Angle-Recession Glaucoma



Angle-recession glaucoma is classified as a type of traumatic secondary open-angle glaucoma.[1] This condition may be underdiagnosed because onset is often delayed and because a history of eye injury may be distant or forgotten.

Traumatic glaucoma refers to a heterogeneous group of posttraumatic ocular disorders with different underlying mechanisms that lead to the common pathway of abnormal elevation of intraocular pressure (IOP) and increased risk of optic neuropathy.

Angle recession, with or without glaucoma, is a common sequela of blunt ocular trauma and one characterized by a variable degree of cleavage between the circular and the longitudinal fibers of the ciliary muscle. Traumatic microhyphema and gross hyphema are both equally associated with a high risk of angle recession.[2, 3]

View Image

Irregular widening of the visible ciliary body in a quadrant with angle recession.

Treacher Collins based the first report of this postcontusional angle deformity on gross examination of enucleated eyes in 1892.

In 1944, D'Ombrain observed the association of ocular trauma and chronic unilateral glaucoma, suggesting abnormalities in the region of the trabecular meshwork as the underlying cause. This theory was substantiated by the classic histologic findings of angle recession published in 1962 by Wolf and Zimmerman,[4] and numerous authors have confirmed the relationship of glaucoma with traumatic angle abnormalities.

Although a relatively uncommon phenomenon, angle-recession glaucoma may be overlooked in the management of nonpenetrating eye trauma.[5] Long-term follow-up care of patients with recognized contusional angle abnormality is warranted because of the risk of delayed asymptomatic onset.


The mechanism of glaucoma associated with angle recession appears to involve 5 processes.

First, blunt force delivered to the globe initiates an anterior to posterior axial compression with equatorial expansion. Sudden indentation of the cornea may be a key factor in angle trauma, creating a hydrodynamic effect by which aqueous is rapidly forced laterally, deepening the peripheral anterior chamber and increasing the diameter of the corneoscleral limbal ring. Ballistic experiments using porcine eyes have demonstrated relatively low energy impact thresholds of 3.5-7.0 joules resulting in moderate-to-severe angle recession.[6]

Second, this transient anatomic deformity results in a shearing force applied to the angle structures, causing disruption at the weakest points if the force applied exceeds the elasticity of the tissues.

Third, although multiple anterior segment structures can be damaged by the above mechanism, a common site of avulsion involves the ciliary muscle. In angle recession, the ciliary body is torn in a manner such that the longitudinal muscle remains attached to its insertion at the scleral spur, while the circular muscle, with the pars plicata and the iris root, is displaced posteriorly. During this process, shearing of the anastomotic branches of the anterior ciliary arteries can occur, resulting in a hyphema. The anterior chamber typically becomes abnormally deep in the meridians of recessed angle due to posterior deviation of the relaxed iris-lens diaphragm. Subsequently, a fissure representing the separation of the longitudinal and circular fibers may be visible by gonioscopy or by histologic examination.

View Image

Angle recession. Note the marked posterior displacement of the iris, with a wide ciliary body band posterior to the scleral spur.

Fourth, in some cases, angle recession progresses to glaucoma. The contusional deformity, when extensive, may result in trabecular dysfunction, which may lead to early or delayed loss of outflow facility and elevation of IOP. The mechanism is not well understood, but evidence suggests an increased incidence of primary open-angle glaucoma (POAG) in the other eye of affected patients. One theory suggests that patients with angle-recession glaucoma have an independent, perhaps genetic, predisposition to chronically diminishing trabecular function in both eyes. A finite portion of the trabecular meshwork in eyes with angle recession is initially rendered dysfunctional by the injury and/or the healing process. With time, the outflow capacity of the remaining meshwork is gradually reduced because of preexisting innate factors; the ultimate result is elevated IOP.

Fifth, chronic elevation of IOP leads to optic neuropathy characterized by progressive optic cupping and visual field loss.



United States

The reported frequency of angle recession as a complication of blunt trauma is 20-94%. Several reports have described incidences of angle recession in more than 75% of bluntly injured eyes.[4] Angle recession after traumatic hyphema occurs in 71-100% of cases.

