(A)

(B)

Fig. 18-14  (A) Goniophotograph of a recessed angle. The angle recess and the width of the ciliary body band vary from area to area. (B)  Blood in the angle following traumatic angle recession. Jugular compression resulted in discharge of blood from Schlemm’s canal into the anterior chamber in this patient who suffered angle recession some months previously. The patient had experienced periodic blurring of vision with pressure elevation as a result of this blood in the anterior chamber. It was resolved with laser applied to the bleeding point.

(From Campbell DG, Netland PN: Stereo atlas of glaucoma, St Louis, Mosby, 1998.)

Fig. 18-15  Histopathology of a previous tear into the ciliary face showing the root of the iris recessed posterior to Schlemm’s canal.

recession include absent or torn iris processes, posterior attachment of the iris root (Fig. 18-15), an anterior chamber deeper than in the fellow eye, and increased visibility and width of the scleral spur. Late glaucoma is more frequent if the recession involves three-quarters or more of the angle but can occur even with recessions of 1 clock hour or less. The angle recession is not the cause of the glaucoma, but rather it is an indicator of previous trauma.

Late glaucoma occurs in an estimated 2–10% of eyes after contusion injuries.250–252

It is thought that eyes with an underlying tendency to develop open-angle glaucoma are more likely to develop late increased IOP after blunt trauma.This theory is supported by the observation that many of the supposedly normal, untraumatized fellow eyes have spontaneous IOP elevations. Furthermore, the normal fellow eyes respond to topical corticosteroids, similar to eyes with POAG.253

The unifying theory is that eyes with marginal outflow facility are more likely to develop pathologic pressure elevations with trabecular injury than are eyes with excess or reserve outflow facility. Because the outflow facility tends to be about equal in the two eyes, a patient with angle recession and glaucoma might well be expected to have poor outflow in the fellow eye.

Histopathologic study of eyes with post-traumatic glaucoma may reveal a cuticular membrane covering the trabecular meshwork. However, it is not clear whether this membrane is the cause of the glaucoma.12

The treatment of late postcontusion glaucoma usually consists of the full antiglaucoma regimen, including miotics.254–258 Argon laser trabeculoplasty is often disappointing in this condition but should be considered before proceeding to filtering surgery. It should be emphasized again that the untraumatized fellow eyes should be watched closely for elevated IOP.

Glaucoma associated with intraocular hemorrhage

Ghost-Cell Glaucoma

Ghost-cell glaucoma is an uncommon condition that occurs in association with intraocular hemorrhage.259 In this entity, RBCs degenerate in the vitreous, migrate forward to the anterior chamber through a disrupted anterior hyaloid face, and then obstruct the trabecular meshwork.260 The vitreous hemorrhage is usually caused by retinal disease, trauma, or surgery; a recent case report associated ghost-cell glaucoma with snake poisoning injury.261 Generally the

anterior hyaloid face has been disrupted by vitrectomy, cataract surgery, or trauma,262,263 but ghost-cell glaucoma has been reported

in non-traumatized phakic eyes as well.264 The RBCs in the vitreous degenerate to tan-colored spheres (ghost cells), which appear empty except for clumps of denatured hemoglobin called Heinz bodies. The ghost cells are more rigid than are normal RBCs and thus are less able to pass through the trabecular meshwork.259 This proposed mechanism is supported by animal experiments in which infusion of fixed RBCs produced elevated IOP.265

When examined, patients with ghost-cell glaucoma have elevated IOP, which may be sufficient to cause pain and corneal edema. Slit-lamp examination shows tiny, tan-colored cells in the vitreous, aqueous, and trabecular meshwork. Sometimes the cells in the

anterior chamber are so numerous that they settle into a pseudohypopyon.259,266 The diagnosis of ghost-cell glaucoma is confirmed

by anterior chamber paracentesis. The anterior chamber aspirates

can be passed through a Millipore filter and then stained,267 or the fluid can be examined by phase-contrast microscopy.266,268

Ghost-cell glaucoma is a transient condition that can last for weeks or months depending on the volume of blood in the vitreous and the ability of the trabecular meshwork to clear the degenerated cells. Many cases are controlled by standard medical therapy, including topical -adrenergic antagonists, agonists, topical CAIs (oral if necessary), and hyperosmotic agents. Resistant cases are treated with anterior chamber washouts, which can be repeated as needed. If IOP cannot be controlled by repeated anterior chamber

lavage, a vitrectomy should be performed to remove as much of the blood as possible.269,270

