Vitreous loss caused by posterior capsule rupture or dialysis of the zonular fibers during complicated cataract surgery is a common and fearsome complication that makes surgery more difficult because it may be associated with severe intraoperative problems such as dropped lens fragments. Moreover, it may lead to blinding postoperative conditions such as corneal edema, secondary glaucoma, retinal detachment (RD), cystoid macular edema (CME), and endophthalmitis, in particular when the prolapsed vitreous strands in the anterior chamber are not completely removed.1–4 However, the transparent vitreous body in the anterior chamber is invisible under an operating microscope, necessitating indirect clues to determine its extent and location for meticulous removal. Therefore, several studies4–7 have described a technique that uses intracameral triamcinolone acetonide to make the vitreous fibers visible in the anterior chamber, thereby alerting the surgeon to residual strands of vitreous that might have gone unnoticed.
However, there is great concern regarding the safety of injecting triamcinolone acetonide into the anterior chamber during complicated cataract surgery with vitreous loss because it can access the vitreous cavity and, thus, may not be completely removed at the end of the surgery. The residual triamcinolone acetonide may cause steroid-induced glaucoma8,9 and inflammatory reactions,10 increase the susceptibility to ocular infection,10 and result in triamcinolone acetonide crystals deposition in the retina and toxic effects to the neurosensory retina and the retinal pigment epithelium (RPE).7,11 In addition, the benzyl alcohol used as a vehicle component in the pharmaceutical preparations of triamcinolone acetonide may be toxic to the corneal endothelium, retina, and RPE.4,7,11,12 As a result, some surgeons recommend using preservative-free triamcinolone acetonide4 or other substances without steroid activity.13–15
We were unable to find a study reporting the long-term outcomes after triamcinolone acetonide–assisted anterior vitrectomy during complicated cataract surgery with vitreous loss. Hence, the purpose of this retrospective study was to evaluate the long-term safety and efficacy of this procedure.
Patients and methods
This study reviewed the medical records of all patients who had complicated cataract surgery with vitreous loss between January 1, 2010, and January 1, 2012, at Tel Aviv Medical Center, a tertiary medical center affiliated with Tel Aviv University, Israel. In routine practice at the medical center, every single use of triamcinolone acetonide during cataract surgery is registered, allowing capture of all cases of triamcinolone acetonide–assisted anterior vitrectomy on a consecutive basis.
Patients were included in this study if they had triamcinolone acetonide–assisted anterior vitrectomy due to vitreous loss during complicated cataract surgery with a follow-up of at least 12 months. Patients were excluded if the vitreous loss was associated with retained lens material, necessitating posterior vitrectomy to remove those fragments and probably the residual triamcinolone acetonide as well.
All patients provided informed consent before their inclusion in the study. The study was reviewed by the institutional review board and followed the tenets of the Declaration of Helsinki.
Surgical Technique and Postoperative Care
When the cataract surgeon suspected vitreous loss (Figure 1, a), triamcinolone acetonide (nonfiltered Kenalog, 40 mg in 1 mL) was injected into the anterior chamber (Figure 1, b1 and b2) to stain the prolapsed vitreous fibers (Figure 1, c). Triamcinolone acetonide was used on an off-label basis. Then, anterior vitrectomy was performed to remove visible vitreous strands from the anterior chamber (Figure 1, d). Afterward, triamcinolone acetonide was injected again to check for residual vitreous with further vitrectomy performed if needed (Figure 1, e1 and e2). At the end of the surgery, the remaining triamcinolone acetonide was washed out (Figure 1, f1 and f2) and acetylcholine chloride intraocular solution (Miochol-E) was injected to constrict the pupil and ensure that no residual vitreous strands were left in the anterior chamber.
Postoperative treatment included topical steroids, antibiotics, and nonsteroidal antiinflammatory agents according to the surgeon’s preference. The patients were followed at the cataract clinic of the medical center during the first postoperative month and then referred for follow-up at community-based clinics of their health maintenance organization.
The following data were retrieved from the patients’ medical records: age, sex, and ocular comorbidities; preoperative ophthalmic examination, including the corrected distance visual acuity (CDVA), intraocular pressure (IOP); complete biomicroscopic examination results; and postoperative procedures performed in the operated eye up to the final follow-up, including intravitreal and sub-Tenon injections.
After a postoperative period of at least 12 months, all appropriate patients were recruited into this retrospective study and were invited to have the following examinations: CDVA, IOP, anterior segment and fundus biomicroscopy, and spectral-domain optical coherence tomography (SD-OCT) (Spectralis, Heidelberg Engineering GmbH) evaluation of the macula.
The paired t test was used to compare the CDVA and IOP results at last examination with the preoperative values. A P value less than 0.05 was considered significant.
Fifteen patients (7 men, 8 women) were included in the study. The mean age was 71 years (range 50 to 92 years), and the mean follow-up time was 21 months (range 12 to 29 months). Posterior chamber intraocular lenses (IOLs) were placed in the ciliary sulcus in 11 eyes and anterior chamber IOLs in 4 eyes.
