angle recession article

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Angle Recession Glaucoma

Joseph Anthony J. Tumbocon, M.D.

Mark A. Latina, M.D.

Recession of the anterior chamber angle is a common finding afternonpenetrating ocular trauma. A small percentage of eyes with this injuryeventually develop secondary glaucoma, often occurring years after theinitial injury. It is desirable to identify individuals at risk of developingangle recession glaucoma so that appropriate follow-up examinations andtreatment can be done at an early stage, long before the vision becomesseriously 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 thecircular and longitudinal ciliary muscles in 2 eyes enucleated after non-penetrating trauma (Fig 1). The iris, the lens, and the circular fibers

moved posteriorly, rendering the anterior chamber wider and deeper. In1949, DOmbrain2 drew attention to trauma as a cause of unilateralchronic glaucoma; however, no gonioscopic or pathological correlation

was mentioned in this study. It was not until 1962 that Wolff and Zimmer-mann3 pointed out the clinical association among trauma, angle reces-sion, and glaucoma. These authors reported the presence of monocularglaucoma in 6 patients who had histories of blunt trauma to the eye withgonioscopic evidence of angle recession. In addition, they described thepathological findings of angle recession in enucleated eyes of patients

with a previous history of ocular contusion. Since then, numerous inves-tigators have studied the epidemiological, clinical, and histopathologicalfindings of this disease entity.

Epidemiology

In a Baltimore population-based survey of persons aged 40 years orolder, the cumulative lifetime prevalence of blunt ocular trauma was es-

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timated to be 52.7 per 1,000 individuals. However, the prevalence ofposttraumatic angle recession was not available, as gonioscopy was notroutinely performed in this study.4

Other investigators have reported that more than 60% of eyes withnonpenetrating traumatic injuries will have some degree of angle reces-sion.59 Although traumatic angle recessions may occur without anteriorchamber hemorrhage, a strong correlation between hyphema and anglerecession has been established. Careful gonioscopy has revealed that be-tween 56% and 100% of patients with traumatic hyphema have somedegree of angle recession (Table 1).510

The most frequent cause of injury-inducing angle recession occurredas 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 of87) in the series of Mermoud and coworkers.12 Less common causes wereautomobile or industrial accidents, projectiles from toy guns or slingshots,and other leisure activities.1216 A small percentage of people will denyany previous episode of ocular trauma despite the presence of obviouseyelid scars and pupillary sphincter tears.12

Figure 1. Schematic drawing of angle recession. (Courtesy of Ms. Julie Kenny.)

Table 1. Presence of Angle Recession in Patients with Traumatic Hyphema

No. of Patients Presentingwith Hyphema

No. (%) of Patients withAngle Recession

Blanton5 182 130 (71)

Tomjun6 160 160 (100)

Kaufman and Tolpin7

50 47 (94)Filipe et al.10 45 25 (56)

Spaeth8 43 26 (60)

Herschler9 17 17 (100)

Total 497 405 (81)

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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 involv-ing 31 eyes with angle recession, they observed that 6% of the patientsdeveloped glaucoma. Similarly, Blanton5 found 9 individuals (7%) withuniocular glaucoma in his review of 130 cases of angle recession. Fivereceived diagnoses within 3 years after injury, and the remaining 4 pa-tients developed glaucoma more than 10 years after the injury. Thereappear to be two peak incidences of glaucoma after angle recession. Thefirst peak occurs within the first few weeks to years after the trauma, andthe 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 hadunilateral glaucoma. Eight received diagnoses within 4 years after theinjury, and the remaining 6 had diagnoses more than 14 years after the

original trauma. Some investigators have even reported cases of anglerecession glaucoma developing more than 50 years after the initial in-

jury.8,17

There is also an association between the extent of angle recession andthe development of glaucoma. Tonjum6 found a significant correlationbetween the extent of angle recession and decrease in the outflow facilityin the injured eyes. Alper17 observed that 13 of 14 patients with anglerecession glaucoma in his study had angle recessions extending approxi-mately 240 degrees or greater, whereas the remaining case had 150 de-grees of recession. Likewise, Blanton5 found that all his angle recessionglaucoma cases that developed 10 years after injury had more than 180degrees of recession. It appears that those eyes with less than 180 degreesof recession are unlikely to develop glaucoma,7,18whereas most investiga-

tors agree that patients with 180 to 360 degrees of angle recession willhave a greater risk of developing late-occurring glaucoma.3,5,6,1720

