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Traumatic Glaucoma
What is traumatic glaucoma?

Traumatic glaucoma is any glaucoma caused by an injury to the eye. This type of glaucoma can
occur both immediately after an injury to the eye or years later. It can be caused by injuries that
“bruise” the eye (called blunt trauma) and injuries that penetrate the eye. Conditions such as
severe nearsightedness, previous injury, infection or prior surgery may also make the eye more
vulnerable to a serious eye injury.

Blunt Trauma

As a result of an immediate injury, traumatic glaucoma is most commonly caused by blunt

trauma, which is an injury that doesn’t penetrate the eye, such as a blow to the head or an injury
directly on the eye. The most common cause is from sports-related injuries, such as baseball or
boxing. Normally, the eye fluid flows out of the front part of the eye through the pupil and then
is absorbed into the bloodstream through a meshwork of drainage canals around the outer edge
of the iris. When a blunt trauma occurs, damage to this system can occur. The most common
cause is the ciliary body, the part of the eye that produces eye fluid, inside the eye tearing. This
can cause bleeding inside the eye. The excess amount of blood, plasma and debris can
accumulate and clog the drainage system. This can lead to an increase in eye pressure, which can
damage the optic nerve.

Elevated eye pressure due to blunt trauma is treated by keeping the eye pressure at safe levels
while the eye drains the excess blood out. Glaucoma medications to control the eye pressure are
usually tried first. If this is not sufficient to control the eye pressure, surgery may be necessary.

The elevated eye pressure following blunt trauma is temporary in most cases. It is important,
however, to make sure to get regular follow-up eye exams. In some cases, the damaged drainage
canals in the eye can build up excess scarring. This scarring blocks fluid flow and can lead to
glaucoma. This type of glaucoma, called angle recession glaucoma, can occur many years after
the initial injury. The angle recession is seen on an exam as a tear at the base of the iris where the
drainage canals are. Angle recession glaucoma can be difficult to treat. Treatments can include
medications that reduce fluid production in the eye, laser surgery or filtering surgery.

Penetrating Eye Injury

Traumatic glaucoma can also be caused by penetrating injuries to the eye, such as those caused
by a sharp instrument or flying debris. The eye pressure is usually lower right after the injury
occurs. Once the wound is closed, tissue inside the eye can become swollen and irritated, and
bleeding can occur, causing the eye pressure to rise.
Short term rises in eye pressure are controlled in ways similar to cases of blunt trauma. However,
damaged tissue and scarring from a penetrating eye injury can lead to blocked drainage canals.
Glaucoma due to a penetrating eye injury is best treated by preventive measures when the initial
wound occurs. Corticosteroid therapy to help prevent tissue damage and scarring and antibiotics
are an important component of initial treatment. Initial treatment can also include surgery to
remove excess eye fluid or reduce swollen tissue.

If glaucoma does develop over the long term, medications that reduce the production of eye fluid
are usually the first method of treatment, followed by filtering surgery.

This article was contributed by Ruth D. Williams, MD, a glaucoma specialist at the Wheaton Eye
Clinic in Wheaton, Illinois.

reviewed 9-4-08
Eye injury may lead to condition known as angle recession, and later, traumatic glaucoma

More than 1 million eye injuries occur in the U.S. each year, most often to men and boys at work
or playing sports. Sometime after trauma to the eye or a head injury, the angle, the area where
the iris and the cornea comes together, begins to narrow or close. This condition is called angle
recession.

Since the angle allows fluids in the eye to drain, a narrow or closed angle causes pressure to
build inside the eye. In up to 20 percent of causes of angle recession, angle recession or
traumatic glaucoma eventually develops. Left unchecked, high pressure in the eye damages the
optic nerve and causes vision loss or blindness.

Angle recession glaucoma is relatively rare and is often hard to diagnose because the symptoms
may appear long after the eye injury occurred. Symptoms are sometimes so delayed that it is not
unusual for the patient to have forgotten that the injury occurred. This also explains why angle
recession glaucoma is usually not diagnosed until middle to late adulthood.

Ideally, angle recession should be discovered before glaucoma develops, so that the actual risk of
glaucoma can be assessed and appropriate care arranged.

After an eye injury has occurred, regular eye examinations with an ophthalmologist are
important to screen for angle recession, and to monitor the eye for any developing glaucoma.
Most people don’t experience any vision loss until glaucoma is fairly advanced. Regular eye
exams are particularly critical for people who are at a higher risk for glaucoma in general, such
as African Americans and the elderly.

If your ophthalmologist doesn’t ask, be sure to mention any previous eye or head trauma, eye
surgeries, or a family history of eye disease.

Top

Exams and tests

Ideally, angle recession should be discovered before glaucoma develops, so that appropriate
schedule for follow-up exams can be arranged.

Different tests show whether you have angle recession. These tests include:

 Gonioscopy checks the drainage angle of the eye. The angle of the eye is formed where
the iris and the cornea come together inside the eye. This test shows if the angles are
open, narrowed, or closed, and rules out any other conditions that might cause elevated
eye pressure. To view the angle, a special contact lens is placed on the eye. Your eye
doctor also compares the affected angle with the angle of the fellow eye. If the eye is
severely traumatized and gonioscopy cannot be performed, a high-frequency ultrasound
biomicroscopy may be used.
  Visual field tests check your peripheral (or side) vision, usually with an automated visual
field machine. This test rules out any visual field defects due to glaucoma. Since visual
filed defects may not be noticeable to a patient until more than 40 percent of the optic
nerve is lost, your ophthalmologist will judge how often you need to repeat visual field
tests. If you are at low risk to develop glaucoma, the test may be repeated once a year. If
you are at high risk to develop glaucoma, the test may be performed up to every 2
months.

