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 for 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 for angle recession.[2, 3]

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 five 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. A mechanism of forceful asymmetric contraction of ciliary fibers combined with an intrinsically weak anatomic zone has been suggested.[7]

During traumatic separation of the circular and longitudinal ciliary structures, 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.[7]

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.[7]

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

Frequency

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,[8] 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, 10, 11, 12] No difference has been shown between the incidences of angle-recession glaucoma when comparing hyphema versus microhyphema.[12]

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.[13] In 1990, the estimated hospitalization rate with ocular trauma was 15.2 cases per 100,000 children per year.[14]

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%).[15, 16, 17, 18, 19, 20, 21] 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.[22] 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, 7-9% subsequently develops glaucoma.[23]

International

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%.[24] 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%.[25] 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.[26] A 1996 report described a predominance of home injuries in Scotland.[27]

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%.[28]

Mortality/Morbidity

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.[29] Angle recession has been reported in 7.5% of cases of zygomatic-complex fractures.[30]

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.[31]

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.

Race

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 for 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.[32]

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

Sex

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.

Age

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. Participation in sports appears to be a risk factor. An 18% incidence of angle recession following cricket ball injury has been reported.[33]

The annual incidence of pediatric eye injuries has been reported at 15 cases per 100,000 population. Pediatric ocular trauma is predominantly associated with playing sports and engaging in outdoor activities. Angle-recession glaucoma has been described in childhood, with a reported pediatric incidence of 19% following closed globe injury and 7% following open globe trauma.[34]

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 for 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.[35] 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.

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.

• Ideally, angle recession should be discovered before glaucoma develops so that the risk of glaucoma can be assessed and follow-up care arranged accordingly.

• High IOPs noted early after injury (within the first few months of injury) may indicate extensive trabecular damage and a poor prognosis.

• Angle recession is typically diagnosed by means of gonioscopy.

  • The clinical appearance of the affected angle varies with the depth of the tear in the ciliary body and with the amount of time passed after the injury.

  • Typically, an irregularly wide ciliary body band is visible with retroplacement of the iris root. The angle appears abnormally deep in the involved areas. This characteristic appearance is due to a cleavage between the longitudinal and circular muscles of the ciliary body. After years of healing, the fissure may no longer be visible. In fact, when many years have passed after the contusional injury, angle recession may be difficult to recognize.

  • A large series of blunt injuries among soccer players found that angle recession is more likely to occur in the superotemporal quadrant.[20]

• Comparison with the angles in the injured and uninjured eyes is important, particularly in cases with subtle findings. Documented asymmetry supports the diagnosis.

• Ipsilateral anterior chamber depth may be increased following a contusion injury even if other signs of angle recession are absent.[36]

• Angle recession should be differentiated from cyclodialysis, which is the disinsertion of the ciliary body from its attachment to the scleral spur.

• A number of anterior segment abnormalities often accompany angle recession, as follows:

  • Cyclodialysis

  • Iridodialysis

  • Iridoschisis

  • Anterior synechia

  • Iris sphincter tears

  • Mydriasis

  • Iris atrophy

  • Transillumination defects

  • Iritis

  • Zonular breaks

  • Phacodonesis

  • Subluxated lens

  • Cataract

• Ultrasound biomicroscopy (UBM) is a useful adjunctive modality for the evaluation of abnormalities in closed-globe injuries (see Imaging Studies),[37] and UBM may be superior to slit-lamp optical coherence tomography (SL-OCT) to image angle recession.[38]

• A strong association exists between traumatic hyphema and angle recession,[12] but the ciliary body also can be severely damaged from blunt trauma, without the appearance of a hyphema. Gross hyphema and traumatic microhyphema are associated with approximately the same increased long-term risks of angle recession and glaucoma.[2, 12]

• Posterior segment abnormalities, which may signify prior episodes of trauma, include the following:

  • Vitreous opacities

  • Chorioretinal scars

  • Macular hole

  • Retinal breaks

  • Retinal detachment

  • Optic atrophy

• An uncontrolled and sustained elevation in IOP in angle-recession glaucoma, as in other forms of glaucoma, ultimately leads to progressive cupping of the optic nerve and loss of the visual field.

• Snellen visual acuity is typically uninvolved until the late stages of glaucoma.

• Formal visual field testing is of paramount importance in diagnosing and monitoring the disorder.

  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.

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[39] or cataract extraction, may also result in angle recession.