In eyes that do develop angle recession glaucoma, the contralateralnontraumatized eye has been reported to have a 50% chance of develop-ing open-angle glaucoma, sometimes years after the pressure rise wasnoted in the traumatized eye.21 After topical corticosteroid provocativetesting, the fellow eye has also been observed to respond in a mannersimilar to that in eyes with primary open-angle glaucoma.8 The results ofthe aforementioned studies bring into play some possible theories withregard to the relationship of angle recession and open-angle glaucoma. Itmay indicate that the angle recession itself is probably not the cause of

Table 2. Incidence of Glaucoma in Patients with Angle RecessionNo. of

Patients DurationPatients

Developing Glaucoma (%)

Blanton3 130 10 years (retrospective) 7

Kaufman7 31 10 years (prospective) 6

Angle Recession Glaucoma 71


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elevated intraocular pressure but, rather, that it may accelerate the ap-

pearance of glaucoma in patients who are already predisposed to developprimary open-angle glaucoma.3,6 This predisposition may render an eyemore susceptible to developing an increase in intraocular pressure aftertraumatic angle recession due to some genetically determined structuralor functional abnormality in the aqueous outflow pathway of the eye.9

Alternatively, it is also conceivable that angle recession, through some yetunknown feedback mechanism, may alter neural factors that affect intra-ocular pressure in both eyes.8

Clinical Presentation

The diagnosis of angle recession is made by patient history and clini-

cal examination. In cases of unilateral glaucoma or traumatic hyphema orafter blunt trauma, angle recession should always be considered.5,7,9,22,23

Slit-lamp gonioscopy with indirect gonioscopy lenses (e.g., Zeiss orGoldman lenses) provides a detailed view of the angle structures withgood magnification.8 However, the examiner must be willing to switch thelenses from eye to eye several times to detect subtle changes in the angleanatomy. With milder injuries, the examiner may have to compare thegonioscopic appearance of both eyes simultaneously with a Koeppe lensor compare two parts of the angle of 1 eye to identify subtle changes in theinjured angle.8 The appearance varies greatly, depending on the degreeand extent of the recession and on the particular eye.24 Minor angledamage can be recognized as a disruption of the regular pattern of inser-tion 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 withthe angle of the opposite eye.18 Small tufts of uveal tissue may be observedbunching up on the iris root and on the trabeculum above the scleralspur.17 The more difficult cases are those in which there is a question ofa 360-degree recession, and comparison between the two eyes is especiallyhelpful in these cases.5,8Alternatively, the recession may be limited to onesmall area, and careful gonioscopy should be performed to detect subtlechanges in the anterior chamber angle.5 The combination of localizeddeepening with change in color and texture of the angle provides a valu-able clue to the presence of recession.3,6

Signs of trauma should be sought: corneal scars, tears in the Desce-mets membrane, pigmentary deposits, a space between the iris and thelens that is wider in one segment of the pupil than elsewhere, ruptures ofthe 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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3). The light gray portion of the ciliary band appears broadened, and thescleral spur is more distinctly prominent.18,24 Small peripheral anteriorareas of synechiae frequently appear at the lateral limits of an angle re-cession and may extend into the peripheral areas of the recession. Thismay hide areas in the angle that were previously recessed.7,9 Patients withsignificant angle recession should be advised to have annual eye exami-nations for an indefinite period to detect late-occurring glaucoma.18

A classification of angle recession with regard to the depth of ciliarymuscle tears has been proposed by Howard and coworkers.24 In shallowtears,separation of the processes of the uveal meshwork is present so thatthe ciliary body band and the scleral spur are more plainly visible than thefellow eye. The separation of the processes may leave pigmented tags onthe 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 spurappears whiter than does the opposite eye. In shallow tears, no actual cleftinto the face of the ciliary body is present.