If you are experiencing vision loss and traumatic glaucoma doesn’t seem to be the cause, these
additional tests may be performed:

 Tonometry measures the pressure inside the eye. Pressure inside the eye is called
intraocular pressure and is often abbreviated as IOP. Measurements are taken for both
eyes on at least two to three occasions. Because IOP varies from hour-to-hour,
measurements may be taken at different times of the day.
 Dilation lets the ophthalmologist see the optic nerve and examine it for any damage or
abnormalities.
 Fundus photographs may be taken to document the status of your optic nerve and help
detect changes over time. Fundus photographs are pictures of your optic disc, the front
surface of your optic nerve.
 Slit lamp photographs record the front of your eyes (or anterior segment), which
includes your cornea, anterior chamber, iris, and lens. A number of abnormalities in the
anterior segment often accompany angle recession.
 Visual acuity tests, when you read an eye chart from across the room, tell the doctor how
well you can see an object. Any changes in visual acuity are not typically seen until the
late stages of glaucoma.

Top

Questions to ask your doctor

 Is my eye pressure elevated?

 Are there any signs of internal eye damage due to an injury?
 Are there any optic nerve abnormalities?
 Is my peripheral vision normal?
 Is treatment necessary?
 How often should I schedule follow-up exams?

Top

Treatment

Treatment for angle recession glaucoma varies according to the severity of the eye injury.
Generally, if your eye pressure (IOP) is elevated soon after the trauma, your doctor may
recommend exams every 4 to 6 weeks during the first year after the injury to monitor your eye
pressure. Sometimes, early elevation of IOP represents a severe form of the disease that may not
respond to standard medical treatment. Severe forms require more frequent follow-up care.

Treatment includes medicated eyedrops to reduce pressure inside the eye and frequent follow-up
appointments to monitor the pressure in the eye. Sometimes it is necessary to try different
medications to find one that works, or one medicine will work for some time and quit working.
In more advanced stages, surgery may be necessary.

Surgery generally is recommended when the maximum amount of medicine has been tried and
failed to reduce eye pressure, and when the risk of vision loss outweighs the risk of surgery.

Either laser surgery or conventional eye surgery may be needed to improve drainage in the eye.
Although favorable results have been reported for surgical intervention of angle recession
glaucoma, success rates are lower when compared to other forms of glaucoma. The most typical
types of surgery include argon laser trabeculoplasty, trabeculectomy or drainage implant
surgery.

If your eyes show no early signs of elevated pressure, the potential for late-onset glaucoma is
still a reasonable concern, even many years after the injury. Therefore, an annual eye exam is
recommended.

by Brian Sullivan, M.D.

To learn more about angle recession glaucoma, visit Dr. Sullivan’s in-depth article on the topic
at http://www.emedicinehealth.com/Articles/41766-1.asp

Top
March 2010

Traumatic Glaucoma

The etiology and management of glaucoma after ocular trauma.

by Anzhelika Vaccaro, MD, and Jeffery M. Liebmann, MD

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In the United States, the average annual rate of hospitalization for ocular trauma as a principal
diagnosis is 13.2 cases per 100,000 hospital admissions.1 Ocular trauma occurs more often in the
young than the old and among men versus women.2 The type and severity of ocular trauma
generally depend on the age group and the circumstances surrounding the injury. Children are
mostly injured while at play; young adults frequently sustain the trauma while involved in sports,
assaults, and car accidents; and older adults are typically injured at work or as a result of
domestic violence.2

Multiple factors determine if an injury will produce blunt, nonpenetrating/nonperforating trauma

with or without hyphema, or penetrating/perforating trauma with or without the presence of an
intraocular foreign body. Other frequent causes of ocular injury include chemical burns,
radiation, and electrical accidents. This article discusses the various etiologies of traumatic
glaucoma and its management.

INTRAOCULAR PRESSURE AFTER OCULAR TRAUMA

During the early posttraumatic period, the IOP may be low or high. Excluding rupture of the
globe, relative hypotony may result from retinal detachment, a reduction in aqueous formation
due to uveitis or uveal effusion, or an increase in outflow secondary to disruption of angle
architecture or cyclodialysis. Elevated IOP may result from associated uveitis, trabecular
dysfunction, or physical obstruction of the angle by hyphema, a dislocated lens, a shallow
anterior chamber due to posterior segment effusion or hemorrhage, disorganization of the
intraocular structures, or angle closure owing to diverse mechanisms such as pupillary block and
more posterior mechanisms.3

After appropriate intervention for the acute cause of elevated IOP without penetrating injury, the
IOP of most patients with mild or moderate trauma and common disorders such as hyphema or
uveitis often normalizes days or weeks after surgery. Some of these patients, particularly those
with a hyphema or traumatic injury to angle structures, may develop persistently elevated IOP
and glaucomatous damage weeks, months, years, or even decades after the initial injury. For this
reason, all individuals with a history of significant ocular trauma require lifelong surveillance for
the onset and progression of ocular hypertension (OHT) and/or glaucoma.
GLAUCOMA ASSOCIATED WITH HYPHEMA
Hyphema is a very common sequela of ocular trauma and is characterized by the presence of
erythrocytes within the anterior chamber. The most common source of bleeding is trauma to the
anterior face of the ciliary body, which disrupts the major arterial circle of iris.