Of eyes with identifiable angle recession, 0-20% develop glaucoma. The onset of glaucoma is extremely variable, ranging from immediately after trauma to months or even many years later. Two peak incidences have been suggested to represent the early and late onset of angle-recession glaucoma; this observation may indicate separate pathologic mechanisms. The underlying differences are not well understood. The risk of eventual progression to glaucoma is generally thought to be proportionate to the extent of the angle recession,[7] though the presence of angle recession alone is not a good predictor of glaucoma. Other risk factors for progression to glaucoma after ocular contusion include chronic elevation of intraocular pressure, poor initial visual acuity, advancing age, lens injury, hyphema, and microhyphema.[8, 9, 7, 10, 11] No difference has been shown between the incidences of angle-recession glaucoma when comparing hyphema versus microhyphema.[11]

Glaucoma after angle recession of less than 180° is unusual; recessions greater than 180° are associated with a 4-9% incidence of glaucoma. Eyes with angle recession of greater than 240° appear to be at the highest risk of chronic glaucoma.

More than 1 million Americans have ocular injuries each year. A 1988 population-based study of adults in New England yielded an annual rate of 9.75 eye injuries per 1000 population based on self-reported histories.[12] In 1990, the estimated hospitalization rate with ocular trauma was 15.2 cases per 100,000 children per year.[13]

Work-related injuries have been reported as 13-18% of all cases of eye trauma. Injuries at home account for 27-31%, followed by assault (11-37%), sports and recreation (about 25%), travel (about 5%), and miscellaneous causes (eg, injuries at school, unknown causes; < 5%).[14, 15, 16, 17, 18, 19, 20] Rates of bilateral injuries are as high as 27%.

The incidence of angle recession in the United States is not reported, but it has been described in 20-94% of eyes affected by blunt trauma. A 1987 study involving the routine examination of asymptomatic boxers found angle recession in 19%, with 8% having bilateral angle recession.[21] Blunt eye injuries are estimated to account for more than 60% of all episodes of eye trauma. Angle recession is one of the most common complications after ocular contusion. Angle recession is observed in 71-100% of cases of traumatic hyphema. By contrast, angle-recession glaucoma occurs relatively infrequently. Of those eyes with known angle recession, 0-20% subsequently develops glaucoma.


Specific epidemiologic data regarding angle recession in other countries is scarce. Limited, worldwide epidemiologic data regarding eye trauma are similar to findings in the United States; however, differences exist in the high-risk activities leading to eye trauma, especially when rural and urban populations are compared. Most reports verify that contusional injuries represent most cases of eye trauma, but rates of angle recession or traumatic glaucoma are not well documented.

A study of Australian adults older than 40 years yielded a lifetime cumulative rate of eye injury of 21.1%.[22] Among men, the rural rate was 42.1% compared with 30.5% for urban men. Workplace injuries predominated at 60%, with home injuries closer to agreement with the US figure of 24%.

Results of 1995 study of ocular trauma in the Nigerian population were in agreement regarding the rate of home injuries, revealing a rate of 26.4%.[23] This study showed that women and children at the greater risk of sustaining eye trauma during domestic activities.

The 1988 Israeli Ocular Injuries Study showed that injuries occurring at home were the most frequent type of eye trauma in Israel.[24] A 1996 report described a predominance of home injuries in Scotland.[25]

In a 1994 population-based survey on gonioscopy in individuals older than 40 years in a community in South Africa, the authors reported a cumulative prevalence of angle recession of 14.6%. Among eyes with 360° of angle recession, 8% had glaucoma, and the overall prevalence of glaucoma of eyes with any degree of angle recession was 5.5%.[26]


Ocular injury is a relatively common comorbidity in patients admitted with major head trauma.

A study in 1999 revealed ocular injuries in 55% of all patients with facial injuries and in 16% of those with major trauma.[27] Angle recession has been reported in 7.5% of cases of zygomatic-complex fractures.[28]

Mortality in association with serious ocular trauma is related to nonophthalmic complications of the underlying trauma, though specific rates have not been reported.

Estimating the public magnitude of visual disability resulting from traumatic glaucoma is difficult because of its chronic nature and the lack of reported outcomes. Published reports of visual outcomes after eye trauma usually describe short-term results.

A 1996 epidemiologic study showed that the annual cumulative incidence of serious ocular trauma necessitating hospital admission is approximately 8 cases per 100,000 population. Of those cases, approximately 13% of patients had a poor visual outcome, and 10.7% had blindness as an outcome.[29]

Angle-recession glaucoma can have onset years after the original episode of trauma. The long-term incidence of substantial vision loss or blindness due to posttraumatic glaucoma has not been reported.