Hemolytic Glaucoma

Hemolytic glaucoma is a rare form of glaucoma associated with intraocular hemorrhage. It resembles ghost-cell glaucoma, except that in hemolytic glaucoma macrophages phagocytize RBC debris and then occlude the trabecular meshwork.271 When examined, these eyes demonstrate elevated IOP, reddish cells in the aqueous humor, open angles, and increased pigmentation of the trabecular meshwork.272 The diagnosis is confirmed by anterior chamber paracentesis, which reveals pigment-containing macrophages rather than khaki-colored ghost cells. Microscopic study of eyes with hemolytic glaucoma shows the trabecular meshwork to be occluded by RBCs, debris, and macrophages laden with pigment.273 Hemolytic glaucoma is usually a self-limited condition that responds to management with topical and systemic pres- sure-lowering medications. If IOP is not controlled, an anterior chamber washout should be performed. If this is not successful, a filtration or cyclodestructive procedure may be indicated.

Hemosiderosis

Hemosiderotic glaucoma is a rare entity associated with intraocular hemorrhage. Hemosiderosis is similar to siderosis, except that the source of iron in hemosiderosis is degenerating RBCs rather than a retained foreign body. Hemoglobin released by degenerated RBCs is phagocytized by trabecular endothelial cells.The iron lib-

erated from the hemoglobin causes siderosis and discoloration of the meshwork.225,274

Hyphema

Blunt trauma to the globe can produce a tear in the ciliary face and bleeding into the anterior chamber. Traumatic hyphemas can

occur in patients of any age or either gender but are typically seen in young men.275,276 Patients with hyphemas complain of redness

and blurred vision; if IOP is elevated, patients may also complain of pain, nausea, and vomiting. The history of the injury reveals trauma that seems severe in some cases and trivial in others. In all cases, however, the object causing the trauma must have been small enough or sufficiently deformable to fit inside the rim of the orbit in order to strike the globe.

When examined, patients with hyphemas demonstrate diminished vision, conjunctival injection, RBCs floating in the aqueous humor, a variable amount of blood settled to the bottom of the anterior chamber, and normal or low IOPs. Children with traumatic hyphemas often appear somnolent. In most patients, the blood clears spontaneously in a few days with no immediate

Fig. 18-16  Blood staining of a cornea that is beginning to clear in the periphery.

­complications. A few weeks after the injury, these patients should have a careful dilated examination to search for retinal tears, retinal dialyses, and choroidal ruptures.They should also undergo gonioscopy to determine whether angle recession is present.

Unfortunately some patients with traumatic hyphemas have recurrent episodes of hemorrhage into the anterior chamber, or re-bleeds. Most episodes of re-bleeding occur within a few days of the trauma. It is postulated that additional bleeding occurs when the blood clot closing the vessel torn in the original injury under-

goes lysis and retraction.277 Reports indicate that re-bleeding after traumatic hyphema occurs in 4–35% of patients.277–287 There is reasonable evidence linking aspirin use to re-bleeding.279,288,289

Some authorities also believe that re-bleeding is more common in blacks and in individuals with larger hyphemas and hypotony.282,285

Re-bleeding is important because it is often associated with complications, including corneal blood staining (Fig. 18-16), optic atrophy, and elevated IOP. In most cases, elevated IOP is caused by RBCs obstructing the trabecular meshwork.290 Less often, the blood clot may produce pupillary block. Glaucoma is more frequent when the hyphema is total. A total hyphema changing color from red to black (black-ball or eightball hyphema) is an ominous sign of impending complications. The exact reason for this is obscure, but it is assumed that the underlying injury is more severe in many eyes with eightball hyphema compared with eyes with subtotal hyphema.

The management of traumatic hyphema has been controversial.291 Typical practice in the past was to hospitalize all patients for bed rest, sedation, and bilateral patching. However, there is evidence

that bed rest and patching are not necessary and that equally good results can be obtained by limiting activity.280,284,292 If there is a

stable family situation, some patients can be managed at home and checked daily in the physician’s office. Despite widespread use, no

evidence suggests that either cycloplegics or miotics facilitate the clearing of blood.293,294 The antifibrinolytic agents epsilon-ami-

nocaproic acid (Amicar) and tranexamic acid have been found to decrease the incidence of rebleeding.277,278,283,295–300 The reported

track record of tranexamic acid remains fairly good, although its use is not entirely without risk. The effectiveness of aminocaproic acid has been questioned by some investigators, who found no significant difference in re-bleed rates between patients treated

with aminocaproic acid and those treated with either corticosteroids or placebo.301–304