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

270 Traumatic Glaucoma

GLAUCOMA COMPLICATING NONPENETRATING TRAUMA

Definition

How Is the Problem Defined?

Nonpenetrating ocular trauma is injury to the eye resulting from impact of a blunt injurious agent that does not penetrate the globe. Whether or not the trauma is penetrating depends on the size, shape, weight, composition, speed, and direction of the injuring object, as well as the impact, location, and the status of the eye and ocular adnexa before the injury. Various types of glaucoma may complicate nonpenetrating ocular trauma.

Epidemiology and Importance

What Type of Patient Is More Liable to Sustain Direct Ocular Trauma?

Most patients sustaining direct ocular trauma—whether penetrating or blunt— are young, typically less than 30 years of age.1–7 The setting of ocular trauma is related to age, play being the most common in children, sports and assaults in young adults, and work and domestic accidents in older adults.8–10 Males are more commonly victims of ocular trauma than females.2,7,11,12 Patients from lower socioeconomic groups experience more severe and frequent ocular trauma.12

Diagnosis and Differential Diagnosis

What Is the Differential Diagnosis of Glaucoma Secondary to Nonpenetrating Trauma?

Table 13–3 lists the various types of glaucoma complicating nonpenetrating trauma. These may occur singly or in combination. For example, hyphema may be associated with lens dislocation and trabecular injury. Figure 13–2 shows the differential diagnosis of elevated IOP in the presence of recent blunt trauma, and Figure 13–3 after an old traumatic incident.

Table 13–3. Types of Glaucoma Associated with Nonpenetrating Trauma

Glaucoma secondary to hyphema Hemolytic glaucoma Hemosiderotic glaucoma

Ghost cell glaucoma Angle recession glaucoma

Glaucoma secondary to trabecular injury Glaucoma secondary to traumatic cataract Glaucoma secondary to lens dislocation

Glaucoma secondary to forward movement of the iris-lens diaphragm Glaucoma secondary to posttraumatic uveitis

274 Traumatic Glaucoma

ocular trauma12 to 55.2% in a survey of penetrating injuries caused by assault.3 Patients with traumatic hyphema are most often young males, with sportsrelated injuries and assaults accounting for the majority of cases associated with blunt trauma.16

The incidence of elevated IOP in traumatic hyphema has been found to correlate well with the size of the hemorrhage. Coles17 studied 235 cases of traumatic hyphema, and found elevated IOP in 13.5% of eyes with hyphema filling less than half of the anterior chamber, 27% with hyphema filling more than half of the anterior chamber, and 52% with total hyphema. Elevated IOP is also more commonly seen in eyes that rebleed. In a series of 113 cases, glaucoma developed in 33% of patients who rebled and in 100% of patients when rebleeding resulted in eight-ball hyphemas.18

Patients with sickle cell hemoglobinopathy may have IOP elevation disproportionate to the amount of the hyphema.19 Their erythrocytes have a tendency to sickle in aqueous humor, and the sickled cells may pass slowly through the trabecular meshwork. These patients are also in greater jeopardy from the elevated IOP because of their predisposition to central retinal artery occlusion.19,20

Diabetes mellitus has also been implicated with delayed clearance of erythrocytes from the anterior chamber, as erythrocytes from patients with proliferative diabetic retinopathy show decreased deformability and increased adherence.21

Diagnosis and Differential Diagnosis

How Is Hyphema Diagnosed?

The clinical diagnosis of hyphema is based on the finding of red blood cells in the anterior chamber. The amount varies from rare circulating cells in the aqueous to subtotal hyphema with a level, or even total hyphema that may darken to become a “black-ball” or “eight-ball” hyphema. The presence of uniformly bright red blood indicates a fresh hemorrhage, although this may darken with time. The presence of layering (i.e., a mixture of fresh and clotted blood) should alert the examiner to the possibility of rebleeding.13

Once hyphema is detected, it should not be immediately assumed that the trauma was blunt. Penetrating trauma, with or without an intraocular foreign body, may also cause hyphema. Therefore, the examiner should reascertain the nature of the injury from the patient, or the accompanying family members. The eyelids, conjunctiva, cornea, and sclera should be carefully examined with the slit lamp for the possibility of penetrating injury. If necessary, plain x-ray and computed tomography (CT) imaging may be performed to exclude intraocular foreign bodies. These imaging techniques are also useful for the exclusion of orbital fractures.

