Angle Recession Glaucoma

Joseph Anthony J. Tumbocon, M.D.

Mark A. Latina, M.D.

Recession of the anterior chamber angle is a common finding after

nonpenetrating ocular trauma. A small percentage of eyes with this injury
eventually develop secondary glaucoma, often occurring years after the
initial injury. 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.
The first description of angle recession was made by Collins1 in 1892.
He observed the presence of a split in the ciliary body separating the
circular and longitudinal ciliary muscles in 2 eyes enucleated after nonpenetrating trauma (Fig 1). The iris, the lens, and the circular fibers
moved posteriorly, rendering the anterior chamber wider and deeper. In
1949, DOmbrain2 drew attention to trauma as a cause of unilateral
chronic glaucoma; however, no gonioscopic or pathological correlation
was mentioned in this study. It was not until 1962 that Wolff and Zimmermann3 pointed out the clinical association among trauma, angle recession, and glaucoma. These authors 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. Since then, numerous investigators have studied the epidemiological, clinical, and histopathological
findings of this disease entity.

Epidemiology
In a Baltimore population-based survey of persons aged 40 years or
older, the cumulative lifetime prevalence of blunt ocular trauma was es69

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Figure 1.

Schematic drawing of angle recession. (Courtesy of Ms. Julie Kenny.)

timated to be 52.7 per 1,000 individuals. However, the prevalence of

posttraumatic angle recession was not available, as gonioscopy was not
routinely performed in this study.4
Other investigators have reported that more than 60% of eyes with
nonpenetrating traumatic injuries will have some degree of angle recession.59 Although traumatic angle recessions may occur without anterior
chamber hemorrhage, 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 have some
degree of angle recession (Table 1).510
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 Archer11 and as a result of assault (65%; 57 of
87) in the series of Mermoud and coworkers.12 Less common causes were
automobile or industrial accidents, projectiles from toy guns or slingshots,
and other leisure activities.1216 A small percentage of people will deny
any previous episode of ocular trauma despite the presence of obvious
eyelid scars and pupillary sphincter tears.12
Table 1. Presence of Angle Recession in Patients with Traumatic Hyphema

Blanton5
Tomjun6
Kaufman and Tolpin7
Filipe et al.10
Spaeth8
Herschler9
Total

No. of Patients Presenting

with Hyphema

No. (%) of Patients with

Angle Recession

182
160
50
45
43
17
497

130 (71)
160 (100)
47 (94)
25 (56)
26 (60)
17 (100)
405 (81)

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71

Although recession of the iridocorneal angle is common after blunt

trauma, only 6%7 to 7%5 of these eyes will eventually develop glaucoma
(Table 2). In a 10-year prospective study by Kaufman and Tolpin7 involving 31 eyes with angle recession, they observed that 6% of the patients
developed glaucoma. Similarly, Blanton5 found 9 individuals (7%) with
uniocular glaucoma in his review of 130 cases of angle recession. Five
received diagnoses 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.5,17,18 Alper17
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 6 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.8,17
There is also an association between the extent of angle recession and
the development of glaucoma. Tonjum6 found a significant correlation
between the extent of angle recession and decrease in the outflow facility
in the injured eyes. Alper17 observed that 13 of 14 patients with angle
recession glaucoma in his study had angle recessions extending approximately 240 degrees or greater, whereas the remaining case had 150 degrees of recession. Likewise, Blanton5 found that all his angle recession
glaucoma cases that developed 10 years after injury had more than 180
degrees of recession. It appears that those eyes with less than 180 degrees
of recession are unlikely to develop glaucoma,7,18 whereas most investigators agree that patients with 180 to 360 degrees of angle recession will
have a greater risk of developing late-occurring glaucoma.3,5,6,1720
In eyes that do develop angle recession glaucoma, the contralateral
nontraumatized eye has been reported to have a 50% chance of developing open-angle glaucoma, sometimes years after the pressure rise was
noted in the traumatized eye.21 After topical corticosteroid provocative
testing, the fellow eye has also been observed to respond in a manner
similar to that in eyes with primary open-angle glaucoma.8 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
Table 2. Incidence of Glaucoma in Patients with Angle Recession

