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Letter
The blood-aqueous barrier breakdown in eyes with endothelial decompensation after argon laser iridotomy
  1. Hisayo Higashihara,
  2. Chie Sotozono,
  3. Norihiko Yokoi,
  4. Tsutomu Inatomi,
  5. Shigeru Kinoshita
  1. Department of Ophthalmology, Kyoto Prefectural University of Medicine, Kyoto, Japan
  1. Correspondence to Shigeru Kinoshita, Department of Ophthalmology, Kyoto Prefectural, University of Medicine, Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto 602-0841, Japan; shigeruk{at}koto.kpu-m.ac.jp

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Argon laser iridotomy-induced bullous keratopathy (ALI-BK) is a growing medical problem in Asian countries.1 This disease is a common reason for either Descemet's stripping automated endothelial keratoplasty or penetrating keratoplasty surgery in Japan.2 3 Our experience with penetrating keratoplasty, combined with cataract extraction and intraocular lens implantation in eyes with ALI-BK, is typically characterised by an aggressive anterior-chamber inflammatory response, both intraoperatively and postoperatively, as compared with pseudophakic and aphakic BK, corneal opacity, and corneal scarring. Therefore, we speculate that in eyes with ALI-BK, the disease tends to weaken the blood-aqueous barrier. We quantitatively evaluated the blood-aqueous barrier in eyes with early endothelial decompensation following ALI using iris fluorescein angiography (IFA) and fluorophotometry.

Subjects and methods

This study involved nine eyes of seven patients with early endothelial decompensation following ALI, as well as eight eyes of four normal volunteers as a control. Relevant ethical committees approved the study protocol. A slit-lamp anterior fluorophotometer (FL-500; Kowa Company, Nagoya, Japan) was used to measure the blood-aqueous barrier function.4 After the autofluorescence values in the anterior chamber were measured, an intravenous injection of 10 ml of 10% sodium fluorescein solution was administered. At 10 and 30 min after the injection, the fluorescence intensity value in the anterior chamber was measured, and the value of autofluorescence was then subtracted. From this value, the blood-aqueous barrier function was evaluated. IFA was performed with a photographic slit-lamp (SL-7F; Topcon, Tokyo, Japan) according to the published method.5 After the intravenous injection of fluorescein, photographs were taken at 10 s intervals at the early phase and at 60 s intervals at the late phase.

Results

The fluorescein intensity values and clinical characteristics of the patients and normal controls are listed in table 1. The fluorescein intensity values in the anterior chamber in eyes with endothelial decompensation after ALI, both at 10 and 30 min after the injection, were significantly higher than those obtained from the normal control eyes (p=0.0004). Patients with a history of acute glaucoma attack had significantly higher fluorescein intensity values compared with patients with prophylactic ALI (at 10 min, p=0.0300; at 30 min, p=0.0098). In all subjects, IFA revealed dye leakage in the pupillary margin and the ALI site, which became more intense in the late phases (figure 1D–F). Especially in cases with a history of acute glaucoma attack, the dye leakage was extensive; the dye spread was patchy and irregular in size and shape in the early phases, and the dye remained bright for a long period of time (figure 1G–I). In our study, a case in which only the ALI-produced atrophic scar remained in the iris without an ALI window was included (Case 2, figure 1J–P). Surprisingly, although the ALI window was not opened, corneal oedema occurred at the lower part of the cornea (figure 1K,L). IFA also revealed spots of dye leakage in the pupillary margin; however, only a slight leakage was observed at the ALI site (figure 1O,P). In the normal control group, IFA revealed no dye leakage from the early to late phases (figure 1A–C).

Table 1

Clinical characteristics and outcome of fluorescein intensity values in eyes with endothelial decompensation after ALI and in normal controls

Figure 1

Clinical appearance in a normal control eye (A–C) and in three representative cases with early endothelial decompensation after argon laser iridotomy (ALI) (D–F, G–I, J–P). Iris fluorescein angiography (IFA) in the early phase (B, E, H, O) and in the late phase (C, F, I, P). Slit-lamp biomicroscopy shows a clear cornea in the normal control eye (A). IFA shows no dye leakage at both the early and late phases in the control eye (B, C). A clear cornea was seen in the left eye of a 63-year-old male patient (Case 1); anterior chamber depth is shallow and a large iridotomy is visible in the 1 o'clock position of the iris (D). IFA sequences of Case 1 (E, F): the dye leakage is seen at the ALI site and the spot leakage is also seen in the pupillary margin in the early phase (E). The dye leakages gradually increase in the late phase (F). Corneal oedema present in the inferior segment of the right eye of an 82-year-old female patient (Case 7); slit-lamp biomicroscopy shows a shallow anterior chamber and ALI is visible at the 10 o'clock position of the iris (G). IFA sequences of Case 7 (H, I); the dye leakage can be seen covering a wide area of the iris as well as at the pupillary margin at the early phase (H). The leaking gradually increases, persisting in the late phases (I). Clinical appearance of an eye with ALI-induced endothelial decompensation in a 77-year-old female patient (Case 2) (J–P). The cornea is clear and ALI is visible at the 10 o'clock position of the iris in the right eye (J). The cornea of the left eye is hazy due to corneal oedema and ALI is visible at the 2 o'clock position of the iris (K). Fluorescein staining demonstrating an irregular staining pattern over the localised area of oedema in the left eye (L). Note that the ALI window was not opened by only the ALI-produced atrophic scar (M, N). IFA sequences in the right eye (O, P); the dye leakage spots are seen in the pupillary margin; on the other hand, slight leakage is only seen at the ALI site in the early phase (O). The dye leakages gradually increase in the late phase (P).

Comment

Our results indicate that eyes with endothelial decompensation after ALI may actually have a chronic postsurgical breakdown of the blood-aqueous barrier. Presumably, the predisposition to postoperative inflammatory reactions in patients with ALI-BK appears to be caused by the manifested impairment of the blood-aqueous barrier. Although the reason why such a subclinical change may continue for a long period of time after ALI is unclear, the post-ALI endothelial decompensation may possibly be due to the humoral transport of substances such as prostaglandins and cytokines (eg, TGF-β1) in the anterior segment.

References

Footnotes

  • Competing interests None.

  • Patient consent Obtained.

  • Ethics approval This study was conducted with the approval of the Institutional Review Board of Kyoto Prefectural University of Medicine (No. MCHS-341).

  • Provenance and peer review Not commissioned; externally peer reviewed.

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