Signs and Symptoms

Patients with angle recession glaucoma are typically asymptomatic, unless the disease is advanced with profound visual field or fixation loss or intraocular pressure (IOP) that has become extremely elevated. Patients with significantly elevated intraocular pressure often are symptomatic with pain and visual disturbances secondary to corneal decompensation.

Angle recession glaucoma is more common in younger males, though any patient may develop this condition.1-3 There is a history of antecedent blunt trauma to the involved eye, often occurring years earlier. Sports injuries and assault are the most common causes.4-6

In some instances, a history of ocular injury may not be available as the patient may either not remember the precipitating incident or, in the case of abuse or assault, may deny the trauma.6 Other signs of ocular trauma, including corneal scars, Descemet’s membrane tears, corneal pigment, correctopia, iridodialysis, phacodonesis and cataract may be found in association with angle recession glaucoma.7

Hyphema is a very common comorbidity and many cases of angle recession glaucoma are associated with traumatic hyphema at inception.8-11 The vast majority of patients with traumatic hyphema have some degree of angle recession.5 Many traumatic eye injuries produce angle recession without ever developing glaucoma.

The rise in IOP may be substantial. Interestingly, there is often an unexplained IOP rise in 50% of the untraumatized, fellow eyes, often years after trauma.12 This could indicate a predisposition to primary open angle glaucoma and that traumatic angle recession only hastens the process rather than being the inciting agent.12

Gonioscopically, there will be a deepening of the angle recess, revealing a greater appearance of the ciliary body (excessive gray tissue posterior to the scleral spur). In minor recessions, there will be a disruption of the insertion of the iris into the ciliary body and the ciliary body will appear more notably compared with the rest of the angle or the fellow eye. In major recessions, the iris root may be torn away and a cleft may extend into the ciliary body with a more visible scleral spur.7 There may be a line of scleral tissue posterior to the ciliary body in severe cases of recession.

Generally, in angle recession, the ciliary body appears wider and the scleral spur appears whiter than the normal fellow eye.7 There may be areas of peripheral anterior synechiae at the lateral edges of the angle recession, which can obscure the total area that has been recessed. For these reasons, in cases when gonioscopy is deemed necessary, it is always recommended it is performed in both eyes. This allows for assessment of both angles as well as inter-eye comparison.


In angle recession, blunt trauma to the eye forces aqueous laterally and posteriorly within the anterior chamber. This hydrodynamic force produces a tear between the longitudinal and circular muscles of the ciliary body. The longitudinal muscles remain attached to the scleral spur. Frequently, there is hyphema at the time of trauma due to tearing of the anterior and posterior ciliary arteries.2,7 Direct damage to the trabecular meshwork may result in an early rise in IOP.7

In angle recession glaucoma, the trabecular meshwork may be damaged at the time of the trauma that causes angle recession, but often there is not enough functional compromise to cause outflow dysfunction. It isn’t until there is a natural age-related decline in trabecular function that the damage is unmasked with IOP elevation.

While angle recession following blunt ocular trauma is rather common, only approximately 6% of patients will develop glaucoma.3 The likelihood of developing glaucoma is related to the extent that the angle is recessed. Typically, greater than 180° of angle recession will result in glaucoma while less than 180° will not.9,14,15

The presence of hyphema at the time of injury greatly increases the risk of late onset open glaucoma angle either with or without angle recession.2,5,8 The presence of increased trabecular pigmentation, elevated baseline IOP, history of concurrent hyphema, lens displacement and recession of more than 180° of the angle are significantly associated with the occurrence of late traumatic and angle recession glaucoma.16

Minimal recession of the anterior chamber angle can heal without sequelae. With more significant angle recession, degeneration atrophy, fibrosis and scarring of the trabecular meshwork and Schlemm’s canal occur. There can be obliteration of the inter-trabecular spaces and closure of Schlemm’s canal years after injury with hyaline membrane development over the inner trabecular meshwork.7 Initially, there may be no increase in IOP. However, after many years, as the outflow facility naturally decreases, the IOP may begin to rise.

Of course, it must be remembered that this rule does not apply to every patient. The recession of the angle itself does not cause IOP elevation. Rather, widespread damage to the trabecular meshwork at the time of trauma, with the long-term changes the injury provokes seems to be the cause. Hence, the trabecular meshwork is not just damaged in the area of the visible recession, but likely a larger portion has been impaired to some degree. Indeed, blunt trauma with minimal recession of the angle can cause glaucoma due to widespread, though not gonioscopically visible, trabecular damage.


