Skip to main content
NIHPA Author Manuscripts logoLink to NIHPA Author Manuscripts
. Author manuscript; available in PMC: 2025 Jul 1.
Published in final edited form as: Ocul Immunol Inflamm. 2023 Apr 20;32(5):673–677. doi: 10.1080/09273948.2023.2194410

Use of Intracameral Tissue Plasminogen Activator During Uveitic Cataract Surgery

Wen F Hu 1, Tyler Etheridge 2, Marissa B Larochelle 2
PMCID: PMC10587359  NIHMSID: NIHMS1925117  PMID: 37079881

Abstract

Purpose:

To report the outcomes of intracameral tissue plasminogen activator (tPA) use during uveitic cataract surgery.

Design:

Retrospective case series from a single United States tertiary center of 36 eyes from 31 consecutive patients with established uveitis who received intraoperative intracameral tPA during cataract surgery between 2016–2020.

Results:

Mean visual acuity (VA) improved from logMAR 1.0±0.7 preoperatively to logMAR 0.7±0.8 by POM12. VA improved from baseline postoperatively (POM1 p=0.0002, POM6 p=0.006 and POM12 p=0.007). Minimal to no anterior chamber inflammation was achieved in 47.2% of eyes by POW1 and 80.0% of eyes by POM1. Mean clock-hours of posterior synechiae improved from 8.2±3.8 pre-operatively to 0.1±0.6 by POM12. Six eyes developed hyphema and/or vitreous hemorrhage, four of which resolved spontaneously.

Conclusions:

Adjunctive intracameral tPA during uveitic cataract surgery improves VA and intraocular inflammation, but risks postoperative hemorrhage. Intraoperative tPA as adjunctive anti-inflammatory therapy warrants randomized prospective studies.

Introduction

Uveitis is a heterogenous group of inflammatory eye disorders. Both uveitis and its first-line treatment, steroid therapy, accelerate cataract formation. Controlling intraocular inflammation peri-operatively is critical for patients with uveitis undergoing cataract surgery, as surgery exacerbates inflammation in these eyes already at high risk of postoperative inflammation.

Tissue plasminogen activator (tPA) is a serine protease that cleaves plasminogen to form plasmin during fibrinolysis. tPA is produced by multiple ocular tissues1, with concentrations in the aqueous humor 30 times greater than plasma2. Following cataract surgery, tPA levels decrease, which has been surmised to contribute to postoperative inflammation and fibrin formation3.

tPA has been used as an adjunctive postoperative therapy to treat severe intraocular inflammation and fibrin after adult and pediatric cataract surgery46 and retina surgery7. However, there are limited reports on its use at the time of cataract surgery8, or in patients with uveitis9. We report the first case series of intraoperative intracameral tPA use during uveitic cataract surgery.

Methods

A single institution retrospective chart review was conducted to identify patients with uveitis who received intracameral tPA during cataract surgery. Institutional review board approval was obtained from the University of Utah Human Subjects Division (IRB 00136659). The research described adheres to the tenets of the Declaration of Helsinki. Under the guidelines of the IRB, informed consent was not necessary for this retrospective review. Surgeries were performed by four anterior segment surgeons between 2015–2021. Thirty-six eyes from 31 patients met inclusion criteria. Thirty-two eyes completed 12 months of follow-up. Surgical data collected included cataract extraction surgical technique, additional surgical procedures performed, type and location of intraocular lens implantation, use of iris expansion devices or capsular tension ring, use of intracameral antibiotics and dose of intracameral tPA administered. Clinical data including uveitis diagnosis, anatomical uveitis subtype, presence of other ocular diseases, best corrected visual acuity, intraocular pressure, anterior chamber cell grade, vitreous haze grade, extent of posterior synechiae, systemic medications, topical medications, ocular surgeries or procedures, were collected at the most recent clinic visit prior to surgery and during postoperative week 1 (POW1), postoperative month 1 (POM1), postoperative month 6 (POM6) and postoperative month 12 (POM12).