The most common types of blunt trauma are the following:

• Sports injuries (eg, boxing, paintball, airsoft gun toys)[22, 17, 16]

• Motor vehicle accidents (eg, airbag deployment, other facial trauma)

• Assaults

• Falls

• Military combat injuries

• Accidents (eg, industrial, farm, home, bungee cord injuries)[15]

• Other (eg, school accidents, natural disasters)

See the list below:

• Nonglaucomatous comorbidity in eyes with angle recession increases the risk of vision loss. Traumatic insults to the cornea, iris, lens, vitreous, retina, or optic nerve may contribute to vision-threatening sequelae.

• Traumatic cataract often accompanies angle recession.

  • Gonioscopy should always be performed when a patient with a unilateral cataract is evaluated, even when his or her history is negative for trauma.

  • After surgical management, the risk of complications is higher with a traumatic cataract than with a senile cataract.

• Intraoperative complications of cataract surgery in traumatized eyes include the following:

  • Zonular dialysis

  • Vitreous loss

  • Intraocular hemorrhage

  • Suboptimal or inadequate posterior intraocular lens (IOL) support: Zonular injury is a common finding in such cases. When zonular defects are small, placement of the IOL into the capsular bag usually can be achieved without further complication. Placement of an anterior-chamber IOL is not preferred in eyes with even minimal angle recession, and it is fully contraindicated when the angle is recessed more than 180°.

• Postoperative complications

  • IOP elevation

  • Inflammation

  • IOL malposition

  • Pupil capture

  • Intraocular hemorrhage

  • Glare

  • Monocular diplopia: Symptoms may result from iris abnormalities.

• Cataract extraction in eyes with known angle-recession deformities should be approached with caution.

• The most common posterior-segment complications after blunt trauma include macular lesions and peripheral retinal tears.

  • Posttraumatic entities involving the macula include the following:

    • Macular cysts

    • Macular holes

    • Hyperplastic-atrophic pigment epitheliopathy

    • Choroidal rupture: This is another possible finding in traumatized eyes and sometimes leads to secondary neovascular degeneration or disciform scarring.

  • Traumatic abnormalities of the peripheral retina include the following:

    • Atrophic holes

    • Horseshoe tears

    • Operculated tears

    • Retinal dialysis

    • Retinal detachment

Imaging studies can include the following:

• The diagnosis of angle recession is confirmed during office examination.

• Usually, imaging is necessary only to evaluate comorbidities due to trauma.

  • Occasionally, CT scanning of the orbits is needed to evaluate for orbital fractures or foreign bodies.

  • Emergency neuroimaging if typically indicated after major head trauma.

• On occasion, gonioscopy is difficult or impossible in traumatized eyes because of corneal edema, corneal scarring, hyphema, synechia, or other opacity. In such cases, high-frequency ultrasound biomicroscopy (as a supplemental tool to standard office examination) is effective for evaluating abnormalities of the angle in the anterior chamber.[37, 41]

  • Ultrasound biomicroscopy (UBM) produces high-resolution axial images of the anterior globe, providing cross-sectional views of the angle in vivo similar to those of a histologic section. This noninvasive procedure is readily performed in a clinical setting in an intact globe, and it provides information otherwise unavailable from convention examination.

  • High-resolution images of angle recession, zonular deficiency, iridodialysis, and cyclodialysis have been described. Zonular deficiency and angle recession are the most common UBM findings in a closed-globe injury.[37]

  • Ultrasound biomicroscopy findings of a wider angle and absence of cyclodialysis have been reported to be significant predictors for the development of traumatic glaucoma in eyes with closed-globe injury.[8]

  • Ciliary body melanoma, although rare, has been differentiated from angle recession using a combination of UBM, PET-CT, and aqueous tap.[40]

• Slit-lamp optical coherence tomography (SL-OCT) has also been described as a method of imaging angle recession, but it may be less reliable than UBM. ^[38]

Other tests include the following:

• Because progressive loss of visual field is a potential outcome, formal visual field testing is the most important adjunctive diagnostic modality in detecting and following up the disorder.

• Several authors have described the use of tonography to evaluate patients with traumatic angle recession.[42]

  • Loss of outflow facility, as measured on tonographic studies, is common after angle-recession injuries, and this finding is statistically significant in cases of angle recession as a group.

  • However, role of tonography in predicting the risk of glaucoma appears to be of little value in any single case.

  • Tonography might not be available to the average practitioner, and it is currently an unnecessary adjunct to the evaluation and management of angle recession.

• Optic nerve photography is also important for documenting and monitoring glaucoma.

• Computerized disk analysis and analysis of nerve-fiber layers has been gaining acceptance in the diagnosis and management of all forms of glaucoma.

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.

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]

• The extent of dissection varied, but the longitudinal muscle remained attached to the scleral spur.

