Trabecular Injury?
This is an IOP elevation that occurs secondary to trabecular injury, without the presence of angle recession.
What Is the Mechanism of Glaucoma Secondary to Trabecular Injury?
Trabecular meshwork injury occurs in the form of edema or tears. Tears of the trabecular meshwork heal in their original position, and may be impossible to detect later. The tear itself does not decrease outflow facility, but the associated scarring of the trabecular meshwork may decrease outflow facility and cause secondary open-angle glaucoma. In addition, the untorn surrounding trabecular meshwork may sustain some reversible damage, which transiently contributes to the IOP rise.13
Typically, glaucoma secondary to trabecular injury occurs in the first few days after trauma. Depending on the extent and reversibility of trabecular damage, and the preexisting facility of outflow, the glaucoma may be transient, or it may persist and require definitive management.
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Epidemiology and Importance
What Is the Incidence of Trabecular Injury
Following Nonpenetrating Trauma?
The occurrence of trabecular injury following nonpenetrating trauma is often overlooked. When specifically sought, the incidence may be as high as 76%, particularly in injuries that are severe enough to cause hyphema.62 As a result, trabecular injury is one of the commonest causes of early IOP elevation following trauma.
Diagnosis and Differential Diagnosis
What Are the Clinical Features of Glaucoma
Complicating Trabecular Injury?
Trabecular injury should be suspected whenever there is early glaucoma following nonpenetrating trauma. The gonioscopic finding may be trabecular edema, or a tear in the trabecular meshwork. Early after trauma, these findings may be masked by concomitant hyphema or uveitis, although a mild hyphema may allow sufficient visualization of the angle to make the diagnosis. Later on, the gonioscopic findings become much more subtle, and the angle may even appear normal. If there is sufficient recovery of the trabecular meshwork, the glaucoma may resolve. Extensive trabecular damage may result in persistent glaucoma.
What Is the Differential Diagnosis of Glaucoma
Complicating Trabecular Injury?
An early IOP rise following trauma can be due to trabecular injury, hyphema, or traumatic uveitis. Hyphema is distinguished by the finding of red blood cells in the anterior chamber, whereas uveitis is characterized by leukocytes in the anterior chamber. However, it is probably common for all three entities to coexist in different combinations, each contributing to IOP elevation.
After the acute phase has subsided, a persistent IOP rise due to trabecular injury should be differentiated from other secondary open-angle glaucomas occurring after trauma. These include entities associated with intraocular hemorrhage, such as hemolytic glaucoma, ghost cell glaucoma, and hemosiderotic glaucoma. Hemolytic glaucoma and ghost cell glaucoma both exhibit cells in the anterior chamber, which are absent in glaucoma resulting solely from trabecular injury. Hemosiderotic glaucoma, especially late, is not associated with cells in the anterior chamber, similar to glaucoma resulting from trabecular injury. However, hemosiderotic glaucoma may show a characteristic rusty brown discoloration, whereas trabecular injury may leave a normalappearing angle. Siderotic glaucoma complicating an old ferrous iron body is another type of late-onset open-angle glaucoma complicating penetrating trauma. In such a case, there will be other signs of siderosis oculi, as discussed
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later in this chapter. Angle-recession glaucoma may be confused with glaucoma complicating trabecular injury. In most cases, gonioscopy will resolve the problem. Again, both angle recession and trabecular injury may coexist in the same patient.
Finally, a late-onset glaucoma associated with ocular trauma and a normalappearing angle may be simply primary open-angle that had been previously undiagnosed, or was accelerated by mild trabecular injury.
Treatment and Management
How Is Glaucoma Due to Trabecular Injury Treated?
Initially, IOP is lowered by aqueous suppressants as described above. If this succeeds, the patient is kept on medical treatment, and periodic attempts are made to taper therapy. If trabecular function recovers, treatment may be discontinued, or at least reduced. If the IOP fails to respond to medical therapy, filtering surgery is warranted.
