Angle Recession Glaucoma 

  • Author: Brian R Sullivan, MD; Chief Editor: Hampton Roy Sr, MD   more...
 
Updated: Apr 18, 2012
 

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 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.

Next

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. Ballistic experiments using porcine eyes have demonstrated relatively low energy impact thresholds of 3.5-7.0 joules resulting in moderate-to-severe angle recession.[4]

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 displacAngle 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.

Previous
Next

Epidemiology

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,[5] 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.[6, 7, 5, 8]

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.[9] In 1990, the estimated hospitalization rate with ocular trauma was 15.2 cases per 100,000 children per year.[10]

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%).[11, 12, 13, 14, 15, 16, 17] 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.[18] 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%.[19] 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%.[20] 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.[21] A 1996 report described a predominance of home injuries in Scotland.[22]

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%.[23]

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.[24]
  • 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.[25]
  • 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.
Previous
 
 
Contributor Information and Disclosures
Author

Brian R Sullivan, MD  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.

Specialty Editor Board

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.

Simon K Law, MD, PharmD  Associate Professor of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine

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.

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: Nothing to disclose.

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.

Additional Contributors

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.

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. Sponsel WE, Gray W, Scribbick FW, Stern AR, Weiss CE, Groth SL, et al. Blunt eye trauma: empirical histopathologic paintball impact thresholds in fresh mounted porcine eyes. Invest Ophthalmol Vis Sci. Jul 2011;52(8):5157-66. [Medline].

  5. 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].

  6. 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].

  7. 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].

  8. Mowatt L, Chambers C. Ocular morbidity of traumatic hyphema in a Jamaican hospital. Eur J Ophthalmol. May-Jun 2010;20(3):584-9. [Medline].

  9. Glynn RJ, Seddon JM, Berlin BM. The incidence of eye injuries in New England adults. Arch Ophthalmol. Jun 1988;106(6):785-9. [Medline].

  10. 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].

  11. Chorich LJ 3rd, Davidorf FH, Chambers RB, Weber PA. Bungee cord-associated ocular injuries. Am J Ophthalmol. Feb 1998;125(2):270-2. [Medline].

  12. 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].

  13. 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].

  14. 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].

  15. 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].

  16. 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].

  17. Vize CJ, Gauba V, Atkinson PL. Eye injury as a result of coat toggle trauma. Eye. Jan 2007;21(1):94-5. [Medline].

  18. Giovinazzo VJ, Yannuzzi LA, Sorenson JA, Delrowe DJ, Cambell EA. The ocular complications of boxing. Ophthalmology. Jun 1987;94(6):587-96. [Medline].

  19. McCarty CA, Fu CL, Taylor HR. Epidemiology of ocular trauma in Australia. Ophthalmology. Sep 1999;106(9):1847-52. [Medline].

  20. Nwosu SN. Domestic ocular and adnexal injuries in Nigerians. West Afr J Med. Jul-Sep 1995;14(3):137-40. [Medline].

  21. 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].

  22. 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].

  23. 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].

  24. Poon A, McCluskey PJ, Hill DA. Eye injuries in patients with major trauma. J Trauma. Mar 1999;46(3):494-9. [Medline].

  25. 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].

  26. 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].

  27. Ozdal MP, Mansour M, Deschênes J. Ultrasound biomicroscopic evaluation of the traumatized eyes. Eye. May 2003;17(4):467-72. [Medline].

  28. 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].

  29. Berinstein DM, Gentile RC, Sidoti PA, et al. Ultrasound biomicroscopy in anterior ocular trauma. Ophthalmic Surg Lasers. Mar 1997;28(3):201-7. [Medline].

  30. 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].

  31. 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].

  32. 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].

  33. 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].

  34. 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].

  35. de Klerk TA, Au L. I-stent for treatment of angle recession with raised intraocular pressure. Clin Experiment Ophthalmol. Nov 2 2011;[Medline].

  36. 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].

  37. Canavan YM, Archer DB. Anterior segment consequences of blunt ocular injury. Br J Ophthalmol. Sep 1982;66(9):549-55. [Medline].

  38. 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].

Previous
Next
 
Irregular widening of the visible ciliary body in a quadrant with angle recession.
Angle recession. Note the marked posterior displacement of the iris, with a wide ciliary body band posterior to the scleral spur.
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.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2012 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.