No known racial predilection exists.

Because of the possible relationship of POAG with angle-recession glaucoma, it can be theorized that African Americans may be at an increased risk of glaucoma after contusional eye trauma.

In addition, one urban study reported in 1991 showed that, at an inner-city hospital in Los Angeles, African American patients had eye injuries more than twice as frequently as Hispanic patients.

A comparison of the rates of progression to angle-recession glaucoma among different races has not yet been reported.


No sex predilection has been reported specifically for angle-recession glaucoma, but blunt eye injuries are significantly more common in males.

A strong predominance of eye trauma exists in men, with a male-to-female ratio of 4:1. Therefore, it may be assumed that angle recession and angle-recession glaucoma occur most frequently in men.

Among children, eye injuries occur more frequently in boys than girls.

Compared with men, women appear to be at greater risk of sustaining eye injuries at home.


Advancing age has been reported as an independent predictive factor for the risk of developing glaucoma after ocular contusion injury.

Because of the potential for delayed or late onset after a blunt injury, angle-recession glaucoma is most likely diagnosed in mid or late adulthood. It may be misidentified as POAG because late angle abnormalities may be subtle on examination. A distant or even forgotten history of eye trauma may result in the condition being overlooked, especially in elderly persons.

In general, ocular trauma occurs most commonly during young adulthood. The annual incidence of pediatric eye injuries has been reported at 15 cases per 100,000 population. Angle-recession glaucoma has been described in childhood.

Among adults, the risk of injury appears to steeply decline with advancing age. Studies of urban populations have indicated that elderly persons have only 1.6% of all eye traumas, and for persons older than 65 years, eye injuries are most often the result of a fall.


Owing to the highly variable clinical course of angle recession and angle-recession glaucoma, the prognosis of these conditions cannot be generalized. It is widely accepted that a greater extent of angle recession, especially over 180°, is associated with an increased long-term risk of glaucoma. No epidemiologic data characterizing long-term visual outcomes of eyes with chronic angle-recession glaucoma have been published. As with other types of glaucoma, angle-recession glaucoma can result in progressive visual field loss and blindness. The risk of vision loss depends on many factors, particularly timeliness of initial diagnosis and response to treatment.

No formal data indicate the long-term visual outcomes of eyes with chronic angle-recession glaucoma. Eyes that develop early-onset angle-recession glaucoma are thought to represent a subgroup with most extensive angle injury, but the visible degree of angle recession is not correlated with the severity of glaucoma in this group.

Angle recession of more than 180° is a risk factor for glaucoma.[2]  Late-onset angle-recession glaucoma almost always occurs in eyes with more than 180° of angle recession, and the risk appears to increase with the extent of angle recession. Eyes with a 360° angle recession are at greatest risk.

As in most types of glaucoma, angle-recession glaucoma can cause progressive visual field loss and blindness.[30]  The risk of visual loss depends on many factors, particularly the timeliness of initial diagnosis and the course of management. Response of elevated IOP to medical therapy varies, and with time, IOP control may deteriorate despite dependence on multiple medications. Favorable results have been reported for surgical intervention of angle-recession glaucoma, but success rates are lower than those of other forms of glaucoma.

Patient Education

Patients with angle recessions of greater than 180°, without evidence of glaucoma, should be advised of the need for lifelong follow-up care.

For patient education resources, see the Glaucoma Center, as well as Angle Recession Glaucoma, Understanding Glaucoma Medications, and Glaucoma FAQs.


Although nonpenetrating eye trauma invariably precedes angle recession, the patient may forget details of the injury or the entire episode after a number of years have passed. In addition, patients with angle-recession glaucoma, like patients with other forms of glaucoma, may present with no specific eye or visual complaints.

A unilateral cataract in a young or middle-aged adult should raise the suspicion of remote trauma, even when the history is negative.

In cases of suspected traumatic angle recession, careful history taking may elicit otherwise forgotten information.

In elderly patients, rule out a history of falls.

Some patients do not report any history of trauma despite extensive questioning. Lack of a positive history does not rule out angle recession.


