Angle-Recession Glaucoma Workup

Updated: Nov 02, 2021
  • Author: Frank X Cao, MD; Chief Editor: Hampton Roy, Sr, MD  more...
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Imaging Studies

Imaging studies can include the following:

  • The diagnosis of angle recession is confirmed during office examination.

  • Usually, imaging is necessary only to evaluate comorbidities due to trauma.

    • Occasionally, CT scanning of the orbits is needed to evaluate for orbital fractures or foreign bodies.

    • Emergency neuroimaging if typically indicated after major head trauma.

  • 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. [37, 41]

    • Ultrasound biomicroscopy (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 a clinical setting in an intact globe, and it provides information otherwise unavailable from convention examination.

    • High-resolution images of angle recession, zonular deficiency, iridodialysis, and cyclodialysis have been described. Zonular deficiency and angle recession are the most common UBM findings in a closed-globe injury. [37]

    • 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. [8]

    • Ciliary body melanoma, although rare, has been differentiated from angle recession using a combination of UBM, PET-CT, and aqueous tap. [40]

  • Slit-lamp optical coherence tomography (SL-OCT) has also been described as a method of imaging angle recession, but it may be less reliable than UBM. [38]

Other Tests

Other tests include the following:

  • 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.

  • Several authors have described the use of tonography to evaluate patients with traumatic angle recession. [42]

    • 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, 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 nerve photography is also important for documenting and monitoring glaucoma.

  • Computerized disk analysis and analysis of nerve-fiber layers has been gaining acceptance in the diagnosis and management of all forms of glaucoma.



Gonioscopy is the only clinical procedure that must be performed before angle recession can be diagnosed.

Use of a 1- or 3-mirror Goldman goniolens, which provides the greatest magnification of angle structures, is recommended.

Use of the Koeppe lens for examining and photographing the anterior chamber angle is also advocated. Use of Koeppe lenses allows for easy comparison with the uninjured eye because they can be placed simultaneously on the eyes.

The Posner 4-mirror gonioprism is not preferred for evaluating suspected angle recession because of the potential for indenting the central cornea, inducing artificial deepening, and/or distorting of the anterior-chamber angle.


Histologic Findings

Histopathologic findings of eyes with angle-recession deformities have been well described and include features of both light microscopy and electron microscopy (EM).

In their classic report in 1962, Wolf and Zimmerman described a characteristic tear extending into the anterior ciliary body, separating the longitudinal and circular fibers. [4]

  • The extent of dissection varied, but the longitudinal muscle remained attached to the scleral spur.

  • Retroplacement of the iris root and ciliary processes was noted microscopically. An association with other abnormal findings, including iridodialysis, rupture of the trabecular meshwork, or cyclodialysis, was documented. Late findings were also reported.

  • Over time, healing of the ciliary body laceration was noted. This was accompanied by atrophy of the circular muscle at involved sites, resulting in a fusiform contour of the ciliary body, as seen on axial sections.

  • Other histopathologic findings in late cases provided clues to the mechanism of glaucoma in angle recession. Marked degeneration of the trabecular meshwork was prominent.

  • In some cases, an abnormal hyaline membrane, continuous with the Descemet membrane, was formed over the inner surface of the trabecular meshwork, sometimes extending further onto the anterior iris surface.

    • Abnormal corneal endothelial proliferation may occur in some eyes with traumatic angle deformities.

    • The histologic examination revealed proliferation of the endothelium posterior to the Schwalbe ring with secretion of a Descemetlike membrane covering the meshwork and perhaps reducing trabecular outflow capacity of the involved angle.

    • Electron microscopy 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 electron microscopy 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. [43]

Although the exact pathology of angle-recession glaucoma is not fully established, the ultrastructural abnormalities described above support a chronic progressive mechanism of trabecular outflow dysfunction, leading to pressure elevation over time.