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REVIEW ARTICLE
Angle Recession Glaucoma
Sunil Ganekal1, Syril Dorairaj2
ABSTRACT
Traumatic glaucomas are a very heterogeneous group of entities due to a variety of mechanisms which increase the
intraocular pressure in the early or late phase after traumatic injury. Glaucoma after closed globe injury is a major
concern because many cases may go unnoticed and are diagnosed many years later as having irreversible glaucomatous
optic nerve damage.[1,2] Angle recession is one of the causes for late onset posttraumatic glaucoma; this condition may
be underdiagnosed because the onset is often delayed and because a history of eye injury may be distant or forgotten.
KEY WORDS: Blunt trauma, Angle recession, Glaucoma
INTRODUCTION
Eyes with an underlying tendency for open-angle
glaucoma will develop a late increase in intraocular
pressure (IOP) following blunt trauma.[3] Glaucoma
after blunt trauma appears to have two peaks of
incidence, at <1 year and about 10 years after
[4]
trauma. A review of data from the eye injury register
found increasing age, poor baseline visual acuity,
angle recession, hyphema, and lens injury to be
independent risk factors for developing posttraumatic
glaucoma.[5]
Angle recession glaucoma is classified as a type of
traumatic secondary open-angle glaucoma.[6] Angle
recession, with or without glaucoma, is a common
sequel of blunt ocular trauma and one characterized
by a variable degree of cleavage between the circular
and the longitudinal fibers of the ciliary muscle.[7]
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, reported the presence
of monocular glaucoma in 6 patients who had histories
of blunt trauma to the eye with gonioscopic evidence
of angle recession. In addition, they described the
pathological findings of angle recession in enucleated
eyes of patients with a previous history of ocular
contusion.[7]
Since then, numerous investigators have studied
the epidemiological, clinical, and histopathological
findings of this disease entity. Although a relatively
uncommon phenomenon, angle recession glaucoma
may be overlooked in the management of blunt
eye trauma.[1] Long-term follow-up care of patients
with recognized contusional angle abnormality is
warranted because of the risk of delayed asymptomatic
onset. It is desirable to identify individuals at risk
of developing angle recession glaucoma so that
appropriate follow-up examinations and treatment
can be done at an early stage, long before the vision
becomes seriously impaired.
Epidemiology
Advancing age has been reported as an independent
predictive factor for the risk of developing glaucoma
after ocular contusion injury. Angle recession
glaucoma is most likely diagnosed in mid or late
adulthood due to the potential delay or late onset
after a blunt injury. It may be misidentified as
primary open-angle glaucoma (POAG) because late
angle abnormalities may be subtle on examination.
A distant or even forgotten history of eye trauma may
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Department of Ophthalmology, Jagadguru Jayadeva
Murugarajendra Medical College, Davangere, Karnataka, India,
2
Department of Ophthalmology, Mayo Clinic, Florida, USA
1
Quick Response Code:
Website:
***
Address for correspondence:
Dr. Sunil Ganekal, Department of Ophthalmology, Jagadguru Jayadeva
Murugarajendra Medical College, Davangere - 577 004, Karnataka,
India. Phone: +91-0819222565. [email protected]
Journal of Vision Sciences/May-Aug 2015/Volume 1/Issue 2
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Ganekal and Dorairaj: Angle recession glaucoma following blunt trauma
result in the condition being overlooked, especially in
the elderly persons.
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 frequent
in men. Among children, eye injuries occur more
frequent in boys than girls.