Unilateral elevation of IOP is a hallmark finding in angle-recession glaucoma, but it may not be noted in early stages of the disorder.


Any cause of nonpenetrating ocular trauma can result in angle-recession glaucoma. The episode may be seemingly trivial and forgotten. The circumstances of the injury can be variable, often involving trauma from high-velocity blunt objects or projectiles (eg, stones, balls, champagne stoppers, bungee cords, toys, tree branches, fruit, airbags, fists). Ocular surgery, such as penetrating keratoplasty[34] or cataract extraction, may also result in angle recession.

The most common types of blunt trauma are the following:


See the list below:

Imaging Studies

See the list below:

Other Tests

See the list below:


Gonioscopy is the only clinical procedure that must be performed before angle recession can be diagnosed.

Use of a 1- or 3-mirror Goldman goniolens, which provides the greatest magnification of angle structures, is recommended.

Use of the Koeppe lens for examining and photographing the anterior chamber angle is also advocated. Use of Koeppe lenses allows for easy comparison with the uninjured eye because they can be placed simultaneously on the eyes.

The Posner 4-mirror gonioprism is not preferred for evaluating suspected angle recession because of the potential for indenting the central cornea, inducing artificial deepening, and/or distorting of the anterior-chamber angle.

Histologic Findings

Histopathologic findings of eyes with angle-recession deformities have been well described and include features of both light microscopy and electron microscopy (EM).

In their classic report in 1962, Wolf and Zimmerman described a characteristic tear extending into the anterior ciliary body, separating the longitudinal and circular fibers.[4]

Although the exact pathology of angle-recession glaucoma is not fully established, the ultrastructural abnormalities described above support a chronic progressive mechanism of trabecular outflow dysfunction, leading to pressure elevation over time.

Medical Care

The necessity of initiating treatment of angle-recession glaucoma depends on the severity of the initial injury and the somewhat variable clinical course as healing progresses. Normotensive eyes with angle recession of more than 180° should be routinely reexamined for an indefinite period to monitor for the development of late glaucoma.

Surgical Care

Surgical intervention in angle-recession glaucoma is usually indicated when maximally tolerated medical treatment has failed[38] and when the risk of progressive visual loss outweighs the estimated risk of the planned surgical management. In general, outcomes of surgical treatment are less favorable than those of POAG.

Laser trabeculoplasty

Laser trabeculoplasty has been associated with short-term success, though the procedure has been reported to have poor long-term effectiveness, particularly in eyes with more than 180° of angle recession.

IOP elevation may become worse in response to argon laser trabeculoplasty (ALT).

In eyes with less than 180° of angle recession, ALT may be beneficial if applied to only the trabecular meshwork of the nonrecessed portions of the anterior-chamber angle. There is insufficient published data describing the use of selective laser trabeculoplasty (SLT) for angle-recession glaucoma.

Alternative laser procedures

Nd:YAG laser trabeculopuncture (YLT) has been used with variable success. However, 1992 study demonstrated a 100% failure rate in eyes with 360° angle recession.[39] Currently, YLT is not recommended for the routine management of angle-recession glaucoma.

Other laser procedures that have shown promise are transscleral krypton laser cyclophotocoagulation, transpupillary argon laser cyclophotocoagulation, and endoscopic cyclophotocoagulation.

Filtration surgery

Filtration surgery has a success rate lower than that of POAG.

Trabeculectomy in eyes with angle recession is associated with decreased postoperative reduction in IOP, increased rates of bleb fibrosis and bleb failure, and increased dependence on postoperative medical treatment of glaucoma.[40] Serous retinal detachment has been reported as an early complication of trabeculectomy in angle-recession glaucoma.[41]

The adjunctive use of antimetabolites, particularly mitomycin C, can improve the success of trabeculectomy. This finding suggests that an antimetabolite should be used during the initial filtering procedure. A 2001 report described effective results with an acceptable complication rate in such cases.[42]

In the management of severe blunt trauma cases involving angle recession with dense vitreous hemorrhage and/or retinal detachment, combined trabeculectomy and pars plana vitrectomy has been reported with some successful outcomes.[43]

Tube shunt devices

Benefits with the implantation of tube shunt devices have been demonstrated, but outcomes are reportedly less successful in angle recession than in other types of refractory glaucoma.