Depending on the severity of the trauma, hyphema can be present in various amounts, including
occasional or nonlayered circulating erythrocytes (microhyphema), layered blood, and complete
filling of the anterior chamber. When the erythrocytes are deoxygenated, they turn dark in color
(sometimes termed an eight-ball hyphema). In most cases of hyphema, normal erythrocytes
gradually exit the anterior chamber through the trabecular meshwork over the course of several
days or weeks. Black patients should be tested for sickle cell disease or trait, because these
deformed erythrocytes may not easily leave the eye and will predispose these individuals to
persistent, more dangerous increases in IOP and the potential for retinal ischemic damage.
“Rebleeding” can occur, most often in the first week. Patients with acute hyphema should be
counseled to avoid significant exertion or strain until healed. The frequency of rebleeding is
influenced by the presence of hypotony or hypertension, the patient’s use of anticoagulants, and
African ancestry.2

The management of uncomplicated hyphema should be conservative, with topical steroids,

cycloplegia, protective eyewear to prevent further trauma, and elevation of the head. The OHT
associated with hyphema also calls for conservative treatment, with or without oral carbonic
anhydrase inhibitors (CAIs), as needed and as tolerated. Elevated IOP in the setting of hyphema
usually responds well to topical suppressants of aqueous humor formation (often in the form of
betaadrenergic antagonists, alpha 2-adrenergic agonists, and CAIs, although prostaglandin
analogues can also be tried). Systemic CAIs in patients with sickle cell hemoglobinopathies
should be avoided when possible, because acidosis increases the propensity for sickling. If the
patient’s elevated IOP cannot be controlled medically, and it threatens corneal staining or the
function of the optic nerve, surgical intervention is appropriate. Treatment can take the form of
paracentesis (once or more than once), anterior chamber washout, or more invasive glaucoma
surgery such as trabeculectomy.2,4

GLAUCOMAS ASSOCIATED WITH DEGENERATED ERYTHROCYTES

Ghost cell glaucoma results from IOP raised by degenerated erythrocytes (ghost cells), which
lose their hemoglobin in the vitreous cavity and subsequently migrate forward to the anterior
chamber via a disrupted anterior hyaloid face. Ghost cells are spherical and more rigid than
normal erythrocytes and have a tendency to obstruct the trabecular meshwork. Although the
diagnosis is made clinically, an anterior chamber paracentesis can confirm the cells’ presence
cytologically. Ghost cell glaucoma will persist until the supply of ghost cells is depleted. The
management is standard glaucoma therapy, but vitrectomy is effective for eliminating the
remaining reservoir of erythrocyte ghosts.

Hemolytic glaucoma is a rare form of open-angle glaucoma that can occur days to weeks after an
intraocular hemorrhage. Gonioscopy reveals an open angle, but the trabecular meshwork is
covered with reddishbrown pigment. The diagnosis is confirmed cytologically: characteristically,
testing reveals macrophages containing golden-brown pigment. The elevated IOP is secondary to
the obstruction of the trabecular meshwork by these hemoglobin-laden macrophages.
Recalcitrant cases may need anterior chamber washout and/or pars plana vitrectomy.

Hemosiderotic glaucoma is a rare condition that occurs when hemoglobin becomes

phagocytosed by endothelial cells of the trabecular meshwork. The iron liberated from
hemoglobin may cause siderosis of the trabecular meshwork, which can lead to increased
outflow resistance.

TRAUMATIC ANGLE DEFORMITY

Nonpenetrating ocular trauma often leads to recession of the anterior chamber angle, which
represents a cleavage into the ciliary body face. This finding can be visualized by gonioscopy or
ultrasound biomicroscopy (Figures 1 and 2). A relatively small proportion (6%-7%) of patients
with angle recession will develop glaucoma, frequently many years after the initial insult.5 It is
crucial to identify individuals at risk of developing anglerecession glaucoma so that appropriate
follow-up can be established and treatment can be initiated prior to any significant vision loss.
The degree of angle recession seems to correlate with the individual’s likelihood of developing
angle-recession glaucoma.5 Eyes with 180° to 360° of recession have a greater risk of developing
late-onset OHT or glaucoma.5,6 Patients with anglerecession glaucoma develop glaucoma in their
fellow eye more often than expected by chance alone. This fact suggests that traumatic angle
recession accelerates the appearance of unilateral glaucoma in patients who are already
predisposed to developing bilateral primary open-angle glaucoma.5

The diagnosis of angle recession is made based on the history of blunt trauma that led to
unilateral glaucoma or a history of traumatic hyphema.7 Gonioscopy is the gold standard for the
diagnosis of angle recession, and it is often aided by a comparison of the two eyes (Figures 1 and
2). Angle recession may encompass small or large areas of the angle. The clinical appearance is
that of a widened ciliary body band during gonioscopy.

The pathophysiology of angle-recession glaucoma consists of mechanical disruption from

physical force to the angle structures and an elevation in IOP. Blunt trauma pushes the iris
against the lens, creating reverse pupillary block and forcing aqueous into the angle recess. This
hydrodynamic pressure splits the circular and longitudinal muscle fibers of the ciliary body. An
acute rupture of the angle vasculature and permanent damage to the angle ensue. Splitting the
ciliary body muscle may lead to hyphema secondary to disruption of the major arterial circle of
the iris located in the ciliary body. Lost tension from the ciliary muscle on the scleral spur can
further compromise outflow. In general, the presence of angle recession should be viewed as a
marker of injury to the trabecular meshwork and a risk factor for the future development of OHT
or glaucoma. The frequency of periodic reassessment should be determined determined by the
health of the eye, age of the patient, level of IOP, and other patient-related and ocular factors.

GLAUCOMA AFTER PENETRATING TRAUMA

Penetrating ocular trauma can result from blunt, sharp, or missile injury. Initially, the IOP tends
to be low because of uveitis and a penetrating injury. An intraocular foreign body is reportedly
present in 6% of assault cases and 35% of occupational injuries.2
Glaucoma secondary to an unsuspected remaining fragment may develop years after the injury.
Iron and copper are known to cause toxicity and damage to intraocular tissues. The former is
toxic to both the retina and the trabecular meshwork. Glaucoma is much more common with
siderosis than chalcosis.