Investigators have reported that more than 60% of
eyes with blunt trauma will have some degree of angle
recession.[4,8-11] Although traumatic angle recessions
may occur without hyphema, a strong correlation
between hyphema and angle recession has been
established. Careful gonioscopy has revealed that
between 56% and 100% of patients with traumatic
hyphema has some degree of angle recession
(Table 1).[4,8-12]
The most frequent cause of injury-inducing angle
recession occurred as a result of sports or other
recreational accidents (55.6%; 114 of 205) in the series
of Canavan and Archer[13] and as a result of assault
(65%; 57 of 87) in the series of Mermoud et al.[14]
Less common causes were automobile or industrial
accidents, projectiles from toy guns or slingshots,
and other leisure activities.[14-18] A small percentage
of people will deny any previous episode of ocular
trauma despite the presence of obvious eyelid
scars and pupillary sphincter tears.[14] Very rarely
ocular surgical procedure like cataract surgery and
penetrating keratoplasty can cause angle recession.[19]
Although recession of the iridocorneal angle is
common after blunt trauma, only 6-8%[4,9,20] of these
eyes will eventually develop glaucoma (Table 2).
In a 10 years prospective study by Kaufman and
Tolpin[9] involving 31 eyes with angle recession, they
observed that 6% of the patients developed glaucoma.
Similarly, retrospective analysis by Blanton[4] found
nine individuals (7%) with uniocular glaucoma in
his review of 130 cases of angle recession. 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
Table 1: Presence of angle recession in patients with
traumatic hyphema
Authors
Number of
patients with
hyphema
Number of
patients with angle
recession (%)
Blanton[4]
182
71
Tomjun
160
100
Kaufman and Tolpin[9]
50
94
Filipe et al.
45
56
Spaeth
43
60
Herschler[12]
17
100
Total
497
405 (81)
[8]
[10]
[11]
prevalence of glaucoma of eyes with any degree of
angle recession was 5.5%.[20]
Five patients were diagnosed within 3 years after
injury, and the remaining 4 patients developed
glaucoma more than 10 years after the injury. There
appear to be two peak incidences of glaucoma after
angle recession. The first peak occurs within the first
few weeks to years after the trauma, and the second
peak occurs 10 or more years after the injury.[4] Alper[21]
reviewed a series of 27 cases of angle recession, and
14 of these had unilateral glaucoma. Eight received
diagnoses within 4 years after the injury, and the
remaining six had diagnoses more than 14 years
after the original trauma. Some investigators have
even reported cases of angle recession glaucoma
developing more than 50 years after the initial
injury.[1,15] There is also an association between the
extent of angle recession and the development of
glaucoma. Tonjum[8] found a significant correlation
between the extent of angle recession and decrease
in the outflow facility in the injured eyes. Alper[21]
observed that 13 of 14 patients with angle recession
glaucoma in his study had angle recessions extending
approximately 240° or greater, whereas the remaining
case had 150° of recession. Likewise, Blanton[4]
found that all his angle recession glaucoma cases that
developed 10 years after injury had more than 180°
of recession. It appears that those eyes with <180°
of recession are unlikely to develop glaucoma,[11,22]
whereas most investigators agree that patients with
180-360° of angle recession will have a greater risk of
developing late-occurring glaucoma.[1,4,7,8,19,23]
In eyes that do develop angle recession glaucoma, the
contralateral nontraumatized eye has been reported
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Ganekal and Dorairaj: Angle recession glaucoma following blunt trauma
Table 2: Incidence of glaucoma in patients with angle recession
Authors
Number
of patients
Duration
(years)
Kaufman and Tolpin[9]
31
10
Prospective
6
Blanton[4]
130
10
Retrospective
7
Salmon
987
‑
Population based survey
8
[20]
to have a 50% chance of developing open-angle
glaucoma, sometimes years after the pressure rise
was noted in the traumatized eye.[22] After topical
corticosteroid provocative testing, the fellow eye has
also been observed to respond in a manner similar
to that in eyes with POAG.[15] The results of the
aforementioned studies bring into play some possible
theories with regard to the relationship of angle
recession and open-angle glaucoma. It may indicate
that the angle recession itself is probably not the cause
of elevated IOP but, rather, that it may accelerate the
appearance of glaucoma in patients who are already
predisposed to develop POAG.[9,10] This predisposition
may render an eye more susceptible to developing an
increase in IOP after traumatic angle recession due to
some genetically determined structural or functional
abnormality in the aqueous outflow pathway of the
eye.[16]
Alternatively, it is also conceivable that angle
recession, through some yet unknown feedback
mechanism, may alter neural factors that affect IOP
in both eyes.[15]
CLINICAL PRESENTATION
The diagnosis of angle recession is made by history
and clinical examination. 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.