A 1993 study showed the superior results of trabeculectomy with antimetabolite over Molteno implantation in cases of posttraumatic angle-recession glaucoma.

Implantation of a trabecular bypass stent in eyes with angle-recession glaucoma has been reported.[44]


Consultation with a glaucoma specialist should be considered in cases with an uncertain diagnosis, with early severe IOP elevation, with a poor response to treatment, or with advanced visual field loss.

Depending on the presence of other posttraumatic ocular or orbital abnormalities, consider referring the patient to subspecialists in corneal and/or external disease, oculoplastics retinal disease, or neuro-ophthalmology.


The incidence of angle-recession glaucoma can be reduced by preventing the underlying trauma.

Data indicate that most pediatric and adult eye injuries (eg, sports-related accidents) are preventable.

Public education on the use of eye, face, or head protection during high-risk activities may lower the incidence of ocular injuries.

Public safety standards to reduce rates of eye injury can be achieved by enacting legislative policies such as seatbelt or helmet laws.

Further Outpatient Care

As in other types of glaucoma, follow-up depends on the degree of IOP control and the risk of progressive loss of the visual field.

Patients with an early increase in IOP after blunt trauma should be reexamined every 4-6 weeks during the first year to monitor their condition. Some early cases are self-limited, but patients should still be observed after their condition appears to resolve. Other early cases represent a severe form of the disease that may be refractory to standard medical treatment; such cases warrant more frequent follow-up.

In cases of angle recession of greater than 180° that initially have no evidence of glaucoma, late-onset glaucoma can potentially occur, even many years after the injury. Annual examinations should be performed for an indefinite period.

Medication Summary

The preferred drugs have the pharmacologic action of aqueous suppression. A beta-antagonist is the common first choice, with subsequent additions of an alpha-agonist and/or a carbonic anhydrase inhibitor, as necessary. Prostaglandin analogs probably have a useful role, but the use of miotic agents is controversial and not routinely recommended.

The goal of therapy is IOP reduction. Medications must often be used long term. IOP should be monitored whenever medications are discontinued or changed, and therapy should be restarted, if necessary.

Timolol maleate (Timoptic, Timoptic XE) 0.25%, 0.5%

Clinical Context:  May reduce elevated or normal IOP, with or without glaucoma, by reducing aqueous humor production.

Levobunolol (Betagan, AKBeta) 0.25%, 0.5%

Clinical Context:  Nonselective beta-adrenergic blocking agent. Lowers IOP by reducing aqueous humor production.

Carteolol ophthalmic (Ocupress)

Clinical Context:  Blocks beta1- and beta2-receptors. Has mild intrinsic sympathomimetic effects.

Betaxolol ophthalmic (Betoptic)

Clinical Context:  Selectively blocks beta1-adrenergic receptors. Reduces IOP by reducing aqueous humor production.

Class Summary

Topical beta-adrenergic receptor antagonists decrease the production of aqueous humor by the ciliary body. Adverse effects are due to systemic absorption of the drug, which causes decreased cardiac output and bronchoconstriction. These agents may cause bronchospasm, bradycardia, heart block, or hypotension. Monitor the patient's pulse rate and blood pressure. Patients may be instructed to perform punctal occlusion after administering the drops. Some patients may have depression or anxiety, and sexual dysfunction may occur or worsen.

Apraclonidine (Iopidine) 0.5%, 1%

Clinical Context:  Selective alpha-adrenergic agonist that suppresses aqueous production. Minimal cardiovascular effect.

Brimonidine (Alphagan)

Clinical Context:  Selective alpha2-receptor agonist. Reduces aqueous humor formation. Possibly increases uveoscleral outflow.

Class Summary

Topical adrenergic agonists (sympathomimetics) decrease aqueous production and reduce resistance to aqueous outflow. Adverse effects include dry mouth and hypersensitivity.

Dorzolamide (Trusopt)

Clinical Context:  Used concomitantly with other topical ophthalmic drugs to lower IOP. If > 1 ophthalmic drug used, administer >10 min apart. Reversibly inhibits carbonic anhydrase, reducing hydrogen ion secretion at renal tubule. Increases renal excretion of sodium, potassium bicarbonate, and water to decrease aqueous humor production.