Other signs of blunt trauma should be sought. These include pupillary sphincter tears, iridodialysis, angle recession, cyclodialysis, trabecular dialysis, lens subluxation or dislocation, retinal dialysis and/or detachment, macular edema (commotio retinae), and choroidal rupture.22 Gonioscopy (to detect angle recession, cyclodialysis, or trabecular dialysis) should not be performed until 4 weeks after the traumatic incident, as the attendant pressure on the globe may reopen an occult rupture of the globe, or promote rebleeding by

dislodging a blood clot from the injured vessel. Likewise, scleral indentation to detect peripheral retinal pathology should be deferred. If the hyphema is total, ultrasound examination may be useful to detect coincidental posterior segment pathology, such as vitreous hemorrhage, retinal detachment, and posterior lens dislocation. Where available, high-frequency ultrasound (ultrasound biomicroscopy) may detect anterior segment conditions masked by a total hyphema, such as lens subluxation or angle recession.23

With the slit lamp, a search is made for corneal blood staining. Pathologic studies of blood staining demonstrate erythrocyte breakdown products and hemosiderin in the keratocytes and corneal stroma.24 Initially, this will manifest as a subtle yellowish discoloration of the posterior corneal stroma. Although corneal blood staining requires a high IOP, it may occur in the absence of glaucoma if there is corneal endothelial damage. When corneal blood staining is detected, this in itself may be an indication for surgical evacuation of the hyphema.

The visual acuity should be correlated with the amount of hyphema and coincidental ocular pathology. The presence of profoundly reduced vision (no light perception or bare light perception) that is not explained by the amount of hyphema or posterior segment problems should alert the examiner to the possibility of traumatic optic neuropathy, which may require megadose steroid therapy or surgical decompression of the optic canal.25 Nevertheless, many patients with hyphema manifest afferent pupillary defects caused by the intraocular blood itself, rather than by the optic nerve injury.13

The IOP is measured by applanation tonometry or pneumatonometry. Ocular pressure by palpation is avoided in the acute period for reasons similar to gonioscopy and scleral indentation. Examination of the fellow eye is essential to provide a baseline IOP or to rule out the possibility of preexisting primary glaucoma in the injured eye.

If the patient is of African descent, a search should be made for sickle cell disease, including hemoglobin electrophoresis. If sickle cell disease is present, management will have to be more aggressive. Similarly, diabetes is also ruled out.

What Is the Differential Diagnosis of Hyphema with Glaucoma?

If the patient does not have a history of trauma, and there are no signs suggestive of trauma, other causes of hyphema should be considered, as any of them may be accompanied by glaucoma. These include neovascular glaucoma, herpetic iridocyclitis, retinoblastoma, uveal malignant melanoma, and juvenile xanthogranuloma.

Treatment and Management

How Is Glaucoma Complicating Hyphema Managed?

Management should be directed toward three main aims: encouraging resorption of hyphema, prevention of rebleeding, and treatment of elevated IOP.

To encourage hyphema resorption, activity should be restricted. For simple hyphema, outpatient management with limited activity and a shield may

276 Traumatic Glaucoma

suffice.26,27 For severe cases and sickle cell patients, hospitalization with bed rest is mandatory.

Many drugs have been used to accelerate resorption of hyphema, including intravenous hyperosmotic agents (urea and mannitol), subconjunctival methylprednisolone,28 systemic acetazolamide, topical atropine and pilocarpine,29 and intracameral tissue plasminogen activator (TPA),30 but none has been shown to have a clinically significant benefit. Although TPA was found in a rabbit model to accelerate hyphema resorption, it also substantially increased rebleeding episodes.30

Prevention of rebleeding is achieved by inhibition of clot lysis. Two antifibrinolytic agents, aminocaproic acid31–33 and tranexamic acid,34 have been tried, with equivocal results. Aminocaproic acid often causes nausea, vomiting, systemic hypotension, and dizziness, and has not been universally accepted. Furthermore, both drugs may precipitate thrombotic episodes in predisposed patients, such as patients with coronary artery disease. Because of these considerations, antifibrinolytics are reserved for patients at high risk of complications related to rebleeding, such as those with sickle cell disease, and perhaps all black patients.13

Elevated IOP associated with hyphema usually responds favorably to topical aqueous suppressant therapy, such as beta-blockers and 2-agonists. CAIs may also be added when required. However, systemic acetazolamide is better avoided in sickle cell patients, as it increases ascorbate levels in the aqueous humor and produces systemic acidosis, both of which exacerbate erythrocyte sickling.19 Methazolamide may be safer as it causes less systemic acidosis than acetazolamide.