Results

Thirty-six eyes from 31 patients were included (Table 1). Mean age was 36.3 years. Anterior uveitis was the most common anatomical subtype (66.7%). Of eyes with anterior uveitis, 58.3% carried a concomitant diagnosis of intermediate or posterior uveitis. Twenty-five percent of eyes had panuveitis. The most common etiology was idiopathic (41.7%), followed by HLA-B27-associated uveitis (16.7%) and sarcoidosis (16.7%). Mean duration of disease quiescence prior to surgery was 5.8 months. Over 90% of eyes had coexisting ocular disease or structural complication, with cystoid macular edema (50.0%), glaucoma (19.4%), and epiretinal membrane (19.4%) being the most common. Twenty-four (66.8%) eyes were on at least one steroid-sparing immunomodulatory therapy. Mean oral prednisone equivalent was 4.9 mg/day and topical prednisolone equivalent was 1.0 drop/day pre-operatively. Ten eyes were on intraocular pressure (IOP)-lowering drops pre-operatively.

Table 1.

Preoperative and intraoperative population data.

Age, mean ± SD 36.3 ± 19.9
Female, number (%) 18 (58.1)
Ethnicity, number (%)
White or Caucasian 19 (61.3)
Hispanic or Latino 6 (19.4)
Black or African American 4 (12.9)
Asian or Pacific Islander 2 (6.4)
Eye laterality, number (%)
Right 14 (38.9)
Left 22 (61.1)
Anatomical Subtype of Uveitis, number (%)
Anterior 24 (66.7)
Intermediate 14 (38.9)
Posterior 3 (8.3)
Panuveitis 9 (25.0)
Diagnosis, number (%)
Idiopathic 15 (41.7)
HLA-B27 6 (16.7)
Sarcoidosis 6 (16.7)
Herpetic/viral 4 (11.1)
Juvenile idiopathic arthritis 2 (5.6)
Tubulointerstitial nephritis and uveitis 1 (2.8)
Syphilis 1 (2.8)
Vogt-Koyanagi-Harada 1 (2.8)
Nodular scleritis and Peripheral ulcerative keratitis associated with granulomatosis with polyangitis 1 (2.8)
MEK-inhibitor associated Vogt-Koyanagi-Harada like syndrome 1 (2.8)
Months of disease quiescence prior to surgery, mean ± SD 5.8 ± 4.7
Other ocular disease, number (%)
Cystoid macular edema 18 (50.0)
Epiretinal membrane 7 (19.4)
Glaucoma 7 (19.4)
Ocular hypertension or steroid response 5 (13.9)
Band keratopathy 3 (8.3)
Narrow angles or angle closure 3 (8.3)
Pupillary membrane or fibrosis 3 (8.3)
Retinal detachment 2 (5.6)
Proliferative diabetic retinopathy 1 (2.8)
Previous ocular procedures, number (%)
Local steroid injection 12 (33.3)
Peripheral iridotomy 5 (13.9)
Glaucoma drainage implant 3 (8.3)
Pars plana vitrectomy 2 (5.6)
Immunomodulatory therapy
Antimetabolite 23 (63.9)
  Methotrexate 17 (73.9)
  Mycophenolate 6 (26.1)
T cell inhibitor 4 (11.1)
  Cyclosporine 3 (75.0)
  Tacrolimus 1 (25.0)
TNF alpha inhibitor 12 (33.3)
  Adalimumab 11 (91.7)
  Infliximab 1 (8.3)
Other biologic 3 (8.3)
  Rituximab 3 (100.0)
Perioperative steroid(s)
Systemic steroids, number (%) 31 (86.1)
  Oral prednisone equivalent mg/day, mean ± SD 45.1 ± 23.2
  Intravenous methylprednisolone 125mg (intraoperative one-time dose), number (%) 2 (5.6)
Local steroid(s), number (%) 14 (38.9)
  Subtenon’s triamcinolone 7 (19.4)
  Intravitreal dexamethasone implant 5 (13.9)
  Intravitreal triamcinolone 2 (5.6)
Topical prednisolone equivalent drops/day, mean ± SD 3.5 ± 2.1
Cataract type, number (%)
Nuclear sclerotic 20 (55.6)
Posterior subcapsular 28 (77.8)
Cortical 4 (11.1)
Other 2 (5.6)
Unknown 2 (5.6)
Surgical procedure, number (%)
Phacoemulsification 36 (100.0)
With synechiolysis, number (%) 34 (94.4)
With combined pars plana vitrectomy with endolaser, number (%) 12 (33.3)
With combined pars plana vitrectomy without endolaser, number (%) 7 (19.4)
Intraocular lens material, number (%)
Acrylic 36 (100.0)
Intraocular lens implanted location, number (%)
Capsular bag 34 (94.4)
Sulcus 2 (5.6)
Iris expansion device 30 (83.3)
Iris hooks 17 (47.2)
Malyugin ring 22 (61.1)
Capsular tension ring, number (%) 3 (8.3)
Intracameral antibiotics, number (%) 35 (97.2)
tPA dose, number (%)
12.5 μg 18 (50.0)
25 μg 18 (50.0)
Complications, number (%)
Anterior capsular tear without posterior extension 1 (2.9)
Posterior capsular tear 1 (2.9)

