Traumatic Glaucoma
Angela V. Turalba
Mary Jude Cox
INTRODUCTION
Following ocular trauma, patients often develop difficulties with intraocular pressure control. Intraocular pressure may be elevated or the eye may be hypotonous. Patients may have difficulty acutely or many years following the injury. In either case, a thorough history and examination will often determine the cause and severity of the intraocular damage and the appropriate course of treatment and follow-up. Open and closed globe injuries can result in damage to any of the ocular structures. This chapter focuses on traumatic hyphemas, angle recession, and cyclodialysis clefts.
TRAUMATIC HYPHEMA
The term hyphema refers to the blood in the anterior chamber. The amount of blood may be microscopic, termed microhyphema, visible only at the slit lamp as nonlayering red blood cells in the aqueous. Red blood cells may also layer or form clots in the anterior chamber (Figs. 16-1, 16-2 and 16-3). As the blood clears from the anterior chamber, it will settle in the angle and is only visible on gonioscopy. A total hyphema refers to layered blood filling the entire anterior chamber (Fig. 16-4). A total hyphema that has clotted and appears black in color is referred to as an eight-ball hyphema (Fig. 16-5). A traumatic hyphema can result from either blunt or penetrating injury to the globe. The majority of hyphemas resolve gradually without sequelae; however, complications such as rebleeding, increased intraocular pressure, and corneal blood staining (Fig. 16-6) can occur. After a hyphema clears, traumatic cataracts and iris damage become more apparent (Figs. 16-7 and 16-8).
Epidemiology
• Traumatic hyphemas are most common in young active men, with a male-to-female ratio of approximately 3:1. In general, the risk of complications such as rebleeding, uncontrolled intraocular pressure, or corneal blood staining increases with the size of the hyphema. Patients with sickling hemoglobinopathies, however, are an exception. These patients are at an increased risk of developing complications regardless of the size of the hyphema.
• Rebleeding occurs in up to 35% of patients. The majority of rebleeding episodes take place within 2 to 5 days of the initial injury. Rebleeding is often larger than the original hyphema and more prone to complications.
Pathophysiology
• Blunt trauma causes compressive forces that result in the shearing of iris and ciliary body vessels. Tears in the ciliary body result in damage to the major arterial circle of the iris. Penetrating injuries can cause direct damage to blood vessels. Clots plug these damaged blood vessels, and rebleeding occurs as these clots retract and lyse (Fig. 16-2B).
• Intraocular pressure rises acutely as red blood cells, inflammatory cells, and debris obstruct the trabecular meshwork (Fig. 16-1C). Elevated intraocular pressure can also be the result of pupillary block caused by the clot in the anterior chamber. Eight-ball hyphemas often cause this form of pupillary block and can impair aqueous circulation (Fig. 16-5). The impaired aqueous circulation causes a reduction in oxygen concentration in the anterior chamber, resulting in the black appearance of the clot.
• In patients with sickle cell disease or trait, sickling causes the red blood cells to be rigid and easily trapped in the trabecular meshwork, leading to elevated intraocular pressure even in the presence of a small hyphema. Sickle cell patients are subject to vascular occlusion and optic nerve damage at lower intraocular pressures as a result of microvascular compromise.
History and Clinical Examination
• For patients presenting with a traumatic hyphema, a thorough evaluation of the timing and nature of the trauma is important to determine the likelihood of additional injuries and the need for close observation and treatment. Patients may be asymptomatic or have reduced vision, photophobia, and pain. Nausea and vomiting may accompany a rise in intraocular pressure. There may be evidence of orbital trauma or damage to other ocular tissues.
• Slit lamp: Slit-lamp examination may show circulating red blood cells alone or in combination with a layered hyphema in the anterior chamber. When there is elevated intraocular pressure associated with a large hyphema, corneal blood staining can occur (Fig. 16-6). There may be evidence of trauma to other ocular structures such as cataract (Fig. 16-7), phacodonesis, subconjunctival hemorrhage, foreign bodies, lacerations, or iris damage such as sphincter tears, iridodialysis, or traumatic aniridia (Figs. 16-7A and 16-8).
• Gonioscopy: Gonioscopy should be delayed until the risk of rebleeding has passed. When performed 3 to 4 weeks after the initial injury, the angle may appear undamaged or may show residual blood (see Fig. 16-1C) or angle recession (Fig. 16-9). Occasionally, peripheral anterior synechiae or a cyclodialysis cleft (Fig. 16-10A) may be present.
• Posterior pole: The posterior pole may show evidence of blunt or penetrating trauma. Commotio retinae, choroidal ruptures, retinal detachments, intraocular foreign bodies, or vitreous hemorrhage may be present. Scleral depression should be delayed until the risk of rebleeding has passed. A persistent vitreous hemorrhage can also cause elevated intraocular pressures in the form of ghost cell glaucoma. Unlike the typical red blood cells seen in hyphemas, tan-colored ghost cells can be observed in the anterior chamber. Ghost cells are degenerated erythrocytes that clog the trabecular meshwork as they make their way from the posterior segment to the anterior chamber presumably through a break in the anterior hyaloid face.
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