Brinzolamide (Azopt) 1%

Clinical Context:  Catalyzes reversible reaction involving hydration of carbon dioxide and dehydration of carbonic acid. May use concomitantly with other topical ophthalmic drug products to lower IOP. If >1 topical ophthalmic drug used, administer >10 min apart.

Dorzolamide HCl/timolol maleate (Cosopt)

Clinical Context:  Dorzolamide is carbonic anhydrase inhibitor that may decrease aqueous humor secretion, decreasing IOP; presumably slows bicarbonate ion formation with subsequent reduction in sodium and fluid transport. Timolol is nonselective beta-adrenergic receptor blocker; decreases IOP by decreasing aqueous humor secretion. Administered together bid may reduce IOP more than either alone, but reduction not as much as that with concomitant dorzolamide tid and timolol bid.

Acetazolamide (Diamox, Diamox Sequels)

Clinical Context:  Reduces aqueous humor formation by inhibiting enzyme carbonic anhydrase, decreasing IOP.

Methazolamide (Neptazane, GlaucTabs)

Clinical Context:  Reduces aqueous humor formation by inhibiting carbonic anhydrase, decreasing IOP.

Class Summary

These drugs reduce secretion of the aqueous humor by inhibiting carbonic anhydrase in the ciliary body. These agents are less effective than many other classes of drugs and have a shorter duration of action. Adverse effects are relatively rare but include superficial punctate keratitis, acidosis, paresthesias, nausea, depression, and lassitude. Corneal decompensation has been reported when this class of drugs is used in patients with corneal endothelial dysfunction.

Latanoprost (Xalatan)

Clinical Context:  Decreases IOP by increasing outflow of aqueous humor.

Bimatoprost ophthalmic solution (Lumigan)

Clinical Context:  Prostamide analog with ocular hypotensive activity. Mimics IOP-lowering activity via the prostamide pathway. Used to reduce IOP in open-angle glaucoma or ocular hypertension.

Travoprost ophthalmic solution (Travatan)

Clinical Context:  Prostaglandin F2-alpha analog. Selective prostaglandin F2 receptors prostanoid receptor agonist; may reduce IOP by increasing uveoscleral outflow. Used to treat open-angle glaucoma or ocular hypertension.

Unoprostone ophthalmic (Rescula)

Clinical Context:  Prostaglandin F2-alpha analog. Selective FP prostanoid receptor agonist; may reduce IOP by increasing uveoscleral outflow. Used to treat open-angle glaucoma or ocular hypertension.

Class Summary

These selective agonists act on prostaglandin receptors in the eye to lower IOP by increasing uveoscleral outflow.


Brian R Sullivan, MD, Professor, Department of Ophthalmology, Chicago Stritch School of Medicine, Loyola University Medical Center

Disclosure: Nothing to disclose.

Specialty Editors

Simon K Law, MD, PharmD, Clinical Professor of Health Sciences, Department of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine

Disclosure: Nothing to disclose.

Martin B Wax, MD, Professor, Department of Ophthalmology, University of Texas Southwestern Medical School; Vice President, Research and Development, Head, Ophthalmology Discovery Research and Preclinical Sciences, Alcon Laboratories, Inc

Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy, Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Disclosure: Nothing to disclose.

Additional Contributors

Andrew I Rabinowitz, MD, Director of Glaucoma Service, Barnet Dulaney Perkins Eye Center

Disclosure: Nothing to disclose.


Supported in part by an unrestricted research grant from Research to Prevent Blindness, Inc., New York, NY

Dr. Sullivan has no financial interests in any of the products mentioned in this article, nor in any of the companies that manufacture or distribute them.


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Irregular widening of the visible ciliary body in a quadrant with angle recession.

Angle recession. Note the marked posterior displacement of the iris, with a wide ciliary body band posterior to the scleral spur.

Gonioscopic examination many years after blunt trauma in a patient with angle-recession glaucoma. Note the irregular contour of the iris, with loss of detail of angle structures. Classic findings of angle recession may become subtle or be obscured over time.

Irregular widening of the visible ciliary body in a quadrant with angle recession.

Angle recession. Note the marked posterior displacement of the iris, with a wide ciliary body band posterior to the scleral spur.

Gonioscopic examination many years after blunt trauma in a patient with angle-recession glaucoma. Note the irregular contour of the iris, with loss of detail of angle structures. Classic findings of angle recession may become subtle or be obscured over time.