OTHER CAUSES OF GLAUCOMA AFTER TRAUMA

Permanent ocular injury can result from alkali, acid, or thermal injury. Alkali burns are more
severe than acid burns and may lead to an early, rapid increase in IOP as a result of initial
corneal and scleral shrinkage.1 Vascular remodeling and venous congestion after radiation may
cause the IOP to rise. Electrical injury only leads to transient increases in IOP and may be
associated with the release of iris pigment.2

CONCLUSION
Caused either by particulate obstruction or frank damage to the outflow structures, glaucoma
associated with trauma can be multifactorial in etiology. The treating clinician must be vigilant
or risk missing early-, intermediate-, or late-onset glaucoma that, if not treated, could lead to a
devastating loss of vision.

Jeffrey M. Liebmann, MD, is a clinical professor of ophthalmology at New York University

School of Medicine and is the director of the Glaucoma Service at Manhattan Eye, Ear, &
Throat Hospital, both located in New York. Dr. Liebmann may be reached at (212) 477-7540;
jml18@earthlink.net.

Anzhelika Vaccaro, MD, is a glaucoma fellow at New York Eye and Ear Infirmary in New York.

1. Allingham RR,Damji K,Freedman S,et al.Shields’Textbook of Glaucoma.5th

ed.Philadelphia,PA:Lippincott Williams and Wilkins;2005:393-409.
2. Mermoud A,Heuer DK.Glaucoma associated with trauma.In:Ritch R,Shields MB,Krupin T,eds.The
Glaucomas.2nd ed.St.Louis,MO:Mosby;1996:1259-1275.
3. Tello C,Tran HV,Liebmann J,et al.Angle closure:classification,concepts,and the role of ultrasound
biomicroscopy in diagnosis and treatment.Semin Ophthalmol.2002;17:69-78.
4. Ozer PA,Yalvac IS,Satana B,et al.Incidence and risk factors in secondary glaucomas after blunt
and penetrating ocular trauma.J Glaucoma.2007;16:685-690.5. Tumbocon JA,Latina MA.Angle
recession glaucoma.Int Ophthalmol Clin.2002;42:69-78.
5. Sihota R,Kumar S,Gupta V,et al.Early predictors of traumatic glaucoma after closed globe
injury.Arch Ophthalmol. 2008;126:921-926.
6. Girkin CA,McGwin G,Long C,et al.Glaucoma after ocular contusion.J Glaucoma.2005;14:470-473.

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Glaucoma, Angle Recession

Author: Brian R Sullivan, MD, Associate Professor, Department of Ophthalmology, University

of Texas Southwestern Medical Center
Contributor Information and Disclosures

Updated: Apr 29, 2010

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Introduction
Background

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 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.

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.
Irregular widening of the visible ciliary body in a quadrant with angle recession.
[ CLOSE WINDOW ]

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,2 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.3 Long-term follow-up care of patients with
recognized contusional angle abnormality is warranted because of the risk of delayed
asymptomatic onset.

Pathophysiology

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.

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.

Angle recession. Note the marked posterior displacement of the iris, with a wide ciliary body
band posterior to the scleral spur.
[ CLOSE WINDOW ]
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.
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.2
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,4 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, and hyphema.5,6,4

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.7 In 1990, the estimated hospitalization rate with ocular trauma was 15.2
cases per 100,000 children per year.8

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%).9,10,11,12,13,14,15 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.16
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.

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%.17 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%.18 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.19 A 1996 report described a predominance of home injuries
in Scotland.20

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%.21

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.22
 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.23
 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 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.

Sex

No sex predilection for angle-recession glaucoma has been reported.

 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. 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.

Clinical
History

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.

Physical

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.
o 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.
o 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.
o A large series of blunt injuries among soccer players found that angle recession is more
likely to occur in the superotemporal quadrant.14
 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.24
 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:
o Cyclodialysis
o Iridodialysis
o Iridoschisis
o Anterior synechia
o Iris sphincter tears
o Mydriasis
o Iris atrophy
o Transillumination defects
o Iritis
o Zonular breaks
o Phacodonesis
o Subluxated lens
o Cataract
 Ultrasound biomicroscopy (UBM) is a useful adjunctive modality for the evaluation of
abnormalities in closed-globe injuries (see Imaging Studies).25
 A strong association exists between hyphema and angle recession, but the ciliary body also can
be severely damaged from blunt trauma, without the appearance of a hyphema.
 Posterior segment abnormalities, which may signify prior episodes of trauma, include the
following:
o Vitreous opacities
o Chorioretinal scars
o Macular hole
o Retinal breaks
o Retinal detachment
o 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.

[ CLOSE WINDOW ]
 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.

Causes

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 keratoplasty26 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)16,11,10

 Motor vehicle accidents (eg, airbag deployment, other facial trauma)
 Assaults
  Falls
 Military combat injuries
 Accidents (eg, industrial, farm, home, bungee cord injuries)9
 Other (eg, school accidents, natural disasters)