• Retroplacement of the iris root and ciliary processes was noted microscopically. An association with other abnormal findings, including iridodialysis, rupture of the trabecular meshwork, or cyclodialysis, was documented. Late findings were also reported.

• Over time, healing of the ciliary body laceration was noted. This was accompanied by atrophy of the circular muscle at involved sites, resulting in a fusiform contour of the ciliary body, as seen on axial sections.

• Other histopathologic findings in late cases provided clues to the mechanism of glaucoma in angle recession. Marked degeneration of the trabecular meshwork was prominent.

• In some cases, an abnormal hyaline membrane, continuous with the Descemet membrane, was formed over the inner surface of the trabecular meshwork, sometimes extending further onto the anterior iris surface.

  • Abnormal corneal endothelial proliferation may occur in some eyes with traumatic angle deformities.

  • The histologic examination revealed proliferation of the endothelium posterior to the Schwalbe ring with secretion of a Descemetlike membrane covering the meshwork and perhaps reducing trabecular outflow capacity of the involved angle.

  • Electron microscopy of some eyes with angle recession may verify the presence of a hyaline membrane over the inner trabecular region, with an endothelial layer structurally similar to that of normal corneal endothelium. Other electron microscopy findings include loss of intertrabecular spaces and a decrease or absence of the trabecular endothelial cells. Thickening of the juxtacanicular connective tissue has been observed, with loss of vacuole lining within the endothelial cells lining the inner wall of the Schlemm canal.[43]

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.

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.

• In patients with an abnormal elevation of IOP, the decision to begin therapy is based on the clinician's overall assessment of the risk of vision loss.

  • The severity of IOP elevation, optic nerve appearance, and visual field findings contribute to the decision-making process. Glaucoma medications should be implemented in the early stage of the condition.[44]

  • Treatment almost always is indicated when the IOP is greater than an arbitrary range of 25-28 mm Hg and/or when glaucomatous optic nerve or visual field changes are documented over time.

• After the diagnosis of angle recession is established, its management is similar to that of POAG, with a few special considerations.

  • Use of topical aqueous suppressants in the initial medical treatment is preferred; these include beta-antagonists, alpha-agonists, and carbonic anhydrase inhibitors.[44]

  • Prostaglandin analogs, which increase uveoscleral outflow, have a theoretical benefit in angle recession because the trabecular meshwork is thought to be dysfunctional in such cases.

  • Use caution in administering miotic agents because pilocarpine has been reported to cause a paradoxical elevation of IOP in angle recession, presumably due to a reduction of uveoscleral outflow.[23]

  • Atropine has been reported to reduce IOP in angle-recession glaucoma; therefore, cycloplegic agents may have a role in treatment.[44]

  • A trial of a cycloplegic agent should be reserved either for cases involving failure of conventional glaucoma therapy or for cases with other indications for cycloplegia (eg, inflammation).

• The response to medical therapy in angle-recession glaucoma is variable.

  • Topical medical treatment may be effective in cases of mild-to-moderate angle recession, while elevated IOP of eyes with extensive angle injury eventually may become refractory to medications.

  • Severe early cases may fail to show an initial response to aggressive medical treatment, indicating a poorer overall prognosis.

Surgical intervention in angle-recession glaucoma is usually indicated when maximally tolerated medical treatment has failed[44] 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.[45]

IOP elevation may become worse in response to argon laser trabeculoplasty (ALT).[46]

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.[46]  There are small case reports suggesting efficacy of SLT in treating some patients with angle recession glaucoma, however long term success rates and generalizability at this time are unknown.[47]  

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.[48] 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.[49]

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.[49] Serous retinal detachment has been reported as an early complication of trabeculectomy in angle-recession glaucoma.[50]

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.[51]

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.[52]

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.[53]

A 1993 study showed the superior results of trabeculectomy with antimetabolite over Molteno implantation in cases of posttraumatic angle-recession glaucoma.[54]

Implantation of a trabecular bypass stent in eyes with angle-recession glaucoma has been reported.[55]

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.

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 to 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.[23]

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.[44]

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.

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.

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

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

Levobunolol (Betagan, AKBeta) 0.25%, 0.5%

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

Carteolol ophthalmic (Ocupress)

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

Betaxolol ophthalmic (Betoptic)

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

Class Summary

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

Apraclonidine (Iopidine) 0.5%, 1%

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

Brimonidine (Alphagan)

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

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.

Dorzolamide (Trusopt)

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%

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)

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)

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

Methazolamide (Neptazane, GlaucTabs)

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

Class Summary

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

Latanoprost (Xalatan)

Decreases IOP by increasing outflow of aqueous humor.

Bimatoprost ophthalmic solution (Lumigan)

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)

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)

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.