Blanton3
Kaufman7

No. of
Patients

Duration

Patients
Developing Glaucoma (%)

130
31

10 years (retrospective)
10 years (prospective)

7
6

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elevated intraocular pressure but, rather, that it may accelerate the appearance of glaucoma in patients who are already predisposed to develop
primary open-angle glaucoma.3,6 This predisposition may render an eye
more susceptible to developing an increase in intraocular pressure after
traumatic angle recession due to some genetically determined structural
or functional abnormality in the aqueous outflow pathway of the eye.9
Alternatively, it is also conceivable that angle recession, through some yet
unknown feedback mechanism, may alter neural factors that affect intraocular pressure in both eyes.8

Clinical Presentation
The diagnosis of angle recession is made by patient history and clinical examination. In cases of unilateral glaucoma or traumatic hyphema or
after blunt trauma, angle recession should always be considered.5,7,9,22,23
Slit-lamp gonioscopy with indirect gonioscopy lenses (e.g., Zeiss or
Goldman lenses) provides a detailed view of the angle structures with
good magnification.8 However, the examiner must be willing to switch the
lenses from eye to eye several times to detect subtle changes in the angle
anatomy. 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.8 The appearance varies greatly, depending on the degree
and extent of the recession and on the particular eye.24 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.5 This leaves the
ciliary body bare in comparison with other quadrants of the angle or with
the angle of the opposite eye.18 Small tufts of uveal tissue may be observed
bunching up on the iris root and on the trabeculum above the scleral
spur.17 The more difficult cases are those in which there is a question of
a 360-degree recession, and comparison between the two eyes is especially
helpful in these cases.5,8 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.5 The combination of localized
deepening with change in color and texture of the angle provides a valuable clue to the presence of recession.3,6
Signs of trauma should be sought: corneal scars, tears in the Descemets 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 processes, phacodenesis,
localized opacities or dislocation of the lens, old vitreous hemorrhage,
retinal or choroidal atrophy, pigmentation, or tears.8
In more severe injuries, the cleft extends into the ciliary body (Figs. 2,

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73

Figure 2. Gonioscopic
photograph of angle recession with
a deep ciliary body cleft that
extends into the ciliary body.

3). The light gray portion of the ciliary band appears broadened, and the
scleral spur is more distinctly prominent.18,24 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.7,9 Patients with
significant angle recession should be advised to have annual eye examinations for an indefinite period to detect late-occurring glaucoma.18
A classification of angle recession with regard to the depth of ciliary
muscle tears has been proposed by Howard and coworkers.24 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.

Figure 3.

Gonioscopic photograph and schematic diagram of angle recession.

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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.
Ultrasonographic biomicrosopy 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.25
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.22,23 Cyclodialysis can be clinically recognized by the presence of an
area of white sclera visible posterior to the scleral spur (Fig 4). Other
differential diagnoses for angle recession include iridodialysis, trabecular
tears, and angle abnormalities secondary to previous ocular surgery.23
Other causes of unilateral or asymmetrical glaucoma should also be ruled
out (e.g., uveitis, anterior segment tumors, lens-induced glaucoma, pseudoexfoliation glaucoma, and glaucoma secondary to elevated episcleral
venous pressure).26 These other conditions can be clinically differentiated
from angle recession after a complete ocular examination and review of
the patients medical and ocular history.

Mechanism
There are two related mechanisms that require discussion in angle
recession glaucoma. The first is the physical force that produces the ciliary

Figure 4. Gonioscopic photographs of cyclodialysis (A) and angle recession (B). The cyclodialysis
cleft can be recognized as an area of white sclera posterior to the scleral spur (arrow).