In cases of unilateral glaucoma or traumatic hyphema
or after blunt trauma, angle recession should always
be considered.[4,12,24,25] A unilateral cataract in a young
or middle-aged adult should raise the suspicion of
remote trauma, even when the history is negative.
Angle recession is typically diagnosed by means
of gonioscopy (Figure 1). The clinical appearance
Type of study
Patients developing
glaucoma (%)
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. Slit-lamp gonioscopy with
indirect gonioscopy lenses (e.g. Zeiss or Goldman
lenses) provides a detailed view of the angle
structures with good magnification.[11] 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. With milder injuries,
the examiner may have to compare the gonioscopic
appearance of both eyes simultaneously with a
Koeppe lens or compare two parts of the angle
of 1 eye to identify subtle changes in the injured
angle.[11] The appearance varies greatly, depending
on the degree and extent of the recession and on
the particular eye.[26] Minor angle damage can be
recognized as a disruption of the regular pattern
of insertion of the iris fibers into the ciliary body
or scleral spur.[4] This leaves the ciliary body bare
in comparison with other quadrants of the angle or
with the angle of the opposite eye.[23] Small tufts of
uveal tissue may be observed bunching up on the iris
root and on the trabeculum above the sclera spur.[21]
The more difficult cases are those in which there
is a question of a 360° recession, and comparison
between the two eyes is especially helpful in these
cases.[4,11] Alternatively, the recession may be limited
to one small area, and careful gonioscopy should be
performed to detect subtle changes in the anterior
chamber angle.[4] The combination of localized
deepening with change in color and texture of the
angle provides a valuable clue to the presence of
recession.[7,8] Signs of trauma should be sought:
Corneal scars, tears in the Descemet’s membrane,
pigmentary deposits, a space between the iris and the
lens that is wider in one segment of the pupil than
elsewhere, ruptures of the iris sphincter, presence
of a vossius ring on the anterior lens capsule,
iridodialysis, iridodenesis, iridoplegia, torn iris
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Ganekal and Dorairaj: Angle recession glaucoma following blunt trauma
Moderate tears are characterized by a definite cleft into
the fibers of the ciliary muscle, and the angle appears
deeper than that of the opposite eye. Deep tears are
characterized by a fissure in the ciliary body, and the
apex of the fissure cannot be seen gonioscopically.
Figure 1: Gonioscopy in patient with angle recession (widening
of the ciliary body band)
processes, phacodenesis, localized opacities, or
dislocation of the lens, old vitreous hemorrhage,
retinal or choroidal atrophy, pigmentation, or
tears.[11] In more severe injuries, the cleft extends into
the ciliary body, the light gray portion of the ciliary
band appears broadened, and the scleral spur is more
distinctly prominent.[23,26] Small peripheral anterior
areas of synechiae frequently appear at the lateral
limits of an angle recession and may extend into the
peripheral areas of the recession. This may hide areas
in the angle that were previously recessed.[9,12] A large
series of blunt injuries among soccer players found
that angle recession is more likely to occur in the
superotemporal quadrant.[27] Patients with significant
angle recession should be advised to have annual eye
examinations for an indefinite period to detect lateoccurring glaucoma.[23]
A classification of angle recession with regard to the
depth of ciliary muscle tears has been proposed by
Howard et al.[26]
In shallow tears, separation of the processes of the
uveal meshwork is present so that the ciliary body
band and the scleral spur are more plainly visible than
the fellow eye. The separation of the processes may
leave pigmented tags on the anterior surface on the
peripheral iris, on the ciliary body band, on the scleral
spur, and on the posterior portion of the trabecular
meshwork. The ciliary body band appears darker and
wider, whereas the scleral spur appears whiter than
does the opposite eye. In shallow tears, no actual cleft
into the face of the ciliary body is present.