Abbreviations: SD, standard deviation; tPA, tissue plasminogen activator

Beginning 1 week prior to surgery, patients were treated aggressively with systemic, local, and/or topical steroids and NSAIDs to control inflammation. Thirty-one eyes (86.1%) received peri-operative systemic steroids, with a mean oral prednisone equivalent dose of 45.1 mg/day. Peri-operative local steroid injections were administered prior to or during surgery in 14 eyes (38.9%). Mean topical prednisolone equivalent dose was 3.5 drops/day, and ketorolac equivalent dose was 2.7 drops/day.

Surgery was performed using phacoemulsification. Posterior synechiolysis was performed in 94.4% of cases. Thirty patients (83.3%) required use of an iris expansion device. A capsular tension ring was placed in 3 cases (8.3%) due to diffuse zonular weakness. Two surgeries experienced complications, including one anterior (2.8%), and one posterior capsular tear (2.8%). Over half of surgeries (52.8%) were combined with planned pars plana vitrectomy (PPV) due to concomitant intermediate or posterior uveitis. tPA was injected intracamerally at the conclusion of surgery. The dose administered (12.5 μg (50.0%) or 25 μg (50.0%)) was at the discretion of the surgeon.

Postoperatively, patients were followed for 12 months (Table 2). Pre-operatively, mean logMAR best corrected visual acuity (BCVA) was 1.0 (Snellen 20/200), which improved to logMAR 0.7 (Snellen 20/100) by POM12. The greatest improvement in BCVA was achieved at POM1 with an average BCVA of logMAR 0.5 (Snellen 20/60). Improvement in BCVA after surgery was statistically significant across time (p=0.0002, mixed effects ANOVA); multiple comparisons test showed sustained improvement from baseline postoperatively (Figure 1a. POM1 p=0.0002, POM6 p=0.006 and POM12 p=0.007). Preoperatively, five eyes (13.9%) had a BCVA of ≤0.3 logMAR (Snellen 20/40), which improved to 50% of eyes at POM12 (Figure 1b). Ocular hypertension was reported in 27.6% of eyes during POW1, coinciding with a transient increase in IOP lowering agent use at POW1 that was not statistically significant (Figure 2a, one way ANOVA p=0.08). Postoperative mean IOP remained stable compared to preoperative IOP (Figure 2b, p=0.67 mixed effects ANOVA).

Table 2.