When elevated IOP cannot be controlled medically and threatens to damage the optic nerve head, or if the hyphema is associated with corneal blood staining, surgical intervention is indicated. The critical level of IOP that warrants intervention depends on the status of the optic nerve head and the patient’s general medical status. A healthy optic nerve may tolerate pressures of up to 40 or 50 mm Hg for a week or longer, whereas a glaucomatous disc may suffer further damage with substantially lower pressures within a shorter time period. Evaluation of the fellow eye may provide important information on preexisting glaucoma. Even the slightest IOP rise should be taken more seriously in sickle cell patients, as they are more prone to retinal artery occlusion.13

The optimal time for surgical intervention is controversial. Rebleeding is more frequent if intervention is instituted early. Furthermore, if intervention is delayed 3 to 5 days, many cases will resolve spontaneously. Four days has been suggested as the optimal time for surgical intervention with total hyphemas, as this allows optimal clot retraction without adherence to adjacent tissues.35

Various surgical approaches have been utilized successfully. The simplest of these is anterior chamber washout by irrigation through a paracentesis, with or without fibrinolytics.36,37 Cases with more extensive clotting may require clot aspiration with the aid of ultrasonic emulsification or vitrectomy instrumentation. 38,39 In such cases, complete clot removal is neither safe nor necessary. Repeated attempts to disengage the clot may result in iris, lens, or angle damage, or invite rebleeding. Alternatively, the clot may be expressed out of the anterior chamber through a corneoscleral incision with the aid of a viscoelastic agent.40,41 Trabeculectomy with gentle irrigation through a separate paracentesis

What Is the Differential Diagnosis?

Hemosiderotic glaucoma should be distinguished from other open-angle glaucomas associated with intraocular hemorrhage. Hemolytic glaucoma is differentiated from hemosiderotic glaucoma by the presence in the former of reddish-brown blood cells, and reddish brown pigment covering the trabecular meshwork, especially inferiorly. Ghost cell glaucoma is characterized clinically by the presence of khaki-colored cells in the aqueous and vitreous, which may settle in the angle, especially inferiorly, or may be so numerous as to cause a pseudohypopyon.

As with all glaucomas associated with intraocular hemorrhage, the inciting hemorrhage may be of traumatic or nontraumatic origin.

Treatment and Management

How Is Hemosiderotic Glaucoma Managed?

The initial management of hemosiderotic glaucoma consists of lowering the IOP using beta-blockers, 2-agonists, CAIs and, when necessary, hyperosmotic agents. If medical treatment fails to control the condition, it may be due to advanced siderotic angle damage, and filtering surgery may be appropriate. However, intraocular hemorrhage may require washout (hyphema) or vitrectomy (vitreous hemorrhage).

GHOST CELL GLAUCOMA

Definition

How Is Ghost Cell Glaucoma Defined?

Ghost cell glaucoma is an open-angle glaucoma associated with degenerated erythrocytes (ghost cells).

What Is the Mechanism of Ghost Cell Glaucoma?

After a prolonged vitreous hemorrhage, ghost cells develop in the vitreous and subsequently migrate to the anterior chamber through a disrupted anterior hyaloid face. As the erythrocytes degenerate in the vitreous, they change from their typical biconvex shape to spherical khaki-colored ghost cells (erythroclasts). The latter are more rigid than normal erythrocytes and less able to pass through the trabecular meshwork.47 The condition is often transient, with the IOP returning to normal levels after the denatured cells clear from the anterior chamber angle. However, this may take months.

The onset of ghost cell glaucoma is typically 2 to 3 weeks following trauma, as it takes at least 1 to 2 weeks for erythrocytes to degenerate into ghost cells.48,49 The degree of IOP elevation depends on the number of ghost cells reaching the anterior chamber. If the number of cells is small, the IOP may be normal, and if sufficient cells are present, the IOP may reach 50 or 60 mm Hg.