Ultrasound biomicrosopy (UBM) can also be used
to detect the presence of moderate to severe angle
recession when visualization of the angle structures
is limited owing to some form of corneal opacity or
associated injury.[28] An angle anomaly that may be
confused with angle recession is cyclodialysis, in
which a sector of the ciliary body is detached from
the sclera. The cleft or separation occurs between the
longitudinal muscle of the ciliary body and the sclera
itself. In contrast, the cleft in angle recession occurs
between the circular and longitudinal muscles of
the ciliary body.[24,25] Cyclodialysis can be clinically
recognized by the presence of an area of white sclera
visible posterior to the scleral spur. Other differential
diagnoses for angle recession include iridodialysis,
trabecular tears, and angle abnormalities secondary
to previous ocular surgery.[25] Other causes of
unilateral or asymmetrical glaucoma should also be
ruled out (e.g. uveitis, anterior segment tumors, lensinduced glaucoma, pseudoexfoliation glaucoma, and
glaucoma secondary to elevated episcleral venous
pressure).[29] These other conditions can be clinically
differentiated from angle recession after a complete
ocular examination and review of the patient’s
medical and ocular history.
PATHOPHYSIOLOGY
The mechanism of glaucoma associated with angle
recession appears to involve following processes.
There are two related mechanisms that require
discussion in angle recession glaucoma. The first is
the physical force that produces the ciliary body cleft,
and the second is the pathogenesis of the elevated IOP
seen in this disease entity. It should be emphasized
that the presence of a ciliary body tear is only an
indicator of previous ocular trauma and is not the
cause of subsequent glaucoma.[7,12]
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,
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Ganekal and Dorairaj: Angle recession glaucoma following blunt trauma
deepening the peripheral anterior chamber and
increasing the diameter of the corneoscleral limbal
ring. 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. 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,[7]
while the circular muscle, with the pars plicata and
the iris root, is displaced posteriorly.[13,26] In addition,
the presence of angle recession can disrupt the tension
exerted by the ciliary muscles on the scleral spur and
trabecular meshwork, which may further compromise
aqueous drainage.[12]
but evidence suggests an increased incidence of
POAG in the other eye of affected patients.
If there is only minimal recession of the angle,
the cleft often heals with little or no scarring.[7] In
the presence of more significant injury, advanced
degeneration, atrophy, fibrosis, and scarring of the
trabecular meshwork and Schlemms canal may
occur years after the initial trauma.[7,12,25,30] Variable
obliteration of the intertrabecular spaces and
Schlemm’s canal accompanied by atrophy of the
inner circular muscles of the ciliary body is a common
finding.[7,12,30] In addition, a hyaline membrane may
be present on the inner trabecular meshwork.[7,30]
With the reduction in aqueous drainage brought about
by the aforementioned events, the IOP can rise with
time as the outflow facility gradually decreases with
increasing age.[4]
HISTOPATHOLOGY
During this process, shearing of the anastomotic
branches of the anterior ciliary arteries can occur,
resulting in a hyphema.[26] 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.
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.[8,12] The mechanism is not well-understood,
One theory suggests that patients with angle recession
glaucoma have an independent, perhaps genetic,
predisposition to chronically diminishing trabecular
function in both eyes.[31]
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.
Chronic elevation of IOP leads to optic neuropathy
characterized by progressive optic cupping and visual
field loss.
Histopathologic findings of eyes with angle recession
deformities have been well described and include
features of both light microscopy and electron
microscopy (EM).
Gross pathology
Yanoff suggested a diagnostic method in sections of the
eye that involves drawing a line through the optic axis
(black line in picture) and then drawing a second line
(white lines in picture) parallel to the first, but which
includes the scleral spur. If the angle recess is located
posteriorly to the line (as the white arrow indicates)
then there is angle recession (Figure 2). The changes
noted on light microscopy (Figure 3) include a tear
extending into the anterior ciliary body, separating the
longitudinal and circular fibers but the longitudinal
muscle remains attached to the scleral spur. Other
findings include the retroplacement of the iris root
and ciliary processes. Overtime with healing of the
ciliary body laceration, atrophy of the circular muscle
at involved sites, resulting in a fusiform contour of
the ciliary body, as seen on axial sections. Associated
findings such as iridodialysis, rupture of the trabecular
meshwork, and cyclodialysis may be noted.
