To assess the feasibility and outcomes of combining fluocinolone acetonide sustained drug delivery implant insertion, pars plana vitrectomy, and silicone oil infusion to treat patients with chronic, refractory ocular hypotony resulting from uveitis.
Retrospective chart review.
A retrospective, institutional chart review was performed. Outcome measures included visual acuity, intraocular pressure, and adverse events.
A total of 13 eyes of 11 patients were studied. All patients were women, had a mean age of 57 years (range, 26 to 73 years), and had a diagnosis of panuveitis. The mean duration of preoperative hypotony was 42 months (range, 11 to 108 months). Patients were followed up on average for 22 months (range, 9 to 46 months) after the combined surgical procedure. The mean preoperative visual acuity was 20/1000 (logarithm of the minimal angle of resolution, 1.7). At the 6- and 12-month visits, the mean visual acuity remained stable at 20/800 (logarithm of the minimal angle of resolution, 1.6; P = .74) and 20/600 ( P = .34), respectively. At baseline, the mean intraocular pressure (IOP) was 2.3 mm Hg. The average IOP was 5.9 mm Hg, 5.1 mm Hg, and 5.0 mm Hg at 6, 12, and 24 months after surgery, respectively. The increase in IOP relative to the baseline IOP was statistically significant at 6 and 12 months ( P = .027 and P = .004, respectively). The duration of preoperative hypotony inversely correlated with the IOP at 6 months ( P = .027). No intraoperative complications were encountered and the procedure was well tolerated.
Fluocinolone acetonide implantation combined with pars plana vitrectomy and silicone oil infusion is feasible and is well tolerated in the management of chronic, refractory ocular hypotony associated with uveitis.
Hypotony typically is described as an intraocular pressure (IOP) of less than 6 mm Hg. Chronic hypotony may result from ocular trauma (such as cyclodialysis cleft), glaucoma surgery, retinal detachment, proliferative vitreoretinopathy, and chronic uveitis. Prolonged ocular hypotony can have permanent and devastating consequences, including visual loss from maculopathy and optic neuropathy. End-stage complications include phthisis and a painful and disfigured eye.
The factors that contribute to uveitis-related hypotony are unique and likely differ between acute and chronic inflammatory processes. Hypotony in acute uveitis may result from ciliary body shutdown, prostaglandin-mediated increased uveoscleral outflow, or suprachoroidal effusions. These processes often are reversible with inflammation control. With chronic uveitis, hypotony may be caused by inflammation and by structural complications such as ciliary body tractional detachment resulting from inflammatory membranes. In some cases with ciliary body traction, removal of ciliary body membranes may restore normal anatomic features and may increase IOP. Permanent atrophy of ciliary processes and associated decreased aqueous production is another important factor in chronic uveitic hypotony. When a tractional component is absent, therapeutic options are limited. Described treatment approaches include periocular or intraocular corticosteroid therapy, topical ibopamine (a nonselective dopaminergic agent), injection of viscoelastic material, or pars plana vitrectomy surgery with or without intraocular gas or silicone oil. However, none of these procedures have shown consistent long-term benefits.
A fluocinolone acetonide implant controls inflammation and maintains visual acuity in eyes with ocular inflammation associated with noninfectious intermediate uveitis, posterior uveitis, or panuveitis. Steroid-induced elevated IOP is a notable adverse event associated with this implant. Vitrectomy and silicone oil injection have been used to treat eyes with chronic ocular hypotony. We hypothesized that it may be feasible to combine fluocinolone implant insertion with vitrectomy and silicone oil injection to treat uveitic eyes with chronic uveitis-associated hypotony. We reasoned that the fluocinolone acetonide implant would help to control subclinical or inadequately treated inflammation that contributed to the hypotony and that in this setting, a steroid-induced IOP elevation actually would be a benefit rather than an adverse event. Furthermore, we predicted that the vitrectomy and silicone oil would maintain intraocular volume and thereby would prevent progression to phthisis.
In the present report, we describe the surgical outcomes of patients with chronic uveitis-related ocular hypotony that were managed with pars plana vitrectomy, placement of a fluocinolone acetonide implant, and silicone oil infusion. The goal of treatment was to salvage eyes from progressive deterioration and phthisis.
A retrospective, institutional chart review was conducted to identify patients with persistent ocular hypotony associated with chronic, noninfectious uveitis that underwent complete pars plana vitrectomy, placement of a fluocinolone acetonide implant, and infusion of silicone oil from January 2006 through January 2009. Hypotony was defined as an IOP of 6 mm Hg or less on 2 visits more than 1 month apart with associated hypotony-related complications. A minimum of 6 months of follow-up was required for study inclusion. Patients with active anterior segment inflammation were not included in the study. Cases with inadequate follow-up or incomplete chart records were excluded. Reversible causes of hypotony such as cyclodialysis cleft, retinal detachment, or overfiltering bleb also were excluded. Finally, eyes with hypotony without associated secondary complications, such as hypotony maculopathy or corneal decompensation, were not included. Ultrasound biomicroscopy was not performed routinely on all patients to assess cyclitic membranes or ciliary process atrophy.
