This gonioscopic view shows the patient’s inferior angle structures, including 2 small synechiae: 1 attached to the scleral spur, and a second attached to the trabecular meshwork.
A 52-year-old patient presented with a chief complaint of a problem reading small print. He was in good health and was taking no systemic or eye medications. He had not had an eye examination for many years, and never wore glasses. However, his ocular history was significant as 15 years earlier he had experienced a penetrating globe injury to his left eye. He recalled being told that the injury caused bleeding inside the eye as well as some eye damage, but his vision and eye would recover, and it did. He remembered being first treated with an eye drop (pilocarpine, as, at that time, beta blockers were not yet available). After being managed with other glaucoma medications, he underwent eye surgeryAt this visit, his visual acuity (VA) was correctable to 20/20 in each eye with minimal myopic correction. His pupillary reactions were normal but his intraocular pressures (IOP) were consistently 17 mm Hg OD and between 27 and 30 mm Hg OS. An optic nerve assessment revealed a normal right disc rim, but inferior temporal thinning of the disc rim tissue in the left eye. No field defects were found with standard 24-2 visual field testing.
A gonioscopic exam showed angle recession in the left eye and inferior angle structures, including 2 small synechiae (1 likely attached to the scleral spur, and another appeared attached to the trabecular meshwork). Note the presence of some pigment spots in the trabecular meshwork. The small triangular dark area underneath and behind the ciliary body band (CBB), is a portion of a cyclodialysis cleft, where aqueous can escape through the ciliary muscles to the suprachoroidal space and bypass the damaged trabecular area. This may have helped keep the IOP lower, and resulted in causing less damage to the optic nerve. In the photo, some of the angle recession can be seen from the 4 o’clock to 8 o’clock positions. The total area of angle recession seen was 180 degrees. The trabecular area and adjacent structures appear small in the gonio view, due to the viewing angle. He was referred to and then followed by a glaucoma specialist.
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Blunt trauma can cause both anterior segment and posterior segment injuries, or both. In the anterior segment, it causes distortion of the angle anatomy area, and a widening of the angle, termed angle recession. It also can cause unilateral glaucoma, termed angle recession glaucoma (ARG). This traumatic event is referred to as traumatic glaucoma and classified as a secondary open angle glaucoma. It is the result of sudden blunt or sharp object trauma to the globe. The force from the trauma causes axial compression and rapid equatorial compensatory equatorial expansion, which can result in significant damage and distortion of ocular tissues including the angle. The sudden equatorial expansion directed at the angle structures and the ciliary body, results in disorganization of the angle, causing irregular widening of the ciliary body band. In addition, there are changes in the depth, color and texture of the angle structures.1 Posterior anterior synechiae (PAS) and remnants of small dark pigment balls or old blood may be present. Histologically the angle recession represents a tear between the longitudinal and circular muscles of the ciliary body, resulting in the posterior displacement of the ciliary body along the iris root.2-4 This posterior displacement of the ciliary body is why see more of the ciliary body band with gonioscopy.
Angle recession glaucoma (ARG) is divided into 2 categories. The first, termed “early onset,” usually occurs within the first few years. The second, “late onset,” can occur many years later.5 In these late onset unilateral glaucoma cases, the angle recession itself is probably not the only cause of the elevated IOP. Late fibrosis and hyalinization of the trabecular meshwork may be sufficient enough to eventually decrease the membrane’s filtering ability. This vulnerability may also be due to the added effect of the aging of the damaged meshwork. The optometrist should have a raised index of suspicion for late ARG in any eye with signs of previous eye trauma including: hyphema, traumatic lens opacification, subluxation, phacodonesis, iris sphincter splits, and changes to the choroid or retina.
Gonioscopy should be performed after healing has occurred from the blunt trauma injury. In a 10-year follow-up of 33 patients with postcontusion hyphema and angle recession, the incidence of glaucoma was 9% and only 2 of the patients developed late onset glaucoma. Angle recessions of less than 180 degrees were not associated with glaucoma in the 10 year study, but that number may have increased with longer follow-up.2
There also appears to be a late alteration of the trabecular meshwork with gradual scarring and fibrosis of the meshwork, which plays a role in the late onset of angle recession glaucoma.3 Pathologic examination should monitor for anatomic changes including hyalinization and formation of a hyaline membrane.3 All of these angles are difficult to evaluate on gonioscopic examination.3 The scarring and fibrosis may alter the anatomy of the angle, and, in some cases, make the angle recession and tissue changes less detectable.4 Researchers suggest performing gonioscopy on both eyes using the uninvolved eye as a reference.5
Our patient was first seen 45 years ago, with a history of blunt trauma, angle recession, and hyphema 15 years prior. He was not followed closely. Today, we know these patients need to be followed with regular annual examinations. Clinicians must be very clear in a discussion with the patient, about possible glaucoma, and document this in the patient’s record. If their IOP increases, gonioscopy will be necessary to see if the recession has changed, and to rule out other angle abnormalities. If the angle recession or IOP increases, the optometrist should document the changes, and treat or refer the patient. For medical treatment, IOP-lowering medications (topical or oral) that suppress the aqueous secretion are preferred in angle recession situations associated with late unilateral pressure increases, due to the compromise of the trabecular outflow pathways. Surgical measures may also be required.6
Regular yearly eye examinations are important in all patients, but critical for patients with a history of blunt trauma to the globe.
Matthew Garston, OD, is an adjunct professor at the New England College of Optometry and was a senior staff optometrist in the medical department at MIT for 43 years.
- Sponsel WE, Gray W, Scribbick Fw, et al. Blunt eye trauma: empirical histopathologic paintball impact thresholds in fresh mounted porcine eyes. Invest Ophth Vis Sci. 2011;52(7):5157-5166. doi:10.1167/iovs.11-7172
- Kaufman JH, Tolpin DW. Glaucoma after traumatic angle recession: A ten-year prospective study. Am J Ophthalmol.1974;78(4):648-654. doi:10.1016/s0002-9394(14)76303-2
- Wolf SM, Zimmerman LE . Chronic Secondary Glaucoma* : Associated with retrodisplacement of iris root and deepening of the anterior chamber angle secondary to contusion. Am J Ophthalmol. 1962;54(4):547-563. doi:10.1016/0002-9394(62)92186-4
- Alper MG. Contusion angle deformity and glaucoma-gonioscopic observations and clinical care. Arch Ophthalmol. 1963;69(4):455-467. doi:10.1001/archopht.1963.00960040461007
- Fisch B. Blunt Trauma-Induced Angle Abnormalities, IN: Gonioscopy and the Glaucomas. Boston: Butterworth-Heineman; 1993:115-122.
- Brenner J, Aref AA, Moore DB, et al. Angle recession glaucoma. EyeWiki. https://eyewiki.aao.org/Angle_Recession _Glaucoma. Updated: February 3, 2022 Accessed July 26, 2022.