Histopathologic findings in late cases like marked
degeneration of the trabecular meshwork, abnormal
corneal endothelial proliferation posterior to the
Schwalbe ring with secretion of a Descemet like
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Ganekal and Dorairaj: Angle recession glaucoma following blunt trauma
abnormal hyaline membrane covering the meshwork,
sometimes extending further onto the anterior iris
surface provided clues to the mechanism of glaucoma
in angle recession.[32]
EM 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
EM 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.[32]
Figure 2: Section of the eye (gross pathology) showing angle
recession, black line indicates optical axis and white line indicates
scleral spur, white arrow indicates angle recession
Differential diagnosis
POAG, primary acute and chronic angle closure
glaucoma, secondary glaucoma like neovacular
glaucoma, pigmentary glaucoma, pseudoexfoliation
glaucoma, iridocorneal endothelial (ICE) syndrome,
uveitis-glaucoma-hyphema syndrome.
Work up
The diagnosis of angle recession is confirmed during
office examination using gonioscopy.
Gonioscopy
A simple diagnostic test, is essential for making the
clinical diagnosis of angle recession. It is usually
deferred for 4-6 weeks after the acute injury. When
gonioscopy is performed, asymmetry of the angle
recess may be noticeable between the affected and the
nontraumatized eye or in different quadrants of the
involved eye. Widening of the ciliary body band may
be present due to retrodisplacement of the iris root.
Other signs include irregular and darker pigmentation
in the angle, whitening of the scleral spur due to visibly
fractured iris processes, or the presence of peripheral
anterior synechiae. Gonioscopy may aid in the diagnosis
of other angle abnormalities from trauma, such as
iridodialysis or cyclodialysis. It’s essential to note that,
in some cases, the gonioscopic findings may become
more difficult to recognize with the passage of time.
Imaging studies
Usually, imaging is necessary only to evaluate
comorbidities due to trauma. Occasionally, CT scan of
the orbits is needed to evaluate for orbital fractures or
foreign bodies. Emergency neuroimaging if typically
indicated after major head trauma.
Figure 3: Angle recession changes noted on histopathology slide
of patient with angle recession glaucoma. (1) sclera spur, reveals
the posterior displacement of the iris-ciliary body complex,
(2) residual meridional ciliary muscle strands are seen attached
to the sclera, (3) the effaced ciliary muscle shows pigment as it
is reflected posteriorly, (4) angle injury to the outflow tract is
indicated by pigment laden macrophages and fibrosis over the
trabecular meshwork, (5) the remaining attached longitudinal
ciliary muscle, (6) circular muscle fibers, (7) radial ciliary muscle
fibers
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.[28]
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
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Ganekal and Dorairaj: Angle recession glaucoma following blunt trauma
a clinical setting in an intact globe, and it provides
information otherwise unavailable from convention
examination. High-resolution images of angle
recession (Figure 4), zonular deficiency, iridodialysis,
and cyclodialysis have been described. Zonular
deficiency and angle recession are the most common
UBM findings in a closed-globe injury.[33]
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.[34]
Anterior
segment
optical
coherence
tomography (AS-OCT) (Figure 5)
Figure 4: Ultrasound biomicrosopy showing the angle recession
(marked posterior displacement of the iris and an abnormally
deep chamber angle)
The noncontact nature of AS-OCT makes it a valuable
tool in identifying angle pathology in posttraumatic
eyes Kawana et al. described the use of a prototype 3D
swept-source, 1310 nm OCT to image post-traumatic
angle recession.[35]
Visual field test
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.