Best-corrected visual acuity was assessed with the Early Treatment Diabetic Retinopathy Study chart. Visual acuities were converted to logarithm of the minimal angle of resolution (logMAR) units for statistical analysis. Non-Early Treatment Diabetic Retinopathy Study visual acuities (eg, hand movements and light perception) were converted to logMAR units using previously described methods.
IOPs were measured with the Goldmann applanation tonometer or with a handheld pneumotonometer. An IOP of 0 was assigned when the eye was too soft to obtain an accurate measurement. Preoperative IOP was defined as the mean of all pressures measured from the onset of hypotony to the date of surgery. Visual acuity and IOP were recorded at the preoperative visit and postoperative months 1, 3, 6, 12, 24, and 36. The highest and lowest measurements also were recorded, even when not at one of the above intervals. A visit that was within 2 weeks of the predetermined intervals was considered valid for the postoperative month 1 and 3 follow-up visits, and if within 4 weeks for the subsequent visits.
The procedure was performed under monitored anesthesia care and retrobulbar block on an outpatient basis. A complete 3-port 20-gauge pars plana vitrectomy was performed, followed by implantation of a 2.1-mg fluocinolone acetonide implant (Bausch & Lomb, Rochester, New York, USA), as previously described. The ciliary body was assessed during surgery for the presence of pathologic features, such as traction or atrophy. A fluid–air exchange then was performed with an infusion light-pipe and soft-tipped aspiration cannula, and the air was replaced with 1000-centistoke silicone oil. Additional pathologic features, when present, such as macular epiretinal membrane, pupillary membrane, or capsular opacity, were treated as part of the vitrectomy procedure. An anterior segment surgeon placed a temporary keratoprosthesis, followed by penetrating keratoplasty when corneal opacity precluded an adequate posterior segment view to perform the vitrectomy safely, when the corneal opacity was thought to contribute to decreased visual acuity, or when both were the case. At the conclusion of surgery, an antibiotic, typically cefazolin 100 mg, and dexamethasone sodium phosphate 5 mg were injected into the subconjunctival space. After surgery, prednisolone acetate 1% and scopolamine 0.25% were given at a frequency dependent on the degree of postoperative inflammation. If a penetrating keratoplasty was performed, a broad-spectrum antibiotic also was administered during the first couple of weeks after surgery.
A total of 13 eyes of 11 patients met the above-described inclusion criteria ( Table 1 ). All patients were women, had a mean age of 57 years (range, 26 to 73 years), and had a diagnosis of panuveitis. The cause of panuveitis was idiopathic in 7 patients (9 eyes, 64% of patients), sarcoidosis in 2 patients (18%), and multiple sclerosis in 2 patients (18%). Patients were followed up, on average, for 22 months after surgery (range, 9 to 46 months).
|Study Eye||Age (y)||Cause||Duration of Hypotony Before Surgery (mos)||Follow-up (mos)||Intraocular Pressure (mm Hg)||Visual Acuity (logMAR)|
|Before Surgery||Postoperative Month 6||Postoperative Month 12||Most Recent||Highest Postoperative||Before Surgery||Postoperative Month 6||Postoperative Month 12||Final||Best Postoperative|
The mean and median duration of preoperative hypotony were 42 and 48 months, respectively (range, 11 to 108 months). Hypotony-related complications included choroidal thickening, macular thickening or retinal fold, corneal decompensation, band keratopathy, anterior and posterior synechiae, and foreshortened globe.
The mean preoperative Snellen equivalent VA was 20/1000 (logMAR, 1.7). At the 6- and 12-month visits, the mean visual acuity remained stable at 20/800 (logMAR, 1.6; P = .74) and 20/600 (logMAR, 1.5; P = .34), respectively ( Table 2 ). At the 6-month visit, 9 of 13 eyes had maintained stable visual acuity (no more than 2 lines of lost visual acuity). Two of 4 eyes with visual loss had preexisting corneal decompensation, band keratopathy, and corneal stromal opacities that were exacerbated after surgery by emulsified silicone oil (study eyes 6 and 9). Another patient had multiple preoperative ocular comorbidities (history of optic neuritis, penetrating keratoplasty, and epiretinal membrane), without any postoperative complications (study eye 2). The final eye had a nonclearing hyphema that required an anterior chamber washout with vitrectomy revision and replacement of silicone oil (study eye 7). At the most recent follow-up, the vision in this patient improved from baseline (20/320) to 20/250. At 12 months, only 1 of 11 eyes had not maintained stable visual acuity (study eye 2), and no eye demonstrated more than 2 lines of visual loss.