Preoperative and postoperative population data.

Preoperative Postoperative
Week 1 Month 1 Month 6 Month 12
Number of eyes 36 36 35 28 32
BCVA (logMAR), mean ± SD 1.0 ± 0.7 0.8 ± 0.8 0.5 ± 0.6 0.7 ± 0.8 0.7 ± 0.8
BCVA (logMAR), number (%)
≤0.3 (Snellen 20/40 or better) 5 (13.9) 16 (44.4) 18 (51.4) 13 (46.4) 17 (53.1)
0.4–0.7 (Snellen 20/50 to 20/100) 12 (33.3) 9 (25.0) 6 (17.1) 8 (28.6) 5 (15.6)
0.8–1.2 (Snellen 20/125 to 20/300) 6 (16.7) 3 (8.4) 6 (17.1) 2 (7.1) 2 (6.3)
≥1.3 (20/400 or worse) 13 (36.1) 8 (22.2) 5 (14.4) 5 (17.9) 8 (25.0)
IOP (mmHg), mean ± SD 15.0 ± 5.2 14.5 ± 7.5 13.6 ± 4.3 14.9 ± 4.9 14.6 ± 4.6
Number of IOP lowering medication(s), mean ± SD 0.6 ± 1.0 1.1 ± 1.1 0.6 ± 1.0 0.4 ± 0.9 0.5 ± 1.1
Anterior chamber cell grade, number (%)
0 28 (77.8) 9 (25.0) 16 (45.7) 14 (50.0) 17 (53.1)
0.5 5 (13.9) 8 (22.2) 12 (34.3) 9 (32.1) 7 (21.9)
≥1 2 (5.6) 17 (47.2) 6 (17.2) 4 (14.3) 7 (25.0)
Unknown 1 (2.8) 2 (5.6) 1 (2.9) 1 (3.6) 0 (0)
Vitreous haze grade, number (%)
0 19 (54.3) 27 (75.0) 32 (91.4) 23 (82.1) 24 (75.0)
0.5 2 (5.7) 0 (0) 0 (0) 1 (3.6) 2 (6.3)
≥1 1 (2.9) 1 (2.8) 0 (0) 1 (3.6) 3 (9.4)
Unknown 13 (37.1) 9 (22.2) 3 (8.6) 3 (10.7) 3 (9.4)
Posterior synechiae (clock hours), mean ± SD 8.2 ± 3.8 0.2 ± 1.0 0.2 ± 1.0 0.2 ± 0.6 0.1 ± 0.6
Other clinical signs of intraocular inflammation, number (%)
Anterior chamber fibrin - 3 (8.3) 1 (2.9) 1 (3.6) 0 (0)
Pupillary membrane - 3 (8.3) 1 (2.9) 0 (0) 0 (0)
Keratic precipitates - 0 (0) 0 (0) 1 (3.6) 2 (6.3)
IOL precipitates - 0 (0) 1 (2.9) 4 (14.3) 3 (9.4)
Cystoid macular edema 18 (50.0) 2 (5.6) 13 (37.1) 6 (21.4) 5 (15.6)
  Central macular thickness (μm)*, mean ± SD 340.8 ± 142.8 644.0 ± 533.2 481.5 ± 214.4 517.7 ± 247.4 461.6 ± 122.2
Oral prednisone equivalent mg/day, mean ± SD 4.9 ± 11.4 34.9 ± 21.3 10.9 ± 16.2 6.3 ± 15.1 2.7 ± 7.3
Topical prednisolone equivalent drops/day, mean ± SD 1.0 ± 1.2 4.4 ± 2.3 2.0 ± 1.6 1.7 ± 2.0 0.6 ± 0.9
Topical ketorolac equivalent drops/day, mean ± SD 0.1 + 0.5 2.4 ± 1.9 1.0 ± 1.5 0.1 ± 0.8 0.1 ± 0.5
New ocular diseases, number (%)
Ocular hypertension - 10 (27.8) 2 (5.9) 0 (0) 1 (3.1)
Retinal detachment - 0 (0) 1 (2.9) 1 (3.6) 1 (3.1)
Hyphema/hemorrhage - 6 (16.7) 1 (2.9) 0 (0) 1 (3.1)
Hypotony 4 (11.1) 0 (0) 0 (0) 0 (0)
New ocular procedures, number (%) -
Intracameral tPA - 2 (5.6) 0 (0) 0 (0) 0 (0)
Anterior chamber paracentesis - 1 (2.8) 0 (0) 0 (0) 0 (0)
Pars plana vitrectomy - 0 (0) 1 (2.9) 2 (7.2) 1 (3.1)
IOL repositioning 0 (0) 2 (5.9) 0 (0) 2 (6.2)