Angle Recession Glaucoma

75

body cleft, and the second is the pathogenesis of the elevated intraocular
pressure (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 the subsequent glaucoma.3,9
Blunt trauma to the eye forces the aqueous laterally and posteriorly
against the iris. This hydrodynamic force exerts traction on the iris root
and can produce a tear between the longitudinal and the circular muscles
of the ciliary body (see Fig 4).3,11,24 The longitudinal muscles of the ciliary
body characteristically remain attached to the scleral spur.3 The tear may
disrupt the branches of the anterior and posterior ciliary arteries, resulting in bleeding into the anterior chamber.24 The same hydrostatic force
can also directly damage the trabecular meshwork and lead to an early
increase in intraocular pressure.6,9 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.9
If there is only minimal recession of the angle, the cleft often heals
with little or no scarring.3 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.3,9,27 Variable obliteration of the intertrabecular spaces and
Schlemms canal accompanied by atrophy of the inner circular muscles of
the ciliary body is a common finding.3,9,27 In addition, a hyaline membrane may be present on the inner trabecular meshwork.3,27 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.5

Treatment
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.19 There have been reports
that miotics may cause a paradoxical increase in intraocular pressure in
patients with angle recession, possibly by decreasing the uveoscleral outflow.28 Glaucoma medications that decrease aqueous formation, such as
beta blockers, carbonic anhydrase inhibitors, or alpha2-agonists, may be
useful.12,22,23 Prostaglandin analogs, which are claimed to increase uveoscleral outflow, may also be of benefit. 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.5,12,17,18 The late
IOP rise that occurs years after the injury is more difficult to treat medically and may require surgical intervention.12
Surgical management of eyes with angle recession glaucoma is more

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challenging than that in patients with open-angle glaucoma.12,29,30 Argon

laser trabeculoplasty is usually unsatisfactory and fails to lower the IOP in
this group of patients.3134 Trabeculectomy has also been reported to have
a lower success rate in eyes with angle recession glaucoma (43%) as compared to eyes in patients with open-angle glaucoma (74%).29 The adjunctive use of antimetabolites (e.g., mitomycin-C or 5-fluorouracil) in trabeculectomy appears to increase the success rate of this procedure.12
Glaucoma drainage implants for angle recession glaucoma have been
used with relative success, especially in eyes that underwent a previous
filtering procedure that failed.30 Mermoud and associates12 observed that
trabeculectomy with antimetabolites was more effective as a first surgical
procedure and that single-plate Molteno implantation was more useful as
a secondary procedure in patients with angle recession glaucoma.
It must be recognized that eyes with traumatic angle recession have an
increased risk of failure after incisional glaucoma surgery. Bleb fibrosis
develops earlier after trabeculectomy, and additional medical or surgical
therapy may be required.29,30 It has been suggested that an increased
tendency for fibroblast proliferation or a change in the aqueous humor
properties (or both) in eyes damaged by trauma may be responsible for
the decrease in the success rate of glaucoma surgery.3,29,35 This could be
secondary to the presence of stimulatory growth factors or the absence of
fibroblast growth inhibitory factors in the aqueous of these eyes.23,35
In summary, angle recession should be suspected in patients presenting with traumatic hyphema or after blunt trauma to the eye. Careful
evaluation of the angle structures should be performed to identify the
group of patients who are at a higher risk in developing late-onset glaucoma. The mechanism of IOP elevation has been postulated to be the
result of trabecular meshwork injury from the original trauma, with the
consequent scarring and related changes that ensue, in combination with
an underlying predisposition for the development of primary open-angle
glaucoma and the passage of time. It should be kept in mind that eyes with
angle recession glaucoma are more refractory to medical or surgical intervention as compared to those in patients with open-angle glaucoma.
Thus, the therapeutic strategy should be adjusted accordingly for effective
control of the progression of this disease entity.

References
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77

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