More on Glaucoma, Angle Recession

Overview: Glaucoma, Angle Recession

Differential Diagnoses & Workup: Glaucoma, Angle Recession

Treatment & Medication: Glaucoma, Angle Recession

Follow-up: Glaucoma, Angle Recession

Multimedia: Glaucoma, Angle Recession

References

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References
1. Shields MB, ed. Glaucomas associated with ocular trauma. In: Textbook of Glaucoma. 4th
ed. Baltimore: Lippincott Williams & Williams; 1988:339-44.
2. Wolff SM, Zimmerman LE. Chronic secondary glaucoma. Association with
retrodisplacement of iris root and deepening of the anterior chamber angle secondary to
contusion. Am J Ophthalmol. 1962;84:547-63.
3. Sihota R, Sood NN, Agarwal HC. Traumatic glaucoma. Acta Ophthalmol
Scand. Jun 1995;73(3):252-4. [Medline].
4. Sihota R, Kumar S, Gupta V, et al. Early predictors of traumatic glaucoma after closed
globe injury: trabecular pigmentation, widened angle recess, and higher baseline
intraocular pressure. Arch Ophthalmol. Jul 2008;126(7):921-6. [Medline].
5. Girkin CA, McGwin G Jr, Long C, Morris R, Kuhn F. Glaucoma after ocular contusion: a
cohort study of the United States Eye Injury Registry. J Glaucoma. Dec 2005;14(6):470-
3. [Medline].
6. Ozer PA, Yalvac IS, Satana B, Eksioglu U, Duman S. Incidence and risk factors in
secondary glaucomas after blunt and penetrating ocular trauma. J
Glaucoma. Dec 2007;16(8):685-90. [Medline].
7. Glynn RJ, Seddon JM, Berlin BM. The incidence of eye injuries in New England
adults. Arch Ophthalmol. Jun 1988;106(6):785-9. [Medline].
8. Strahlman E, Elman M, Daub E, Baker S. Causes of pediatric eye injuries. A population-
based study. Arch Ophthalmol. Apr 1990;108(4):603-6. [Medline].
9. Chorich LJ 3rd, Davidorf FH, Chambers RB, Weber PA. Bungee cord-associated ocular
injuries. Am J Ophthalmol. Feb 1998;125(2):270-2. [Medline].
10. Endo S, Ishida N, Yamaguchi T. Tear in the trabecular meshwork caused by an airsoft
gun. Am J Ophthalmol. May 2001;131(5):656-7. [Medline].
11. Fineman MS, Fischer DH, Jeffers JB, Buerger DG, Repke C. Changing trends in
paintball sport-related ocular injuries. Arch Ophthalmol. Jan 2000;118(1):60-
4. [Medline].
12. Roller RA, Almond NB, Anderson W. Traumatic iridodialysis in a student naval aviator
applicant. Aviat Space Environ Med. Feb 2005;76(2):147-50. [Medline].
13. Morris DS. Ocular blunt trauma: loss of sight from an ice hockey injury. Br J Sports
Med. Mar 2006;40(3):e5; discussion e5. [Medline].
14. Capao Filipe JA, Fernandes VL, Barros H, Falcao-Reis F, Castro-Correia J. Soccer-
related ocular injuries. Arch Ophthalmol. May 2003;121(5):687-94. [Medline].
15. Vize CJ, Gauba V, Atkinson PL. Eye injury as a result of coat toggle
trauma. Eye. Jan 2007;21(1):94-5. [Medline].
16. Giovinazzo VJ, Yannuzzi LA, Sorenson JA, Delrowe DJ, Cambell EA. The ocular
complications of boxing. Ophthalmology. Jun 1987;94(6):587-96. [Medline].
17. McCarty CA, Fu CL, Taylor HR. Epidemiology of ocular trauma in
Australia. Ophthalmology. Sep 1999;106(9):1847-52. [Medline].
18. Nwosu SN. Domestic ocular and adnexal injuries in Nigerians. West Afr J Med. Jul-
Sep 1995;14(3):137-40. [Medline].
19. Koval R, Teller J, Belkin M, Romem M, Yanko L, Savir H. The Israeli Ocular Injuries
Study. A nationwide collaborative study. Arch Ophthalmol. Jun 1988;106(6):776-
80. [Medline].
20. Desai P, MacEwen CJ, Baines P, Minassian DC. Epidemiology and implications of
ocular trauma admitted to hospital in Scotland. J Epidemiol Community
Health. Aug 1996;50(4):436-41. [Medline].
21. Salmon JF, Mermoud A, Ivey A, Swanevelder SA, Hoffman M. The detection of post-
traumatic angle recession by gonioscopy in a population-based glaucoma
survey. Ophthalmology. Nov 1994;101(11):1844-50. [Medline].
22. Poon A, McCluskey PJ, Hill DA. Eye injuries in patients with major trauma. J
Trauma. Mar 1999;46(3):494-9. [Medline].
23. Desai P, MacEwen CJ, Baines P, Minassian DC. Incidence of cases of ocular trauma
admitted to hospital and incidence of blinding outcome. Br J
Ophthalmol. Jul 1996;80(7):592-6. [Medline].
24. Kashiwagi K, Tateno Y, Kashiwagi F, Tsukahara S. Changes in Anterior Chamber Depth
due to Contusion. Ophthalmic Res. Aug 7 2009;42(4):193-198. [Medline].
25. Ozdal MP, Mansour M, Deschênes J. Ultrasound biomicroscopic evaluation of the
traumatized eyes. Eye. May 2003;17(4):467-72. [Medline].
26. Rumelt S, Bersudsky V, Blum-Hareuveni T, Rehany U. Preexisting and postoperative
glaucoma in repeated corneal transplantation. Cornea. Nov 2002;21(8):759-
65. [Medline].
27. Berinstein DM, Gentile RC, Sidoti PA, et al. Ultrasound biomicroscopy in anterior ocular
trauma. Ophthalmic Surg Lasers. Mar 1997;28(3):201-7. [Medline].
 28. Iwamoto T, Witmer R, Landolt E. Light and electron microscopy in absolute glaucoma
with pigment dispersion phenomena and contusion angle deformity. Am J
Ophthalmol. Aug 1971;72(2):420-34. [Medline].
29. Bai HQ, Yao L, Wang DB, Jin R, Wang YX. Causes and treatments of traumatic
secondary glaucoma. Eur J Ophthalmol. Mar-Apr 2009;19(2):201-6. [Medline].
30. Fukuchi T, Iwata K, Sawaguchi S, Nakayama T, Watanabe J. Nd:YAG laser
trabeculopuncture (YLT) for glaucoma with traumatic angle recession. Graefes Arch Clin
Exp Ophthalmol. Oct 1993;231(10):571-6. [Medline].
31. Mermoud A, Salmon JF, Straker C, Murray AD. Post-traumatic angle recession
glaucoma: a risk factor for bleb failure after trabeculectomy. Br J
Ophthalmol. Oct 1993;77(10):631-4. [Medline].
32. Manners T, Salmon JF, Barron A, Willies C, Murray AD. Trabeculectomy with
mitomycin C in the treatment of post-traumatic angle recession glaucoma. Br J
Ophthalmol. Feb 2001;85(2):159-63. [Medline].
33. Melamed S, Ashkenazi I, Gutman I, Blumenthal M. Nd:YAG laser trabeculopuncture in
angle-recession glaucoma. Ophthalmic Surg. Jan 1992;23(1):31-5. [Medline].
34. Canavan YM, Archer DB. Anterior segment consequences of blunt ocular injury. Br J
Ophthalmol. Sep 1982;66(9):549-55. [Medline].
35. Tesluk GC, Spaeth GL. The occurrence of primary open-angle glaucoma in the fellow
eye of patients with unilateral angle-cleavage
glaucoma. Ophthalmology. Jul 1985;92(7):904-11. [Medline].