Abbreviations: IOP, intraocular pressure; SD, standard deviation; tPA, tissue plasminogen activator

*

Postoperative central macular thickness was only obtained from eyes with cystoid macular edema

Figure 1. Preoperative and postoperative visual acuity.

Figure 1.

(A) Mean logMAR best corrected visual acuity (BCVA) improved with time (mixed effects ANOVA, p=0.0002). BCVA at postoperative time points improved compared to preoperative baseline (multiple comparisons test POM1 p=0.0002, POM6 p=0.006 and POM12 p=0.007). Error bars represent standard error of the mean. (B) Distribution of pre-operative and postoperative BCVA.

Figure 2. Preoperative and postoperative intraocular pressure.

Figure 2.

(A) Mean number of IOP-lowering agents increased transiently at POW1 but was not statistically significant (one way ANOVA, p=0.08). (B) Mean IOP (mmHg) did not vary by visit (mixed effects ANOVA, p=0.67. Error bars represent standard error of the mean.

Prior to surgery, almost all eyes (91.7%) had minimal anterior chamber (AC) cell (grade ≤0.5). At POW1, 47.2% achieved AC cell grade of ≤0.5, and by POM1, 80.0% achieved AC cell grade of ≤0.5, which remained stable through POM12 (Figure 3a). Two eyes underwent repeat intracameral tPA injection at POW1 for fibrin formation. Pre-operatively, 60.0% of eyes had a vitreous haze grade of ≤0.5, which improved to 81.3% at POM12 (Figure 3b). Pre-operatively, mean posterior synechiae was 8.2 clock hours, which improved to 0.1 clock hours at POM12 (Figure 3c). Improvement in posterior synechiae after surgery was sustained over time (mixed effects ANOVA, p<0.0001; multiple comparisons test p<0.0001 at POW1, POM1, POM6, POM12 compared to preoperatively). Two eyes exhibited posterior synechiae at POM12. One eye returned to surgery at POM12 for worsening posterior synechiae causing IOL tilt, iris chafing and persistent inflammation.

Figure 3. Preoperative and postoperative inflammation.

Figure 3.

(A) Anterior chamber (AC) cell grade categorized by a grade of 0 or 0.5 and ≥1 across visits. (B) Vitreous cell grade categorized by a grade of 0 or 0.5 and ≥1 by visit. (C) Average clock hours of posterior synechiae improved after surgery (mixed effects ANOVA, p<0.0001), at all post-operative time points compared to pre-operative baseline (multiple comparisons test p<0.0001 at POW1, POM1, POM6, POM12).

Six eyes (16.7%) experienced hyphema or postoperative hemorrhage during POW1, two of which were associated with vitreous hemorrhage. All 6 eyes had undergone combined cataract surgery and pars plana vitrectomy procedures. Five of the eyes received tPA at a dose of 12.5ug; one eye received tPA at a dose of 25ug. Four cases of hyphema resolved spontaneously. One eye was found to have iris chafing from a mal-placed haptic in the sulcus; the hyphema and vitreous hemorrhage resolved after surgical re-positioning. One eye underwent PPV for nonclearing vitreous hemorrhage. Other cases of return to surgery included a rotated toric lens at POM1, and proliferative vitreoretinopathy, macula-on retinal detachment, and IOL dislocation, all after POM6.