Glaucoma medications that reduce aqueous production, such as beta-blockers, alpha-2 adrenergic agonists and carbonic anhydrase inhibitors, are all very effective.

In that the genesis of glaucoma in angle recession is severe trabecular meshwork dysfunction, miotics typically are ineffective due to the disruption of the ciliary muscle-scleral spur dynamic.13 For this reason, laser trabeculoplasty is likewise ineffective.17-19 Prostaglandin analogs, which increase aqueous outflow through the uveoscleral meshwork, offer an excellent alternative for egress and can be very effective in IOP reduction.7

In cases of recent trauma involving angle recession, vitreous hemorrhage and severe IOP elevation, combined trabeculectomy and vitrectomy is a viable surgical option with no incidence of recurrent vitreous hemorrhage or retinal detachment in one study, though these complications are certainly possible.20 Overall as a sole surgery, trabeculectomy demonstrates a lower success rate in angle recession glaucoma compared to primary open angle glaucoma. Bleb fibrosis forms earlier and more significantly in cases with angle recession.21 For this reason, the use of antifibrolytic agents are desirable in conjunction with trabeculectomy.22

Clinical Pearls

In cases of apparent unilateral or asymmetric glaucoma, a history of antecedent trauma should be sought.

It can be difficult to identify a recessed angle. When performing gonioscopy, it is usually necessary to compare two sections of the angle in one eye or, occasionally, switch from eye to eye repeatedly to identify subtle recessions. If there is 360° of angle recession, comparison with the fellow eye is necessary. By examining only the suspect eye, the diagnosis can be elusive.

IOP level in angle recession glaucoma can be quite dramatic. We have seen IOP exceed 70mm Hg.

We have seen exceptional responses to prostaglandin analogs in patients with angle recession glaucoma.

Due to the potential for IOP to rise years after trauma, patients with angle recession must be followed closely for their entire lives.

Angle recession glaucoma may be an antiquated term. Early traumatic glaucoma can occur from microhyphema or angle structure damage without recession. More accurate and descriptive would be the term late-onset traumatic glaucoma with angle recession.

Gonioscopy is never indicated immediately after blunt trauma. Late traumatic glaucoma and angle recession glaucoma typically occur months to years following the injury. Gonioscopy at the time of the injury adds to the patient’s discomfort, has the potential to dislodge a clotted hyphema causing bleeding and serves no purpose toward the rendering of acute management. The examination can be completed after the sequelae of the blunt force injury have resolved.

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8. Girkin CA, McGwin G Jr, Long C, et al. Glaucoma after ocular contusion: a cohort study of the United States Eye Injury Registry. J Glaucoma. 2005;14(6):470-3.

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13. Pilger IS, Khwarg SG. Angle recession glaucoma: review and two case reports. Ann Ophthalmol. 1985;17(3):197-9.

14. Charfi Ben Ammar O, Chaker N, Soukah M, et al. Posttraumatic glaucoma. J Fr Ophtalmol. 2002;25(2):126-9.

15. Sihota R, Sood NN, Agarwal HC. Traumatic glaucoma. Acta Ophthalmol Scand. 1995;73(3):252-4.

16. 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. 2008;126(7):921-6.

17. Goldberg I. Argon laser trabeculoplasty and the open-angle glaucomas. Aust N Z J Ophthalmol. 1985;13(3):243-8.

18. Lieberman MF, Hoskins HD Jr, Hetherington J Jr. Laser trabeculoplasty and the glaucomas. Ophthalmology. 1983;90(7):790-5.

19. Robin AL, Pollack IP. Argon laser trabeculoplasty in secondary forms of open-angle glaucoma. Arch Ophthalmol. 1983;101(3):382-4.

20. Wang XY, Hu RR, Shen LP, et al. Combined trabeculectomy and vitrectomy for intractable glaucoma with severe ocular contusion involving the posterior segment. Chin Med J (Engl). 2011;124(15):2316-20.

21. Mermoud A, Salmon JF, Straker C, et al. Post-traumatic angle recession glaucoma: a risk factor for bleb failure after trabeculectomy. Br J Ophthalmol. 1993;77(10):631-4.

22. Manners T, Salmon JF, Barron A, et al. Trabeculectomy with mitomycin C in the treatment of post-traumatic angle recession glaucoma. Br J Ophthalmol. 2001;85(2):159-63.