Severe preoperative ocular comorbidities were found in 3 patients. The first had advanced age-related macular degeneration (AMD) with a macular scar in addition to end-stage glaucoma with optic atrophy. The second had neovascular AMD previously treated with 3 bevacizumab injections. The third had diabetic retinopathy formerly treated with scatter and focal laser for proliferative diabetic retinopathy and clinically significant macular edema, respectively. Other ocular comorbidities included intermediate AMD in 1 patient, epiretinal membrane (ERM) in 1 patient, and high myopia in addition to glaucoma controlled with 2 IOP-lowering medications in 1 patient. Three patients had dense cataract precluding preoperative retinal clinical examination.
Postoperatively, 1 patient required 5 bevacizumab injections for neovascular AMD and another patient was successfully treated with 2 sub-Tenon injections of triamcinolone acetonide for pseudophakic CME that subsequently resolved by last examination. In addition, 1 patient developed branch retinal vein occlusion (BRVO) without ocular hypertension 13 months after surgery. No patient developed endophthalmitis or RD.
The mean preoperative Snellen CDVA was 20/157 (0.89 logMAR ± 0.81 [SD]; range light perception to 20/28), improving to 20/35 (0.24 ± 0.31 logMAR; range 20/400 to 20/20) at last examination (P=.0033). All the patients had improved CDVA over the preoperative values.
One patient with a macular scar and optic atrophy had a preoperative CDVA of counting fingers, improving to 20/400 at last follow-up. Three patients with other retinal pathologies had a CDVA of 20/40 at final examination. The first had BRVO with CME awaiting bevacizumab injections. The second had thick ERM with vitreomacular traction syndrome and CME. The third had intermediate AMD. The remaining 11 patients had a CDVA of 20/30 or better at last follow-up.
The mean preoperative IOP was 14.8 ± 3.8 mm Hg, reaching 15.3 ± 2.4 mm Hg at the last follow-up (P=.50). One patient required 2 IOP-lowering medications preoperatively and at the last examination.
At the last follow-up, slitlamp examinations showed clear corneas and quiet anterior chambers in all the eyes with no evidence of flare, cells, or residual vitreous fibers. On posterior segment examination, the vitreous in all eyes was clear, with no cells or triamcinolone acetonide crystal deposits. There were no cases of untreated retinal breaks or RD.
Retinal examination and SD-OCT performed at the last follow-up showed retinal pathology with secondary CME in 2 patients. One patient had a thick ERM and vitreomacular traction, and the other had BRVO. There were no cases of pseudophakic CME.
In this study, triamcinolone acetonide–assisted anterior vitrectomy during complicated cataract surgery with vitreous loss was highly effective in helping the meticulous removal of the vitreous strands from the anterior chamber; the safety profile was high. This resulted in significant improvement in the mean postoperative CDVA compared with preoperative values (20/28 versus 20/157) (P=.0033). To our knowledge, this is the first study reporting the long-term results of this surgical technique after a follow-up of at least 12 months; previous case series5–7 report short-term outcomes only.
In none of our patients were vitreous strands left in the anterior chamber. This finding is consistent with results in previous studies4–7 that found intracameral triamcinolone acetonide was highly efficacious in allowing visualization of the vitreous body in the anterior chamber, thus facilitating its complete removal. The absence of RD after complicated cataract surgery with vitreous loss in our patients is in contrast to results in earlier studies showing a higher risk for RD after complicated cataract surgery with vitreous loss than after uncomplicated cataract surgery.3 This difference can be explained by the meticulous anterior vitrectomy performed in our patients, which may have decreased the incidence of postoperative retinal breaks and thus the incidence of rhegmatogenous RD.
Similarly, chronic pseudophakic CME is a severe complication occurring at a higher incidence after complicated cataract surgery with vitreous loss than after uncomplicated cataract surgery,2 especially when residual vitreous fibers are left in the anterior chamber.7 In the present study, postoperative topical medications to prevent and treat pseudophakic CME failed in 1 patient only. The patient was successfully treated with 2 sub-Tenon injections of triamcinolone acetonide; thus, no patient had pseudophakic CME at the last follow-up. The absence of chronic pseudophakic CME at the last examination may be explained by the use of triamcinolone acetonide, which enabled thorough anterior vitrectomy and thus decreased the incidence of pseudophakic CME; this is in addition to the therapeutic effect of triamcinolone acetonide resulting from its anti-inflammatory characteristics.7 However, randomized controlled studies are required to evaluate the efficacy of triamcinolone acetonide–assisted anterior vitrectomy in preventing pseudophakic CME.
Nevertheless, there might be a concern regarding the safety of triamcinolone acetonide–assisted anterior vitrectomy because triamcinolone acetonide left in the vitreous cavity at the end of the surgery may be associated with long-standing risk for severe complications.4–12 The delayed effect of residual triamcinolone acetonide may be related to its prolonged intraocular existence, as previously reported. Jonas et al.8 found that triamcinolone acetonide crystals may be found in the vitreous and soluble triamcinolone acetonide may be detected in the aqueous humor for 9 months or more after intravitreal injection.