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Further Reading
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Keywords
angle-recession glaucoma, angle recession glaucoma, posttraumatic angle-recession glaucoma,
contusion angle-recession glaucoma, contusion angle deformity, traumatic glaucoma, traumatic
angle-recession glaucoma, intraocular pressure, IOP, optic neuropathy, open-angle glaucoma

[ CLOSE WINDOW ]

Contributor Information and Disclosures

Author

Brian R Sullivan, MD, Associate Professor, Department of Ophthalmology, University of

Texas Southwestern Medical Center
Brian R Sullivan, MD is a member of the following medical societies: American Academy of
Ophthalmology and American Society of Cataract and Refractive Surgery
Disclosure: Nothing to disclose.

Medical Editor

Andrew I Rabinowitz, MD, Consulting Staff, Department of Ophthalmology, Barnet Dulaney

Perkins Eye Center
Andrew I Rabinowitz, MD is a member of the following medical societies: Aerospace Medical
Association, American Academy of Ophthalmology, and American Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Simon K Law, MD, PharmD, Assistant Professor of Ophthalmology, Jules Stein Eye Institute;
Chief of Section of Ophthalmology Surgical Services, Department of Veterans Affairs
Healthcare Center, West Los Angeles
Simon K Law, MD, PharmD is a member of the following medical societies: American
Academy of Ophthalmology, American Glaucoma Society, and Association for Research in
Vision and Ophthalmology
Disclosure: Nothing to disclose.

Managing Editor

Martin B Wax, MD, Clinical Professor, Department of Ophthalmology, University of Texas

Southwestern Medical School; Vice President, Ophthalmology Research and Development,
Head, Ophthalmology Discovery Research, Alcon Labs, Inc
Martin B Wax, MD is a member of the following medical societies: American Academy of
Ophthalmology, American Glaucoma Society, and Society for Neuroscience
Disclosure: Alcon Labs Salary Employment

CME Editor

Lance L Brown, OD, MD, Ophthalmologist, Affiliated With Freeman Hospital and St John's
Hospital, Regional Eye Center, Joplin, Missouri
Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University
of Arkansas for Medical Sciences
Hampton Roy Sr, MD is a member of the following medical societies: American Academy of
Ophthalmology, American College of Surgeons, and Pan-American Association of
Ophthalmology
Disclosure: Nothing to disclose.
 medscapecme

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Glaucoma, Angle Recession: Differential Diagnoses & Workup

Author: Brian R Sullivan, MD, Associate Professor, Department of Ophthalmology, University

of Texas Southwestern Medical Center
Contributor Information and Disclosures

Updated: Apr 29, 2010

 Print This
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 Overview
 Differential Diagnoses & Workup
 Treatment & Medication
 Follow-up
 Multimedia

 References
 Keywords

Differential Diagnoses
Glaucoma, Angle Closure, Acute Glaucoma, Primary Open Angle

Glaucoma, Angle Closure, ChronicGlaucoma, Pseudoexfoliation

Glaucoma, Lens-Particle Glaucoma, Unilateral

Glaucoma, Neovascular Glaucoma, Uveitic

Glaucoma, Phacolytic Melanoma, Ciliary Body

Glaucoma, Pigmentary Melanoma, Iris

Other Problems to Be Considered

Elevated episcleral venous pressure/carotid cavernous fistula

Iridocorneal endothelial (ICE) syndrome
Uveitis-glaucoma-hyphema (UGH) syndrome
Angle recession refers to a tear between the circular and longitudinal fibers of the ciliary body.
Cyclodialysis is defined as a detachment of the ciliary body from its insertion at the scleral spur.
Iridodialysis is separation of the iris root from its attachment to the anterior ciliary body. By
comparison, iridoschisis refers to splitting of layers of iris stroma. All of these conditions are
sequelae of blunt ocular trauma, and any of these conditions may coexist.

Workup
Imaging Studies

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

 Usually, imaging is necessary only to evaluate comorbidities due to trauma.
o Occasionally, CT scanning of the orbits is needed to evaluate for orbital fractures or
foreign bodies.
o 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.27,25
o 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.
o 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.25
o 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.4

Other Tests

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

 Gonioscopy is the only clinical procedure that must be performed before angle recession can be
diagnosed.
o Use of a 1- or 3-mirror Goldman goniolens, which provides the greatest magnification of
angle structures, is recommended.
o 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.
o 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.2

 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.
o Abnormal corneal endothelial proliferation may occur in some eyes with traumatic angle
deformities.
o 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.
o 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.28
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.