Figure 2. Gonioscopicphotograph of angle recession witha deep ciliary body cleft thatextends into the ciliary body.

Figure 3. Gonioscopic photograph and schematic diagram of angle recession.



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Moderate tearsare characterized by a definite cleft into the fibers of the

ciliary muscle, and the angle appears deeper than that of the opposite eye.Deep tearsare characterized by a fissure in the ciliary body, and the apex ofthe fissure cannot be seen gonioscopically.

Ultrasonographic biomicrosopy can also be used to detect the pres-ence of moderate to severe angle recession when visualization of the anglestructures is limited owing to some form of corneal opacity or associatedinjury.25

An angle anomaly that may be confused with angle recession is cyclo-dialysis, in which a sector of the ciliary body is detached from the sclera.The cleft or separation occurs between the longitudinal muscle of theciliary body and the sclera itself. In contrast, the cleft in angle recessionoccurs between the circular and longitudinal muscles of the ciliarybody.22,23 Cyclodialysis can be clinically recognized by the presence of an

area of white sclera visible posterior to the scleral spur (Fig 4). Otherdifferential diagnoses for angle recession include iridodialysis, trabeculartears, and angle abnormalities secondary to previous ocular surgery.23

Other causes of unilateral or asymmetrical glaucoma should also be ruledout (e.g., uveitis, anterior segment tumors, lens-induced glaucoma, pseu-doexfoliation glaucoma, and glaucoma secondary to elevated episcleral

venous pressure).26 These other conditions can be clinically differentiatedfrom angle recession after a complete ocular examination and review ofthe patients medical and ocular history.

Mechanism

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

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



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body cleft, and the second is the pathogenesis of the elevated intraocular

pressure (IOP) seen in this disease entity. It should be emphasized thatthe presence of a ciliary body tear is only an indicator of previous oculartrauma and is not the cause of the subsequent glaucoma.3,9

Blunt trauma to the eye forces the aqueous laterally and posteriorlyagainst the iris. This hydrodynamic force exerts traction on the iris rootand can produce a tear between the longitudinal and the circular musclesof the ciliary body (see Fig 4).3,11,24 The longitudinal muscles of the ciliarybody characteristically remain attached to the scleral spur.3 The tear maydisrupt the branches of the anterior and posterior ciliary arteries, result-ing in bleeding into the anterior chamber.24 The same hydrostatic forcecan also directly damage the trabecular meshwork and lead to an earlyincrease in intraocular pressure.6,9 In addition, the presence of anglerecession can disrupt the tension exerted by the ciliary muscles on the

scleral spur and trabecular meshwork, which may further compromiseaqueous drainage.9

If there is only minimal recession of the angle, the cleft often healswith little or no scarring.3 In the presence of more significant injury,advanced degeneration, atrophy, fibrosis, and scarring of the trabecularmeshwork and Schlemms canal may occur years after the initialtrauma.3,9,27 Variable obliteration of the intertrabecular spaces andSchlemms canal accompanied by atrophy of the inner circular muscles ofthe ciliary body is a common finding.3,9,27 In addition, a hyaline mem-brane may be present on the inner trabecular meshwork.3,27 With thereduction in aqueous drainage brought about by the aforementionedevents, the IOP can rise with time as the outflow facility gradually de-creases with increasing age.5

