Intravitreal crystalline triamcinolone acetonide as an additional tool in pars plana vitrectomy for complicated proliferative vitreoretinopathy?

Abstract

Sir, Intravitreal injections of triamcinolone acetonide have recently been applied as treatment for various intraocular, neovascular, proliferative or oedematous diseases (Jonas et al. 2003). The effect of intravitreal injection of triamcinolone acetonide as an adjunctive procedure in pars plana vitrectomy for proliferative vitreoretinopathy was examined in a previous pilot study (Jonas et al. 2000). That study concluded that an intravitreal injection of crystalline cortisone may not be toxic to intraocular structures, that it reduces postoperative intraocular inflammation, and that it may be a potentially useful additional tool in the treatment of proliferative vitreoretinopathy. The purpose of the present study, which included a larger group of patients with longer follow-up periods than in the earlier pilot study, was to re-address the question of whether intravitreal injection of crystalline triamcinolone acetonide as an additional step in pars plana vitrectomy for proliferative vitreoretinopathy is beneficial in terms of reducing the rate of retinal re-detachments and improving clinical outcome. This consecutive clinical interventional case series study included 33 patients undergoing pars plana vitrectomy for complicated proliferative vitreoretinopathy due to preceding retinal detachment surgeries (n = 25) or traumatic retinal lesions (n = 8). The Ethics Committee of the Faculty of Clinical Medicine Mannheim, of the University of Heidelberg approved the study according to the tenets of the Declaration of Helsinki. Mean preoperative visual acuity (VA) was 0.03 ± 0.05 (median: hand movements; range: light perception to 0.25). The surgical procedure in the present study consisted of a standard three-port pars plana vitrectomy with encircling band, membrane peeling, retinotomy and retinectomy, intraoperative use of perfluorcarbon liquids, silicone oil endotamponade, retinal endolaser coagulation or exocryocoagulation, and an intravitreal injection of 25 mg triamcinolone acetonide (0.2 ml) with the preservative removed. The triamcinolone was injected at the end of the surgery through the closed sclerotomies into the vitreous cavity towards the peripheral retina at the 6 o'clock position. The vitreous cavity was completely, or almost completely, filled with silicone oil. The patients were asked to sit up and to remain in an upright position for at least 2 hours after surgery to prevent the cortisone crystals from sedimenting onto the macular region. Mean follow-up time was 8.6 ± 6.6 months (median: 9.5 months; range: 0.2–23.9 months). The inclusion of patients with short follow-up periods indicates that the figures for postoperative re-detachment rates may be falsely low, and may have increased if the follow-up periods had been long enough for all patients to develop detectable retinal re-detachment. Proliferative vitreoretinopathy with retinal re-detachment was detected in 10 (30%) patients. Postoperative retinal re-detachment was marginally significantly correlated with the number of retinal surgeries prior to inclusion into the study (p = 0.06). In five of the 10 patients with postoperative retinal re-detachment, the detachment was observed within the first 3 months after surgery. The shortest intervals between surgery and detection of re-detachment were 1 week and 3 weeks. Best postoperative VA was 0.06 ± 0.07 (median: 0.03; range: no light perception to 0.25). For all patients included in the study, best postoperative VA was significantly better than preoperative VA (p = 0.024). In two of the 33 (6%) patients, cortisone crystals settled on the macular region. Three months after surgery, they had totally resolved. Upon ophthalmoscopy, no tissue damage was detected. The patients receiving an intravitreal injection of 25 mg triamcinolone acetonide in combination with pars plana vitrectomy as treatment for complicated proliferative vitreoretinopathy showed a relatively high recurrence rate of proliferative vitreoretinopathy with retinal re-detachment. This result was unexpected in view of the presumed antiphlogistic and antiproliferative effect of steroids such as triamcinolone acetonide (Machemer et al. 1979). It may be explained by a previous experimental study in which triamcinolone acetonide inhibited the proliferation of rabbit dermal and conjunctival fibroblasts in cell culture at 150 mg/l, but paradoxically increased proliferation almost two-fold at concentrations ranging from 1 mg/l to 30 mg/l under identical culture conditions (Blumenkranz et al. 1984). As long as the influence of steroids on the proliferation of retinal pigment epithelium cells remains unclear, intravitreal triamcinolone acetonide may be taken cautiously as an adjunct treatment for proliferative vitreoretinopathy. However, it must be remembered that the silicone oil endotamponade and the vitrectomy itself will influence the pharmacokinetics of intraocular triamcinolone acetonide. Additionally, the retinal re-detachments usually occurred in the inferior periphery. It remains unclear whether the location of the retinal re-detachments was associated with the site of the triamcinolone acetonide crystals resting on the retina, or whether they occurred in the inferior periphery because the silicone oil tamponade is usually less marked at that location than in the superior fundus region. Future randomized studies as well as investigations evaluating the effect of triamcinolone acetonide combined with other drugs such as 5-fluorouracil (Chenet al. 1992; Berger et al. 1996; Asaria et al. 2001) may be warranted.