More on Glaucoma, Angle Recession

Overview: Glaucoma, Angle Recession

Differential Diagnoses & Workup: Glaucoma, Angle Recession

Treatment & Medication: Glaucoma, Angle Recession

Follow-up: Glaucoma, Angle Recession

Multimedia: Glaucoma, Angle Recession

References
eMedicine Specialties > Ophthalmology > Intraocular
Pressure

Glaucoma, Angle Recession: Treatment & Medication

Author: Brian R Sullivan, MD, Associate Professor, Department of Ophthalmology, University

of Texas Southwestern Medical Center
Contributor Information and Disclosures

Updated: Apr 29, 2010

 Print This
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 Overview
 Differential Diagnoses & Workup
 Treatment & Medication
 Follow-up
 Multimedia

 References
 Keywords

Treatment
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.

 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.
o The severity of IOP elevation, optic nerve appearance, and visual field findings
contribute to the decision-making process.
o 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.
 o Use of topical aqueous suppressants in the initial medical treatment is preferred; these
include beta-antagonists, alpha-agonists, and carbonic anhydrase inhibitors.
o 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.
o 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.
o Atropine has been reported to reduce IOP in angle-recession glaucoma; therefore,
cycloplegic agents may have a role in treatment.
o 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.
o 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.
o Severe early cases may fail to show an initial response to aggressive medical treatment,
indicating a poorer overall prognosis.

Surgical Care

Surgical intervention in angle-recession glaucoma is usually indicated when maximally tolerated

medical treatment has failed29 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.

 Argon laser trabeculoplasty

o Argon laser trabeculoplasty (ALT) 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.
o IOP elevation may become worse in response to ALT.
o 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.
 Alternative laser procedures
o Nd:YAG laser trabeculopuncture (YLT) has been used with variable success. A 1992 study
demonstrated a 100% failure rate in eyes with 360° angle recession.30
o Currently, YLT is not recommended for the routine management of angle-recession
glaucoma.
o Other laser procedures that have shown promise are transscleral krypton laser
cyclophotocoagulation, transpupillary argon laser cyclophotocoagulation, and
endoscopic cyclophotocoagulation.
 Filtration surgery
o Filtration surgery has a success rate lower than that of POAG.
o 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.31
 o 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.32
 Tube shunt devices
o 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.
o A 1993 study showed the superior results of trabeculectomy with antimetabolite over
Molteno implantation in cases of posttraumatic angle-recession glaucoma.

Consultations

 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.

Medication
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.

Beta-agonists

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.
  Dosing
 Interactions
 Contraindications
 Precautions

Adult

Timoptic: 1 gtt in affected eye bid

Timoptic XE: 1 gtt in affected eye qd

Pediatric

Not established

 Dosing
 Interactions
 Contraindications
 Precautions

May cause bradycardia and asystole in combination with systemic beta-blockers (may cause
additive effects)

 Dosing
 Interactions
 Contraindications
 Precautions

Documented hypersensitivity; bronchial asthma; sinus bradycardia; second- and third-degree AV

block; severe COPD; overt cardiac failure; cardiogenic shock

 Dosing
 Interactions
 Contraindications
 Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may
use if benefits outweigh risk to fetus

Precautions

May contain sulfites, which can cause allergic-type reactions in susceptible patients
Levobunolol (Betagan, AKBeta) 0.25%, 0.5%

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

production.

 Dosing
 Interactions
 Contraindications
 Precautions

Adult

1 gtt in affected eye bid

Pediatric

Not established
Glaucoma, Angle Recession: Treatment & Medication

Author: Brian R Sullivan, MD, Associate Professor, Department of Ophthalmology, University

of Texas Southwestern Medical Center
Contributor Information and Disclosures

Updated: Apr 29, 2010

 Print This
 Email This

 Overview
 Differential Diagnoses & Workup
 Treatment & Medication
 Follow-up
 Multimedia

 References
 Keywords

Treatment
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.

 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.
o The severity of IOP elevation, optic nerve appearance, and visual field findings
contribute to the decision-making process.
o 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.
o Use of topical aqueous suppressants in the initial medical treatment is preferred; these
include beta-antagonists, alpha-agonists, and carbonic anhydrase inhibitors.
o 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.
 o 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.
o Atropine has been reported to reduce IOP in angle-recession glaucoma; therefore,
cycloplegic agents may have a role in treatment.
o 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.
o 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.
o Severe early cases may fail to show an initial response to aggressive medical treatment,
indicating a poorer overall prognosis.

Surgical Care

Surgical intervention in angle-recession glaucoma is usually indicated when maximally tolerated

medical treatment has failed29 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.

 Argon laser trabeculoplasty

o Argon laser trabeculoplasty (ALT) 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.
o IOP elevation may become worse in response to ALT.
o 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.
 Alternative laser procedures
o Nd:YAG laser trabeculopuncture (YLT) has been used with variable success. A 1992 study
demonstrated a 100% failure rate in eyes with 360° angle recession.30
o Currently, YLT is not recommended for the routine management of angle-recession
glaucoma.
o Other laser procedures that have shown promise are transscleral krypton laser
cyclophotocoagulation, transpupillary argon laser cyclophotocoagulation, and
endoscopic cyclophotocoagulation.
 Filtration surgery
o Filtration surgery has a success rate lower than that of POAG.
o 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.31
o 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.32
 Tube shunt devices
 o 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.
o A 1993 study showed the superior results of trabeculectomy with antimetabolite over
Molteno implantation in cases of posttraumatic angle-recession glaucoma.

Consultations

 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.

Medication
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.

Beta-agonists

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.