One of the most fearful complications of injecting intraocular triamcinolone acetonide is development or progression of severe chronic steroid-induced glaucoma. In our study of the long-term outcomes after triamcinolone acetonide–assisted anterior vitrectomy, no patient required postoperative IOP-lowering medications except 1; this patient had been using these medications preoperatively. In addition there was no difference between the mean preoperative and postoperative IOP levels in any of the patients included (14.8 mm Hg versus 15.3 mm Hg). Similarly, Kasbekar et al.7 found no clinically significant IOP elevation 1 month and 3 months after triamcinolone acetonide–assisted anterior vitrectomy and no significant difference between the preoperative and the postoperative IOP levels. As opposed to our findings, a single study, by Angunwela et al.,6 found elevated IOP 3 months after surgery in 2 of 14 patients; 1 of them (7%) required IOP-lowering therapy. This cumulative data suggest that uncontrolled elevated IOP levels are unusual 3 months or later after triamcinolone acetonide–assisted anterior vitrectomy. More studies are required to confirm our findings.
Another important concern is the probable intraocular toxic effect of benzyl alcohol found in the vehicle of triamcinolone acetonide commercial formulations. Two laboratory studies report the possible toxicity of benzyl alcohol to corneal endothelial cells when injected into the anterior chamber. Using an in vivo rabbit model, Oh et al.16 found that intracameral injection of triamcinolone acetonide with its vector reduced the microvilli on the corneal endothelial surface, suggesting possible microstructural damage. In addition, an in vitro experimental study by Chang et al.12 showed that commercial triamcinolone acetonide suspension had a cytotoxic effect on rabbit corneal endothelial cells. On the other hand, 2 previous studies6,7 of humans did not find corneal damage 3 months after use of nonfiltered Kenalog containing benzyl alcohol during anterior vitrectomy. In keeping with these studies, no patient in our study developed corneal edema when examined 12 months or more after anterior vitrectomy with nonfiltered Kenalog, suggesting no clinical harmful effect to the corneal endothelial cells. Further clinical studies measuring the preoperative and postoperative endothelial cell counts and evaluating corneal morphology for a longer follow-up is required to validate our findings.
Furthermore, there is a concern that residual triamcinolone acetonide in the vitreous cavity after triamcinolone acetonide–assisted anterior vitrectomy may have a harmful effect on the retina because several in vitro and animal studies report probable retinal toxicity of triamcinolone acetonide and its vector.11 Nevertheless, former widespread clinical and electrophysiological studies of intravitreal triamcinolone acetonide have not shown anatomic or functional retinotoxic effect in humans.17
Moreover, sterile inflammatory reaction and endophthalmitis can occur after intravitreal injection of triamcinolone acetonide.10,18 Similar to results in previous studies,6,7 none of our patients developed such reactions after triamcinolone acetonide–assisted anterior vitrectomy, possibly because the majority of the injected triamcinolone acetonide was removed at the end of the surgery. However, in view of the low incidence of these conditions, larger case series are required to validate our findings.
This study is limited by the absence of a control group of patients who had vitrectomy without triamcinolone acetonide and lack of a randomized setting to standardize the confounding factors. However, because the use of triamcinolone acetonide for anterior vitrectomy has been regularly practiced with excellent outcomes by the surgeons participating in this study, such a randomized comparative study may not be feasible for ethical reasons.
Table 1 shows the incidence of postoperative complications in our study and in previous series of vitreous loss patients before the triamcinolone acetonide era.3,19–22 The incidence of new-onset glaucoma, persistent corneal edema, and RD was similarly low in all series. On the other hand, there is a significant variability in the incidence of CME, ranging from 0% to 21%. However, except for the series of Spigelman et al.,3 who had no cases of clinical CME, other series had an incidence of CME similar to20,22 or higher than19,21 the 13% incidence in our study. Moreover, the 2 cases of CME in our study resulted from retinal pathologies (eg, ERM and BRVO) that were not related to the cataract surgery, and there were no cases of pure chronic pseudophakic CME 12 months or more postoperatively.
Our study shows promising results of using Kenalog, a triamcinolone acetonide preparation containing benzyl alcohol preservative, to visualize the vitreous gel during anterior vitrectomy. However, Triescence, a preservative-free triamcinolone acetonide preparation, may be used for the same purpose.
In conclusion, our data suggest that triamcinolone acetonide–assisted anterior vitrectomy during complicated cataract surgery with vitreous loss is highly effective, facilitating complete removal of the prolapsed vitreous without long-term complications.
What Was Known
- Intracameral triamcinolone acetonide can be used as an adjunct for anterior vitrectomy during complicated cataract surgery with vitreous loss; however, there has been concern regarding its safety because if left in the vitreous cavity at the end of the surgery, it may cause severe long-standing ocular complications.
What This Paper Adds
- In a long-term study, intracameral triamcinolone acetonide was highly effective in helping the surgeon perform meticulous anterior vitrectomy without long-term complications such as glaucoma, inflammatory reactions, infections, or ocular toxicity.
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