Treatment

Angle recession glaucoma is initially treated medically with the real-ization that miotics may be ineffective because of the disruption of thenormal ciliary musclescleral spur relationship.19 There have been reportsthat miotics may cause a paradoxical increase in intraocular pressure inpatients with angle recession, possibly by decreasing the uveoscleral out-flow.28 Glaucoma medications that decrease aqueous formation, such asbeta blockers, carbonic anhydrase inhibitors, or alpha2-agonists, may beuseful.12,22,23 Prostaglandin analogs, which are claimed to increase uveo-scleral outflow, may also be of benefit. The IOP rise that occurs immedi-ately after blunt trauma to the eye is usually self-limited and, in the ma-

jority of cases, can be controlled with medication alone.5,12,17,18 The lateIOP rise that occurs years after the injury is more difficult to treat medi-cally 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.12,29,30Argon

laser trabeculoplasty is usually unsatisfactory and fails to lower the IOP inthis group of patients.3134 Trabeculectomy has also been reported to havea lower success rate in eyes with angle recession glaucoma (43%) as com-pared to eyes in patients with open-angle glaucoma (74%).29 The adjunc-tive use of antimetabolites (e.g., mitomycin-C or 5-fluorouracil) in trabec-ulectomy appears to increase the success rate of this procedure.12

Glaucoma drainage implants for angle recession glaucoma have beenused with relative success, especially in eyes that underwent a previousfiltering procedure that failed.30 Mermoud and associates12 observed thattrabeculectomy with antimetabolites was more effective as a first surgicalprocedure and that single-plate Molteno implantation was more useful asa 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 fibrosisdevelops earlier after trabeculectomy, and additional medical or surgicaltherapy may be required.29,30 It has been suggested that an increasedtendency for fibroblast proliferation or a change in the aqueous humorproperties (or both) in eyes damaged by trauma may be responsible forthe decrease in the success rate of glaucoma surgery.3,29,35 This could besecondary to the presence of stimulatory growth factors or the absence offibroblast growth inhibitory factors in the aqueous of these eyes.23,35

In summary, angle recession should be suspected in patients present-ing with traumatic hyphema or after blunt trauma to the eye. Carefulevaluation of the angle structures should be performed to identify thegroup of patients who are at a higher risk in developing late-onset glau-coma. The mechanism of IOP elevation has been postulated to be the

result of trabecular meshwork injury from the original trauma, with theconsequent scarring and related changes that ensue, in combination withan underlying predisposition for the development of primary open-angleglaucoma and the passage of time. It should be kept in mind that eyes withangle recession glaucoma are more refractory to medical or surgical in-tervention as compared to those in patients with open-angle glaucoma.Thus, the therapeutic strategy should be adjusted accordingly for effectivecontrol of the progression of this disease entity.

References

1. Collins ET. On the pathological examination of three eyes lost from concussion. Trans

Ophthalmol Soc UK 1892;12:1801862. DOmbrain. Traumatic or concussion chronic glaucoma. Br J Ophthalmol 1949;33:

395400

3. Wolff SM, Zimmermann LE. Chronic secondary glaucoma associated with retrodis-placement of the iris root and deepening of anterior chamber angle secondary tocontusion. Am J Ophthalmol 1962;54:547563



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4. Katz J, Tielsch JM. Lifetime prevalence of ocular injuries from the Baltimore EyeSurvey. Arch Ophthalmol 1993:111(11):15641568

5. Blanton FM. Anterior chamber angle recession and secondary glaucoma: a study of theafter effects of traumatic hyphemas. Arch Ophthalmol 1964;72:39 44

6. Tonjum AM. Intraocular pressure and facility of outflow late after ocular contusion.Acta Ophthalmol 1968;46:886908

7. Kaufman J, Tolpin D. Glaucoma after traumatic angle recession. Am J Ophthalmol1974;78:648654

8. Spaeth GL. Traumatic hyphema, angle recession, dexamethasone hypertension, andglaucoma. Arch Ophthalmol 1967;78:714721

9. Herschler J. Trabecular damage due to blunt anterior segment injury and its relation-ship to traumatic glaucoma. Trans Am Acad Ophthalmol Otolaryngol 1977;83:239

10. Filipe JA, Barros H, Castro-Correia J. Sports-related ocular injuries. A three-year follow-up study. Ophthalmology 1997;104(2):313318

