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Anterior chamber depth and angle-closure glaucoma after central retinal vein occlusion
© The Author(s). 2016
Received: 30 August 2015
Accepted: 26 May 2016
Published: 31 May 2016
The purpose of this study was to report the anterior chamber (AC) depth and the attack of angle-closure glaucoma (ACG) in eyes with the recent onset of central retinal vein occlusion (CRVO).
This retrospective case series included 24 patients with recent onset of CRVO (within one month of attack) from July 2001 to December 2002. The mean follow-up period of the patients was 46 months (range: 3 to 92 months). AC depth was measured using an ultrasound biomicroscopy. Clinical data, including systemic disorders, intraocular pressure, and visual outcomes were recorded. The main outcome measures were AC depth in the diseased eye and the fellow eye of the same patient and the attack of ACG after CRVO.
The mean AC depth in the diseased eyes was significantly shallower than in the unaffected fellow eyes (2.43 ± 0.45 mm vs. 2.55 ± 0.46 mm; p < 0.001). Four patients (17 %) developed ACG after the onset of CRVO within one month of the CRVO attack. In these four patients, the mean AC depth in the diseased eyes was 1.91 ± 0.21 mm, which was much shallower than the eyes without ACG attack (2.53 ± 0.40 mm).
AC depth is significantly shallower following the onset of CRVO. ACG can occur in patients after the onset of CRVO.
Glaucoma may be a contributory factor in the etiology of central retinal vein occlusion (CRVO), or may be a result of CRVO . Neovascular glaucoma (NVG) is the most common form of glaucoma following CRVO [2, 3]. NVG mostly results from an elevated expression of vascular endothelial growth factor (VEGF) following the ischemic onset of vessel occlusion in the retina [4, 5]. However, shallowing of the anterior chamber (AC) following the onset of occlusion in CRVO, therefore resulting in asymmetric AC depths in the same patient, has been observed . Clinical observations have shown that angle-closure glaucoma (ACG) can occur following CRVO without the formation of neovascularization in the angle of the eyes, although with a much lower incidence than NVG [7–11]. However, these previous studies are mainly case reports. The shallowing of AC is mainly observational without actual measurement of it. The purpose of this study was to investigate the AC depth by an ultrasound biomicroscopy (UBM) in patients with acute onset of CRVO and the incidence of ACG following CRVO in a consecutive series of CRVO patients. We hope that our findings can provide more in-depth observations and a better understanding of the association of CRVO and the onset of ACG.
Anterior chamber depth in the diseased eyes with central retinal vein occlusion and the unaffected fellow eyes in 24 patients
Mean ± SD
2.43 ± 0.45 mm
2.55 ± 0.46 mm
0.12 ± 0.1 mm*
Differences of anterior chamber depth in 23 patients with shallower anterior chamber depth in the central retinal vein occlusion eyes than the fellow unaffected eyes
Differences of AC (mm)
Number of eyes
Profiles of the patients with angle-closure glaucoma attacks after central retinal vein occlusion
In this study, we found that the AC depth was significantly shallower in the eyes with CRVO attack than in the fellow eyes. Four patients (17 %) developed ACG after the onset of CRVO, and the mean AC depth in these eyes was only 1.91 ± 0.21 mm. Lin et al.  reported that in acute ACG patients in Taiwan, the mean AC depth (corneal thickness included) was 2.28 ± 0.23 mm. Subtracting the average corneal thickness of 0.5 mm, the AC depth was around 1.78 mm in the patients with ACG attack in Lin et al.’s study, and was consistent with our findings. An AC depth less than 2 mm may pose a greater risk for ACG clinically. ACG after CRVO has not been reported extensively. However, these issues are particularly important for Asians, as Asians have a shallower AC or a steeper cornea and a much higher prevalence of ACG than Caucasians [13–18].
Most of the previous studies on non-rubeotic ACG following CRVO are case reports or small case series and lack of actual measurement of AC depth [6–9]. Our study includes a series of CRVO patients with the actual measurement of AC depth. According to previous case reports, some common characteristics can be seen in those patients. First, temporary shallowing of the AC and reversible ACG without visible vascularization of the angle were noted. Second, neither evidence of pupillary block nor iris bombe was found; however, all of the patients had a rather forward displacement of the entire lens - iris diaphragm. Third, IOP control was usually achieved by medical treatment, and laser or surgical procedures were used as a back-up treatment if the IOP could not be controlled with anti-glaucoma medications. In our current study, we also had a very consistent clinical course. The four patients developing ACG had very shallow AC and revealed no vascularization over the angles. The mechanism of angle closure glaucoma was not due to papillary block in the two patients since they had received prophylactic laser iridotomy before. All the patients got good IOP control after laser surgery and glaucoma medications.
The mechanisms of AC shallowing after CRVO are uncertain. It has been hypothesized that marked swelling and vascular congestion of the ciliary body with anterolateral displacement after CRVO could lead to decreased AC depth. It is also likely that the increase in volume within the posterior segment, either due to blood or transudative fluid following CRVO pushes the lens-iris diaphragm forward. This condition may be under-diagnosed, especially in Asians with a shallower AC than Caucasians [13–18]. Further prospective studies including evaluation of AC depth, angle, and ciliary body changes in CRVO need to be performed to highlight this much neglected disorder.
The limitations of this study include its retrospective design, small sample size, and variable follow-up of the patients. In addition, no longitudinal follow-up of AC depth of these patients was performed. However, our comparative study showed significant shallowing of the AC following the onset of CRVO. This implies that the patients with recent-onset CRVO need to be monitored closely, not only for the presence of NVG, but also for attacks of ACG.
AC shallowing by up to 0.3 mm in eyes after CRVO attack may occur compared with fellow unaffected eyes. It is important to evaluate AC depth and perform gonioscopic examinations in cases of recent-onset CRVO to assess the possible development of NVG as well as the frequently ignored ACG. An AC depth of less than 2 mm may pose a greater risk for ACG clinically. Secondary non-rubeotic ACG from CRVO must be distinguished from NVG, because the treatment and the prognosis may differ among the two disease entities.
AC, anterior chamber; ACG, angle-closure glaucoma; CRVO, central retinal vein occlusion; IOP, intraocular pressure; NVG, neovascular glaucoma; SD, standard deviation; UBM, ultrasound biomicroscopy; VEGF, vascular endothelial growth factor.
Availability of data and materials
All the data supporting the findings is contained within the manuscript.
SCW drafted the manuscript and participated in the design of the study; YSL and WCW were involved in the acquisition, analysis and interpretation of data; SHC conceived of the study, and participated in its design and coordination and helped to draft the manuscript. All authors reviewed and approved the final manuscript.
The authors declare that they have no competing interests.
Consent for publication
Ethics approval and consent to participate
This study was approved by the Institutional Review Board of Chang Gung Memorial Hospital and conforms to the provisions of the Declaration of Helsinki.
Written informed consent was obtained from the patients or the legal guardian for publication of this research article and any accompanying images. One patient was illiterate so the consent was obtained from the legal guardian. A copy of the written consent is available for review by the Editor of this journal.
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