Capsular fibrosis is one of the major late postoperative complications following cataract extraction and implantation of an intraocular lens (IOL). It includes posterior capsular opacification and opacified anterior capsulotomy edge.1,2 Although an opacified anterior capsular edge may not affect the patient's postoperative vision, contraction of the anterior capsulotomy window may lead to the complete closure of the window.3–5 Local cellular mechanism in lens cells, intraocular cytokines, and attenuation in the zonules might be involved in the occurrence of this complication.6–9 This condition can be treated by neodymium:YAG (Nd:YAG) laser-anterior capsulotomy in less severe cases. However, we have experienced 2 cases of complete closure of the anterior capsulotomy window with contraction by thick fibrous tissue formed at the edge of the capsulotomy and surgically well treated. We examined the histology to investigate the mechanism of such severe tissue contraction using light and electron microscopy as well as immunohistochemistry.
A healthy 76-year-old woman had uneventful phacosurgery and implantation of a silicone IOL on March 14, 2002, in her left eye. Surgery was done under local anesthesia. Sodium hyaluronate (0.1%) was used to facilitate the insertion of an IOL (SI-40NB Allergan). Time for the operation was 9.5 minutes. Visual acuity in the operated left eye was 0.4 (0.8) on the next day and 0.6 (1.0) at day 3. The patient consulted us again with reduced visual acuity 3 months after the initial surgery. Her visual acuity in the left eye at that time was 0.05 (0.15). The anterior capsulotomy window was found to be completely closed with a fibrous plaque and wrinkles in the anterior capsule (Figure 1). Neodymium:YAG laser irradiation failed to reopen the capsular window, and the patient was surgically treated on September 9, 2002.
Surgical procedure was as follows: Central anterior capsular closure was punctured with scleral blade for vitreoretinal surgery and sodium hyaluronate 1.0% was injected into the capsular bag to reopen the adhesion between anterior and posterior capsule in the periphery. Then the central anterior capsular closure was removed with a forceps. The postoperative visual acuity in the affected eye was 0.6 (0.8). The excised tissue was routinely fixed with 10% formalin, embedded in paraffin, and processed for immunohistochemistry or processed for transmission electron microscopy.
A 78-year-old woman had uneventful phacosurgery and implantation of an IOL in her left and right eyes on July 15 and 22, 2002, respectively. Surgery was done under local anesthesia. Sodium hyaluronate was used to facilitate the insertion of IOL (Allergan SI-40NB). The required time for the operation was 10.5 or 8.5 min in left or right eye, respectively. The patient had long-standing diffuse corneal stromal opacity, presumably caused by some inflammatory disease. The visual acuity was 0.2 (0.5) and 02 (0.7) in the right and left eyes, respectively. She had suffered from chronic renal failure for over 40 years and had been receiving hemodyalysis and also had received systemic oral steroid to control rheumatoid arthritis for around 10 years. She consulted us 3 months after the initial discharge from our hospital with impaired vision. Her visual acuity was 0.3 (0.4) or 0.15 (0.2) in her right and left eyes, respectively. Opacification in the posterior capsule was observed in her right eye, and complete closure of anterior capsulotomy window in association with upward dislocation of the IOL was observed in her left eye. Posterior capsule in the left eye was not seen because of the anterior capsular opacification. The patient had an operation under local anesthesia for removal of the capsulotomy window closure and repositioning of the decentrated IOL. Surgical procedure was quite similar to that employed in case 1. Her visual acuity in the left eye was 0.2 (0.4) on December 17, 2002. Excised tissue was processed for histology in the same way as in Case 1.
Excised tissues embedded in paraffin were cut at 5 μm, deparaffinized, and processed for hematoxylin and eosin (H&E) staining or immunostaining. The specimens were allowed to react with a battery of primary antibodies (Table 1). After a wash in phosphate-buffered saline, the specimens were treated with peroxidase-conjugated secondary antibody and then processed for diaminobenzidine color reaction as previously reported. Pieces of specimens for electron microscopy were fixed in glutaraldehyde 2.0% in 0.1 M phosphate buffer for 48 hours. Specimens were then postfixed and embedded in Epon 812 mixture, and ultrathin sections were cut, as previously reported. Electron-stained ultrathin sections were observed under transmission electron microscopy.
Ultrastructural examination with H&E staining revealed the presence of elongated, fibroblast-like lens epithelial cells in association with extracellular matrix accumulation (Figures 2 and 3, A). Electron microscopy revealed the presence of fibroblast-like lens cells and accumulation of extracellular matrix. The cells seemed attenuated with accumulation of intracellular lipid droplets and presumedly damaged intracytoplsmic organelles. The matrix includes amorphpos matrix substance and collagen fibers. Because these morphological examinations by light and electron microscopy did not reveal the nature of cells and matrix substance, immunohistochemistry was performed. The cells were labeled with antivimentin antibody (Figure 3, B) anti-α-smooth muscle actin (αSMA) antibody (Figure 3, C). Anterior capsule was uneven. Immunohistochemistry revealed the presence of collagen types I, III, IV, and VI, as well as fibronectin and osteopontin (Figure 3, D–H).
We presented 2 cases of complete closure of the anterior capsulotomy window by contraction of fibrous tissue formed at the edge of the capsulotomy. Both cases required surgical reopening of the window to restore the patients' vision. Immunohistochemistry revealed a histology in the specimens of the present series of 2 cases similar to those previously reported by us in capsular opacification without extensive capsular contraction.10–14 Expression of αSMA and extracellular matrix accumulation, as revealed by the present immunohistochemistry, might lend the tissue contraction during healing. However, both the contraction of the newly formed fibrous tissue by the appearance of αSMA-expressing lens epithelial cells in it and also possible attenuation of the zonnules might be responsible for the total closure of the capsulotomy. Although inflammatory cytokines induced by the operation might be involved in activation of lens epithelial cell,15,16 slit-lamp examinations in both cases postoperatively failed to detect any unusual inflammation in the anterior chamber, as imaginable from the intraoperative course without complications. Although patients with pigmentary retinal degeneration, uveitis, atopic dermatitis, pseudoexofoliation syndrome, or high myopia may have an increased risk for such high-degree contraction of the anterior capsulotomy edge,3–9 the former 3 diseases may induce the condition through exaggerated postoperative intraocular inflammation, and the latter 2 conditions may result in attenuated zonules. However, our 2 cases were not associated with such local or systemic disorders; the relationship between rheumatoid arthiritis and marked contraction of the capsulotomy edge was not clear in Case 1.
A silicone IOL was used in each of 2 cases. Hydrophilic characteristic of this material might affect the postoperative behavior of lens epithelial cells on the anterior capsule. It has been reported that fibrous change in the anterior capsule was marked with a silicone IOL as compared with other material IOLs. It is better to use a nonsilicone IOL in patients with a presumed higher risk of anterior capsulotomy fibrosis and closure of the capsulotomy.
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