11. Canavan YM, Archer DB. Anterior segment consequences of blunt ocular injury.Br J Ophthalmol 1982;66:549555

12. Mermoud A, Salmon JF, Barron A, et al. Surgical management of post-traumatic glau-

coma. Ophthalmology 1993;100:63464213. Chorich LJ 3rd, Davidorf FH, Chambers RB, et al. Bungee cordassociated ocular

injuries. Am J Ophthalmol 1998;125(2):27027214. Michaeli-Cohen A, Neufeld M, Lazar M. Bilateral corneal contusion and angle reces-

sion caused by an airbag. Br J Ophthalmol 1996;80(5):48715. Farr AK, Fekrat S. Eye injuries associated with paintball guns. Int Ophthalmol 1998

99;22(3):16917316. Bullock JD, Ballal DR, Johnson DA, et al. Ocular and orbital trauma from water balloon

slingshots. A clinical, epidemiologic, and experimental study. Ophthalmology 1997;104(5):878887

17. Alper MG. Contusion angle deformity and glaucoma. Arch Ophthalmol 1963;69:455467

18. Mooney D. Anterior chamber tears after non-perforating injury. Br J Ophthalmol 1972;56:418424

19. Pilger IS, Khwarg SG. Angle recession glaucoma: review and two case reports. Ann

Ophthalmol 1985;17:19719920. Sihota R, Sood NN, Agarwal HC. Traumatic glaucoma. Acta Ophthalmol Scand 1995;

73(3):25225421. Tesluk GC, Spaeth GL. The occurrence of primary open angle glaucoma in the fellow

eye of patients with unilateral angle-cleavage glaucoma. Ophthalmology 1985;92(7):904911

22. Hoskins HD, Kass MA. Becker Shaffers diagnosis and therapy of glaucoma, ed 6. St.Louis: Mosby, 1989:324327

23. Herschler J, Cobo M. Trauma and elevated intraocular pressure. In: Ritch R, ShieldsMB, Krupin T, eds. The glaucomas. St. Louis: Mosby, 1989:12281232

24. Howard GM, Hutchinson BT, Frederick AR. Hyphema resulting from blunt oculartrauma: gonioscopic, tonographic and ophthalmoscopic observations following resolu-tion of hemorrhage. Trans Am Acad Ophthalmol Otolaryngol 1965;69:294305

25. Berinstein DM, Gentile RC, Sidoti PA. Ultrasound biomicroscopy in anterior oculartrauma. Ophthalmic Surg Lasers 1997;28(3):201207

26. Miles D, Boniuk M. Pathogenesis of unilateral glaucoma. Am J Ophthalmol 1966;62:493499

27. Jensen OA. Contusion angle recession, a histopathological study of a Danish material.Acta Ophthalmol 1968;46:12071212

28. Bleiman BS, Schwartz AL. Paradoxical intraocular pressure response to pilocarpine:a proposed mechanism and treatment. Arch Ophthalmol 1979;97:13051306



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29. Mermoud A, Salmon JF, Straker C, et al. Post-traumatic angle recession glaucoma riskfactor for bleb failure after trabeculectomy. Br J Ophthalmol 1993;77:651654

30. Mermoud A, Salmon JF, Straker C, et al. Use of single plate molteno implant forrefractory glaucoma. Ophthalmologica 1992;205:113120

31. Thomas JV, Simmons RJ, Belcher CD III. Argon laser trabeculoplasty in the presurgicalglaucoma patient. Ophthalmology 1982;89:187191

32. Goldberg I. Argon laser trabeculoplasty and the open-angle glaucomas. Aust N Z JOphthalmol 1985;13(3):243248

33. Robin AL, Pollack IP. Argon laser trabeculoplasty in secondary form of open angleglaucoma. Arch Ophthalmol 1983;101:382384

34. Leiberman MF, Hoskins HD, Herrington J. Laser trabeculoplasty and the glaucomas.Ophthalmology 1983;90:790795

35. Joseph JP, Miller MH, Hitchings RA. Wound healing as a barrier to successful filtrationsurgery. Eye 1988;2:S113S123


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