|Period (mos)||No.||Visual Acuity (logMAR)||Lines of Visual Acuity Gained or Lost (No. of Eyes)|
|Median||Mean (Range)||P Value||2 or More Lines Lost||No Change||2 or More Lines Gained|
|Baseline||13||2||1.7 (1 to 3)||—||—||—||—|
|3||11||1||1.3 (1 to 2)||.17||2||4||5|
|6||12||1||1.6 (1 to 3)||.74||4||5||3|
|12||11||1||1.5 (1 to 3)||.34||1||7||3|
The mean and median preoperative IOP was 2.3 mm Hg (n = 13; range 0 to 6 mm Hg). The average IOP was 3.8 mm Hg (n = 11; range, 0 to 12 mm Hg), 5.9 mm Hg (n = 12; range, 0 to 21 mm Hg), 5.1 mm Hg (n = 11; range, 0 to 12 mm Hg), and 5.0 mm Hg (n = 6; range, 0 to 16 mm Hg) at 3, 6, 12, and 24 months after surgery, respectively ( Table 3 ). IOP was unchanged or improved in all but 1 eye at both the 6- and 12-month follow-up and in 11 of 13 eyes at the most recent visit. The increase in IOP relative to the baseline IOP was statistically significant at 6 and 12 months ( P = .027 and P = .004, respectively). For all eyes taken together, the average IOP at the most recent visit was 7.0 mm Hg (n = 13; range, 0 to 29 mm Hg). This level also was statistically higher than baseline ( P = .028). The duration of preoperative hypotony was correlated significantly and inversely with the IOP at 6 months ( P = .027), but was not associated with visual outcome ( P = .46).
|Period (mos)||No.||IOP (mm Hg)||P Value|
|Baseline||13||3||2.3 (0 to 6)||—|
|3||11||4||3.8 (0 to 12)||.217|
|6||12||5||5.9 (0 to 21)||.027|
|12||11||5||5.1 (0 to 12)||.003|
|24||6||4||5 (0 to 16)||.172|
|Most recent||13||5||7 (0 to 29)||.028|
There were no intraoperative complications. After surgical intervention, many of the preoperative hypotony-related complications resolved or improved ( Table 4 ). Two patients underwent penetrating keratoplasty at the time of the initial surgery. None of the study eyes had ciliary body traction requiring surgical intervention. Postoperative procedure-related adverse events included hyphema in 2 eyes. In one of these eyes, the hyphema resolved spontaneously, and in another, as described above, an anterior chamber washout and removal and replacement of silicone oil was performed. Silicone oil in the anterior chamber was present on at least 1 postoperative visit in 8 eyes. Among those with pre-existing corneal decompensation, penetrating keratoplasty was required in 1 eye. Two eyes required short-term treatment with ocular antihypertensive drops (highest IOP was 28 mm Hg in one patient and 30 mm Hg in another). Among patients taking systemic immunosuppressants (n = 7), it was possible to decrease the dosage in 2 patients and to stop treatment in 1 patient ( Table 5 ).
|Study Eye||Baseline||Postoperative Month 6||Postoperative Month 12|
|1||Choroidal thickening, maculopathy, foreshortened eye||Posterior synechiae||Posterior synechiae|
|2||Choroidal thickening, maculopathy, IOL capsular opacities||None||None|
|3||Choroidal thickening, maculopathy, ERM, posterior synechiae, PAS, corneal edema, IOL capsular opacities||Corneal edema, PAS||Corneal edema, PAS|
|4||Choroidal thickening, corneal edema, posterior synechiae, PAS, shallow AC, IOL capsular opacities||Choroidal thickening, corneal edema, capsular opacities||Corneal edema, SO in anterior chamber, shallow AC, irregular pupil|
|5||Choroidal thickening||None||Corneal edema|
|6||Maculopathy, band keratopathy, corneal edema, aphakia||Maculopathy, band keratopathy, corneal edema, aphakia||N/A (no visit)|
|7||Maculopathy||None||N/A (no visit)|
|8||Choroidal thickening, maculopathy, foreshortened eye, band keratopathy, aphakia||Band keratopathy, aphakia||Peripapillary edema, band keratopathy, aphakia|
|9||Choroidal thickening, maculopathy, optic nerve edema, band keratopathy, corneal edema/stromal opacification, aphakia||Band keratopathy, aphakia, epikeratophakia||Band keratopathy, aphakia, epikeratophakia|
|10||Choroidal thickening, dense cataract||N/A (no visit)||Pupillary membrane|
|11||Maculopathy, corneal edema||Corneal edema||Corneal edema|
|12||Choroidal thickening, maculopathy, aphakia, corneal decompensation||Aphakia||Aphakia|
|13||Maculopathy, corneal edema and stromal scarring, aphakia||Corneal decompensation, aphakia||Corneal decompensation, aphakia|