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Traumatic glaucoma is a multifactorial group of disorders that results from closed- or open-globe injuries. Although different underlying mechanisms may be involved with the initial injury, the resulting optic neuropathy and visual field loss is secondary to elevated IOP from reduction in aqueous outflow through the trabecular meshwork. Secondary glaucoma after trauma is more likely to occur with a closed-globe injury, but it is often underdiagnosed because its onset may be delayed and the history of eye injury may be remote or overlooked.
Angle recession is a common manifestation of blunt ocular trauma and involves rupture of the ciliary body face, resulting in a tear between the longitudinal and circular fibers of the ciliary muscle. Angle recession is reported to occur in 20 to 94 percent of eyes after blunt trauma and is often masked initially due to the presence of concomitant hyphema, which results from shearing of the anterior ciliary arteries. Approximately 5 to 20 percent of eyes with angle recession develop angle-recession glaucoma.
This brief review will discuss the pathophysiology and clinical course and signs of angle-recession glaucoma, along with differential diagnosis and treatment strategies.
Blunt force to the globe causes an anterior to posterior axial compression with equatorial distension. Abrupt indentation of the cornea forces posterior and lateral displacement of aqueous humor, deepening the peripheral anterior chamber and increasing the diameter of the corneoscleral limbal ring. These resultant shock waves traversing the interior of the globe are responsible for other anterior segment damage accompanying angle recession, such as pupillary sphincter tears, iridodialysis, cyclodialysis and zonular tears.
The shearing forces to the drainage angle result in a tear between the longitudinal and circular fibers of the ciliary muscle. While the longitudinal muscle insertion at the scleral spur remains intact, the circular muscle is displaced posteriorly along with the iris root and pars plicata. The resultant glaucoma is not due to angle recession per se, but is secondary to initial trauma to the trabecular meshwork, with subsequent degenerative changes and scarring, which leads to obstruction of aqueous outflow.
Less often, a hyalinized membrane may cover the inner surface of the trabecular meshwork. This membrane may be continuous with Descemet’s membrane and may extend peripherally into the recessed angle and onto the anterior surface of the iris. The membrane obstructs aqueous outflow, causing an open-angle form of glaucoma. In some cases, this membrane may contract, resulting in angle-closure glaucoma.
Clinical Course and Signs
As mentioned previously, 5 to 20 percent of eyes with angle recession develop angle-recession glaucoma. Onset is extremely variable and may occur soon after the initial trauma or even years later, indicating possibly separate pathologic mechanisms.
The risk of developing angle-recession glaucoma appears to be related to the extent of angle recession. Angle recession of more than 180 degrees is deemed a considerable risk for secondary glaucoma, although glaucoma can develop when the area of recession is smaller than this.
In one study, researchers found that approximately 50 percent of patients with traumatic glaucoma developed open-angle glaucoma in the unaffected, contralateral eye, suggesting that these patients may have an underlying genetic predisposition to developing glaucoma, which may be accelerated by a traumatic insult.1
IOP may rise immediately after the injury, as a result of associated comorbidities such as hyphema, iridocyclitis or pupillary block from ectopia lentis (with or without vitreous prolapse).
In some cases, IOP may be low secondary to decreased production of aqueous humor from associated inflammation, a transient increase in aqueous outflow facility from disruption of structures in the angle, or the presence of a cyclodialysis cleft.
Anterior segment examination is important. Once the acute inflammation and hyphema resolve, attention should be paid to the anterior chamber depth of the affected eye, which may appear deeper. The meticulous physician will also look for other abnormalities encountered with trauma, such as iris sphincter tears, mydriasis, iris atrophy, iridoschisis, iridodonesis, phacodonesis and a subluxated lens.
Gonioscopy, a simple diagnostic test, is essential for making the clinical diagnosis of angle recession. It is usually deferred for four to six weeks after the acute injury. When gonioscopy is performed, asymmetry of the angle recess may be noticeable between the affected and the nontraumatized eye or in different quadrants of the involved eye. Widening of the ciliary body band may be present due to retrodisplacement of the iris root. Other signs include irregular and darker pigmentation in the angle, whitening of the scleral spur due to visibly fractured iris processes, or the presence of peripheral anterior synechiae.
Gonioscopy may aid in the diagnosis of other angle abnormalities from trauma, such as iridodialysis or cyclodialysis. It’s essential to note that, in some cases, the gonioscopic findings may become more difficult to recognize with the passage of time.
Posterior segment examination will detect abnormalities that may also be present, and a dilated fundus exam should be performed after gonioscopy.
After the trauma occurs, elevated IOP may be secondary to obstruction of the trabecular meshwork by red blood cells, inflammatory cells or pigmented cells. Later, ghost-cell glaucoma may develop from long-standing vitreous hemorrhage and a disrupted anterior hyaloid face or an open posterior capsule. Chronic treatment with steroids can lead to steroid-induced glaucoma.
Although the diagnosis of angle-recession glaucoma is evident after careful gonioscopy and optic nerve examination, other differential diagnoses for unilateral glaucoma should be considered. These include—but are not limited to—pseudoexfoliative glaucoma, neovascular glaucoma, uveitic glaucoma, lens-particle glaucoma and phacolytic glaucoma.
Three Options for Treatment
Medication. In the acute setting, treatment should be directed at lowering IOP and controlling inflammation. Topical steroids and cycloplegic agents are used to control inflammation and pain. Aqueous suppressants are preferred as initial IOP-lowering agents. Prostaglandin analogs have a theoretical benefit of bypassing the dysfunctional trabecular meshwork by increasing uveoscleral outflow. Miotics should be avoided because they can cause a paradoxical rise in IOP, presumably due to a reduction in uveoscleral outflow.
Laser. Laser trabeculoplasty is not effective in angle-recession glaucoma due to distortion of the angle anatomy and trabecular meshwork scarring. An alternative laser procedure, Nd:YAG laser trabeculopuncture, has produced variable success rates, with better responses seen in cases where some trabecular meshwork structure was intact on gonioscopy, permitting penetration into Schlemm’s canal with an increase in aqueous outflow facility.
Surgery. Filtration surgery has a lower success rate in angle-recession glaucoma than it does in primary open-angle glaucoma. The adjunctive use of antimetabolites can improve the success of trabeculectomy. Researchers have found greater IOP reduction in cases where antimetabolites were employed with trabeculectomy than in trabeculectomy alone or Molteno tube implantation alone.2
Glaucoma drainage devices have demonstrated some benefit, but their success rates are lower in angle-recession glaucoma than with other types of glaucomas. In eyes with limited visual potential, a cyclodestructive procedure may be an alternative option.
A patient who has experienced blunt ocular trauma should receive a comprehensive eye exam to check for the presence of angle recession and other abnormalities. The risk of angle-recession glaucoma correlates with the extent and severity of angle recession.
In general, angle-recession glaucoma is more difficult to control medically and surgically than other types of glaucomas. Because angle-recession glaucoma can occur even many years after trauma, patients should receive adequate counseling, and follow-up examinations should be performed regularly.
1 Tesluk, G. C. and G. L. Spaeth. Ophthalmology 1985;92:904–911.
2 Mermoud, A. et al. Ophthalmology 1993;100:634–642.
Dr. Boonyaleephan is a visiting research scholar in ophthalmology and Dr. Salim is associate professor of ophthalmology; both are at the University of Tennessee, Memphis.
Coding in Chicago
Attend Glaucoma Coding, event code “213.” It walks you through successful glaucoma documentation and coding and takes place Sunday, Oct. 17, from 2 to 3 p.m.