Discussion

In this retrospective case series, we report the surgical outcomes of intraoperative intracameral tPA use at the time of cataract surgery in patients with uveitis. We show that best corrected visual acuity and multiple indicators of intraocular inflammation improved after cataract surgery with our peri-operative anti-inflammatory regimen that includes intracameral tPA at the conclusion of cataract surgery.

Patients with uveitis are at high risk for postoperative inflammation, and our population has a propensity towards severe inflammation, as indicated by the large percentage of eyes with extensive posterior synechiae, concomitant intermediate, posterior or panuveitis, and disease necessitating systemic immunosuppression. Nearly all eyes required posterior synechiolysis and iris manipulation during surgery, which further exacerbates postoperative inflammation10.

We undertook an aggressive approach to control postoperative inflammation, utilizing perioperative systemic or local steroids, and intraoperative intracameral tPA. Our data show that cataract surgery with tPA in this population improves BCVA. A slightly lower percentage of patients achieved BCVA ≤0.3 logMAR compared to prior published reports11,12, likely attributed to the higher disease severity in our cohort. tPA is not associated with a sustained increase in IOP or IOP-lowering drug requirement in our series, similar to prior reports8.

Anterior chamber inflammation was most active during POW1, as expected. Despite this, almost half of eyes achieved minimal to no AC inflammation at POW1, which further improved by POM1. Vitreous haze also improved, likely augmented by the effects of vitrectomy. Importantly, re-formation of posterior synechiae was rare, with only two eyes developing recurrent synechiae. One patient required adjunctive intracameral tPA at POW1 and due to poor medication adherence and follow-up, required re-operation to release posterior synechiae causing IOL tilt and iris chafing.

There were several cases of hyphema with or without vitreous hemorrhage in the early postoperative period. This is within the range of previously reported rates when tPA is administered postoperatively1315. In four of the six eyes, the hyphema resolved spontaneously by POM1, although two eyes did require additional surgery to clear vitreous hemorrhage. Future studies are necessary to determine whether intracameral tPA at the time of surgery increases the risk of postoperative hyphema and hemorrhage.

Limitations to this study include its retrospective nature, the heterogenous patient population, and the nonrandomized selection of patients. Future randomized prospective studies are warranted to more clearly assess the effect of tPA on surgical outcomes.

Funding Details

This research was supported in part by Unrestricted Grants from Research to Prevent Blindness, New York, NY, to the Department of Ophthalmology & Visual Sciences, University of Utah, and to the Flaum Eye Institute at the University of Rochester. WFH was supported by a Heed Ophthalmic Foundation Fellowship.

Footnotes

Disclosure Statement

The authors report there are no competing interests to declare.