GLAUCOMA SECONDARY TO TRAUMATIC CATARACT
Definition
What Is Meant by Glaucoma Secondary to Traumatic Cataract?
This is an IOP elevation occurring in a patient having traumatic cataract resulting from nonpenetrating trauma.
What Is the Mechanism of IOP Elevation from Traumatic Cataract?
In some cases, the IOP elevation presumably results from lens swelling that produces relative pupillary block, which leads to angle closure. This may lead to glaucoma relatively early following the trauma. In other cases, the patient may present with an old traumatic cataract and pressure elevation due to associated angle recession.
Epidemiology and Importance
Is Traumatic Cataract a Risk Factor for Traumatic Glaucoma?
Patients who develop cataract as a result of nonpenetrating injury are more prone to glaucoma than patients who do not develop cataract. Coles17 reported that in a series of patients with traumatic hyphema, glaucoma occurred in 42%
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of patients with traumatic cataract versus only 15% of patients who did not have traumatic cataract.17
Traumatic cataract is also associated with a high risk of angle recession, as the trauma that is severe enough to cause cataract usually causes concomitant angle recession. In a series of 46 eyes with traumatic cataract in which gonioscopy was possible, Canavan and Archer2 found a 96% incidence of angle recession.
Diagnosis and Differential Diagnosis
How Is Glaucoma Secondary to Traumatic Cataract
Diagnosed?
Glaucoma due to pupillary block occurs relatively early after trauma. Examination will reveal a shallow anterior chamber together with cataractous changes in the lens. Gonioscopy may show anterior bowing of the iris (iris bombé) with iridocorneal apposition obscuring a variable portion of normal angle structures.
If the pressure rise is due to concomitant angle recession, it typically occurs years after the trauma (as previously discussed). The patient’s main complaint may be visual due to the cataract, as the glaucoma associated with angle recession is asymptomatic. On examination, the lens is cataractous, and the anterior chamber is deep. Gonioscopy may show the typical changes of angle recession (see Angle Recession Glaucoma, above).
What Is the Differential Diagnosis of Glaucoma
Complicating Traumatic Cataract?
Glaucoma due to pupillary block should be differentiated from other causes of traumatic glaucoma associated with a shallow anterior chamber and angle closure (Fig. 13–5). These include traumatic uveitis with ring synechiae, lens subluxation with incarceration of the lens in the pupil, forward rotation of the ciliary body with forward displacement of the iris-lens diaphragm, and malignant glaucoma.13 Traumatic uveitis is usually associated with white blood cells and flare. Iris bombé is observed when posterior synechiae develop over 360 degrees around the pupil. The anterior chamber is relatively deep centrally, as opposed to the other conditions where the anterior chamber is shallow centrally, and the iris appears to be draped over the lens. Lens subluxation may be associated with phakodonesis. Forward rotation of the ciliary body is suspected when there is choroidal effusion, which may be seen ophthalmoscopically if the media are clear, or diagnosed by B-scan ultrasonography. Definitive diagnosis of ciliary body rotation is now possible with highfrequency ultrasound biomicroscopy.79 Malignant glaucoma (aqueous misdirection syndrome) may also be differentiated from ciliary body rotation by ultrasound biomicroscopy.79,80 The differential diagnosis of angle recession glaucoma is discussed above.
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Figure 13–5. High IOP and a shallow anterior chamber after recent blunt trauma.
Treatment and Management
How Is Glaucoma Secondary to Traumatic Cataract Treated?
If a pupillary block mechanism is evident, neodymium:yttrium-aluminum- garnet (Nd:YAG) laser iridotomy is indicated to relieve pupillary block. If the cataract is visually significant, it may be removed at a later date. If the lens is severely cataractous, or if there is evidence of phakolytic glaucoma, cataract extraction may improve vision and restore normal IOP. The management of angle recession glaucoma is discussed above.