Tonography
The previous study has described the use of tonography
to evaluate patients with traumatic angle recession.[36]
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, the 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 disc photography is also important for
documenting and monitoring glaucoma
Fourier domain OCT
Optic disc analysis and analysis of nerve fiber layers
has been gaining acceptance in the diagnosis and
management of all forms of glaucoma.
Figure 5: Anterior segment optical coherence tomography
showing hyphema and angle recession in a patient with blunt
trauma
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 re-examined 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 decisionmaking process. Treatment almost always is
indicated when the IOP is greater than an arbitrary
range of 25-28 mmHg 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
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Ganekal and Dorairaj: Angle recession glaucoma following blunt trauma
a few special considerations. Angle recession
glaucoma is initially treated medically with the
realization that miotics may be ineffective because
of the disruption of the normal ciliary musclescleral spur relationship.[37] There have been reports
that miotics may cause a paradoxical increase in
IOP in patients with angle recession, possibly by
decreasing the uveoscleral outflow.[38] Use of topical
aqueous suppressants in the initial medical treatment
is preferred; these include beta-antagonists, alphaagonists, and carbonic anhydrase inhibitors.[14,24,25]
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.
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.
Atropine has been reported to reduce IOP in angle
recession glaucoma;[39] therefore, cycloplegic
agents may have a role in treatment. 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).
Angle recession glaucoma has a success rate lower
than that of POAG (43% vs. 74%).[14,45] Bleb failure
occurred a mean of 3.1 months after surgery in patients
with angle recession glaucoma compared with
9.4 months in those with POAG.[14] Trabeculectomy
in eyes with angle recession is associated with
decreased post-operative reduction in IOP, increased
rates of bleb fibrosis and bleb failure, and increased
dependence on post-operative medical treatment of
glaucoma.[45] The adjunctive use of antimetabolites,
particularly mitomycin C, can improve the success of
trabeculectomy.
The response to medical therapy in angle recession
glaucoma is variable - The IOP rise that occurs
immediately after blunt trauma to the eye is usually
self-limited and, in the majority of cases, can be
controlled with medication alone.[14,21,23] The late
IOP rise that occurs years after the injury is more
difficult to treat medically and may require surgical
intervention.[14]
Laser treatment
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. IOP elevation may become worse in
response to ALT.[40-43] In eyes with <180° of angle
recession, ALT may be beneficial if applied to only
the trabecular meshwork of the nonrecessed portions
of the anterior chamber angle.[40-43]
Alternative laser procedures – neodymium: Doped
yttrium aluminium garnet laser trabeculopuncture
(YLT) has been used with variable success.
A study demonstrated a 100% failure rate in eyes
with 360° angle recession.[44] Currently, YLT is
Surgical care
Surgical intervention in angle recession glaucoma is
usually indicated when maximally tolerated medical
treatment has failed and when the risk of progressive
visual loss outweighs the estimated risk of the planned
surgical management.
Filtration surgery
Artificial
drainage
devices
(tube
shunt
devices) - Benefits with the implantation of tube
shunt devices have been demonstrated, but outcomes
are reportedly less successful in angle recession
than in other types of refractory glaucoma. A study
showed the superior results of trabeculectomy with
antimetabolite over molteno implantation (78% vs.
69%) in the cases of posttraumatic angle recession
glaucoma, but the difference was not statistically
significant.[46]
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.
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35
Ganekal and Dorairaj: Angle recession glaucoma following blunt trauma
Follow up
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 1st 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
>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.
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. 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.
Special concerns
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.
CONCLUSION
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.
Education on the use of eye, face, or head protection
during high-risk activities may lower the incidence
of ocular injuries. Nonglaucomatous comorbidity in
eyes with angle recession increases the risk of vision
loss. Gonioscopy should always be performed when
a patient with a unilateral cataract is evaluated, even
when his or her history is negative for trauma.
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How to cite this article: Ganekal S, Dorairaj S. Angle
Recession Glaucoma. J Vis Sci 2015;1(2):28-37.
Financial Support: None; Conflict of Interest: None
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37