References

  • 1.Geanon JD, Tripathi BJ, Tripathi RC, Barlow GH. Tissue plasminogen activator in avascular tissues of the eye: a quantitative study of its activity in the cornea, lens, and aqueous and vitreous humors of dog, calf, and monkey. Exp Eye Res. 1987;44(1):55–63. doi: 10.1016/s0014-4835(87)80025-8 [DOI] [PubMed] [Google Scholar]
  • 2.Tripathi RC, Park JK, Tripathi BJ, Millard CB. Tissue Plasminogen Activator in Human Aqueous Humor and Its Possible Therapeutic Significance. Am J Ophthalmol. 1988;106(6):719–722. doi: 10.1016/0002-9394(88)90707-6 [DOI] [PubMed] [Google Scholar]
  • 3.Yoshitomi F, Utsumi E, Hayashi M, Futenma M, Yamada R, Yamada S. Postoperative fluctuations of tissue plasminogen activator (t-PA) in aqueous humor of pseudophakes. J Cataract Refract Surg. 1991;17(5):543–546. doi: 10.1016/s0886-3350(13)81039-5 [DOI] [PubMed] [Google Scholar]
  • 4.Dotan A, Kaiserman I, Kremer I, Ehrlich R, Bahar I. Intracameral recombinant tissue plasminogen activator (r-tPA) for refractory toxic anterior segment syndrome. Br J Ophthalmol. 2014;98(2):252–255. doi: 10.1136/bjophthalmol-2013-304294 [DOI] [PubMed] [Google Scholar]
  • 5.Mehta JS, Adams GG. Recombinant tissue plasminogen activator following paediatric cataract surgery. Br J Ophthalmol. 2000;84(9):983–986. doi: 10.1136/bjo.84.9.983 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 6.Heiligenhaus A, Steinmetz B, Lapuente R, et al. Recombinant tissue plasminogen activator in cases with fibrin formation after cataract surgery: a prospective randomised multicentre study. Br J Ophthalmol. 1998;82(7):810–815. doi: 10.1136/bjo.82.7.810 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 7.Jaffe GJ, Abrams GW, Williams GA, Han DP. Tissue plasminogen activator for postvitrectomy fibrin formation. Ophthalmology. 1990;97(2):184–189. doi: 10.1016/s0161-6420(90)32618-0 [DOI] [PubMed] [Google Scholar]
  • 8.Siatiri H, Beheshtnezhad AH, Asghari H, Siatiri N, Moghimi S, Piri N. Intracameral tissue plasminogen activator to prevent severe fibrinous effusion after congenital cataract surgery. Br J Ophthalmol. 2005;89(11):1458–1461. doi: 10.1136/bjo.2005.071407 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 9.Lerner LE, Patil AJ, Kenney MC, Minckler D. Use of intraocular human recombinant tissue plasminogen activator as an adjunct treatment of posterior synechiae in patients with uveitis. Retin Cases Brief Rep. 2012;6(3):290–293. doi: 10.1097/icb.0b013e31822a2f4f [DOI] [PubMed] [Google Scholar]
  • 10.Williams ER, Patnaik JL, Miller DC, et al. Iris manipulation during phacoemulsification: intraoperative and postoperative complications. Int J Ophthalmol-chi. 2021;14(5):676–683. doi: 10.18240/ijo.2021.05.06 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 11.Mehta S, Linton MM, Kempen JH. Outcomes of cataract surgery in patients with uveitis: a systematic review and meta-analysis. Am J Ophthalmol. 2014;158(4):676–692.e7. doi: 10.1016/j.ajo.2014.06.018 [DOI] [PubMed] [Google Scholar]
  • 12.Ozates S, Berker N, Ozdal PC, Erol YO. Phacoemulsification in patients with uveitis: long-term outcomes. BMC Ophthalmol. 2020;20(1):109–8. doi: 10.1186/s12886-020-01373-5 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 13.Wedrich A, Menapace R, Ries E, Polzer I. Intracameral tissue plasminogen activator to treat severe fibrinous effusion after cataract surgery. J Cataract Refract Surg. 1997;23(6):873–877. doi: 10.1016/s0886-3350(97)80246-5 [DOI] [PubMed] [Google Scholar]
  • 14.Rehfeldt K, Höh H. [Therapeutic and prophylactic application of TPA (recombinant tissue plasminogen activator) into the anterior chamber of the eye]. Ophthalmologe. 1999;96(9):587–593. doi: 10.1007/s003470050457 [DOI] [PubMed] [Google Scholar]
  • 15.Wedrich A, Menapace R, Mühlbauer-Ries E. The use of recombinant tissue plasminogen activator for intracameral fibrinolysis following cataract surgery. Int Ophthalmol. 1994;18(5):277–280. doi: 10.1007/bf00917830 [DOI] [PubMed] [Google Scholar]

RESOURCES