 Dosing
 Interactions
 Contraindications
 Precautions
Adult

Timoptic: 1 gtt in affected eye bid

Timoptic XE: 1 gtt in affected eye qd

Pediatric

Not established

 Dosing
 Interactions
 Contraindications
 Precautions

May cause bradycardia and asystole in combination with systemic beta-blockers (may cause
additive effects)

 Dosing
 Interactions
 Contraindications
 Precautions

Documented hypersensitivity; bronchial asthma; sinus bradycardia; second- and third-degree AV

block; severe COPD; overt cardiac failure; cardiogenic shock

 Dosing
 Interactions
 Contraindications
 Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may
use if benefits outweigh risk to fetus

Precautions

May contain sulfites, which can cause allergic-type reactions in susceptible patients

Levobunolol (Betagan, AKBeta) 0.25%, 0.5%

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

production.
  Dosing
 Interactions
 Contraindications
 Precautions

Adult

1 gtt in affected eye bid

Pediatric

Not established
Glaucoma, Angle Recession: Follow-up

Author: Brian R Sullivan, MD, Associate Professor, Department of Ophthalmology, University

of Texas Southwestern Medical Center
Contributor Information and Disclosures

Updated: Apr 29, 2010

 Print This
 Email This

 Overview
 Differential Diagnoses & Workup
 Treatment & Medication
 Follow-up
 Multimedia

 References
 Keywords

Follow-up
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.
o Some early cases are self-limited, but patients should still be observed after their
condition appears to resolve.
o 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.

Inpatient & Outpatient Medications

 See Medication.

Deterrence/Prevention

 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.

Complications

 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.
o Gonioscopy should always be performed when a patient with a unilateral cataract is
evaluated, even when his or her history is negative for trauma.
o After surgical management, the risk of complications is higher with a traumatic cataract
than with a senile cataract.
 Intraoperative complications include the following:
o Zonular dialysis
o Vitreous loss
o Intraocular hemorrhage
o 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
o IOP elevation
o Inflammation
o IOL malposition
o Pupil capture
o Intraocular hemorrhage
o Glare
o 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.
o 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.
o Traumatic abnormalities of the peripheral retina include the following:
 Atrophic holes
 Horseshoe tears
 Operculated tears
  Retinal dialysis
 Retinal detachment

Prognosis

 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.
 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.33
o The risk of visual loss depends on many factors, particularly the timeliness of initial
diagnosis and the course of management.
o Response of elevated IOP to medical therapy varies, and with time, IOP control may
deteriorate despite dependence on multiple medications.
o 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 excellent patient education resources, visit eMedicine's Glaucoma Center. Also, see
eMedicine's patient education articles Angle Recession Glaucoma, Understanding Glaucoma
Medications, and Glaucoma FAQs.

Miscellaneous
Medicolegal Pitfalls

 Medicolegal concerns may arise from an allegation of a failure to diagnose the disorder or from
delays in providing appropriate care.
o Angle recession should be suspected in any patient with a unilateral cataract or with a
history of eye injury, even if the traumatic event seems trivial.
o Gonioscopy should be routinely performed in the evaluation of a patient with a
history—even a remote history—of blunt trauma, particularly after a hyphema resolves.
o Gonioscopy should be performed in all patients with suspected POAG.
o Angles should be examined in patients with asymmetric IOPs, unilateral cataract,
zonular weakness, iridodialysis, or other abnormalities of the anterior segment.
 Failure to recommend appropriate follow-up care is a pitfall.
o Patients with greater than 180° of angle recession should receive lifelong follow-up care,
usually on an annual basis, to monitor for the development of glaucoma.
 o Patients should not be discharged from clinic because the onset of glaucoma may be
many years after the injury.
 Suboptimal monitoring of the relative effectiveness of the treatment provided is another pitfall.
o Angle-recession glaucoma responds to both medical and surgical interventions
somewhat unpredictably and with less favorable results than those of other types of
glaucoma.
o Adjustments to therapy or proceeding to more aggressive treatment measures may
need to be accelerated in eyes with recalcitrant glaucoma.
o Progression of visual field loss during a period with few or no changes in patient care
may lead to medicolegal complaints or claims of an inappropriate treatment delay.

Special Concerns

 Sickle cell anemia or trait is a systemic disorder that has multiple links to eye disease; therefore,
it should be considered during the evaluation and treatment of patients with hyphema in the
immediate period after blunt trauma.
 Sickle cell anemia is a concern during the long-term management of eyes that develop angle-
recession glaucoma because of the increased tendency for microvascular occlusions.
 In general, patients with sickle cell anemia require more aggressive IOP control with glaucoma
treatment than other patients because their eyes have a decreased tolerance of even moderate
elevations in IOP.
 In addition, carbonic anhydrase inhibitors and hyperosmotic agents are contraindicated in
patients with sickle cell disease because of the effects of acidosis and diuresis.

Acknowledgments

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.

More on Glaucoma, Angle Recession

Overview: Glaucoma, Angle Recession

Differential Diagnoses & Workup: Glaucoma, Angle Recession

Treatment & Medication: Glaucoma, Angle Recession

Follow-up: Glaucoma, Angle Recession

Multimedia: Glaucoma, Angle Recession

References

ultimedia
Media file 1: Irregular widening of the visible ciliary body in a quadrant
with angle recession.

(Enlarge Image)

[ CLOSE WINDOW ]
Irregular widening of the visible ciliary body in a quadrant with angle recession.
Media file 2: Angle recession. Note the marked posterior displacement
of the iris, with a wide ciliary body band posterior to the scleral spur.

(Enlarge Image)

[ CLOSE WINDOW ]
Angle recession. Note the marked posterior displacement of the iris, with a wide ciliary body
band posterior to the scleral spur.
Media file 3: 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 becom

(Enlarge Image)