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Postcataract surgical inflammation

Taravati, Parisa; Lam, Deborah L.; Leveque, Thellea; Van Gelder, Russell N.

Current Opinion in Ophthalmology: January 2012 - Volume 23 - Issue 1 - p 12–18
doi: 10.1097/ICU.0b013e32834cd60e

Purpose of review To describe the epidemiology, pathogenesis, and recent developments in the diagnosis and management of postcataract surgery inflammation.

Recent findings In patients with pre-existing uveitis, control of inflammation with topical and/or systemic therapy for 3 months preoperatively continues to be important in lessening the risk of postoperative inflammation and complications. During cataract surgery, intraocular lens selection in these patients is important. Recent literature suggests that modern intraocular lenses (IOLs), particularly hydrophilic or hydrophobic acrylic lenses, generally have good uveal biocompatibility in uveitic patients. The postoperative course can be complicated by inflammation and cystoid macular edema (CME), and in uveitic patients, intensive perioperative steroid treatment can lessen these complications. Recent studies show that in uveitic patients, the improvement in CME and inflammation after intravitreal triamcinolone is better than after orbital floor triamcinolone injection, but that a single intraoperative orbital floor injection of triamcinolone is as effective as a 4-week course of postoperative oral prednisolone. Although postoperative inflammation in uveitic patients may be due to recurrence of uveitis, one must recognize other important potential causes of postoperative inflammation and treat accordingly.

Summary Most patients with postcataract inflammation have good visual outcomes provided that the cause is recognized and that there is adequate perioperative planning in patients predisposed to inflammation.

Department of Ophthalmology, University of Washington School of Medicine, Seattle, Washington, USA

Correspondence to Parisa Taravati, MD, Department of Ophthalmology, UW Medicine Eye Institute, Campus Box 359608, 325 9th Avenue, Seattle, WA 98104, USA. Tel: +1 206 543 7250; fax: +1 206 543 4414; e-mail:

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Although postoperative inflammation following cataract surgery is a typical occurrence, it is usually easily managed and of limited clinical impact. However, in a subset of patients, postoperative inflammation can be severe and/or prolonged, causing visual disability and requiring aggressive and sometimes extended therapy. In this review, we will detail the causes of postoperative inflammation, discuss approaches to minimize this inflammation, and discuss appropriate workup and management of patients with various etiologies of postoperative inflammation.

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Normal postcataract surgical inflammation is thought to be due to the breakdown of the blood aqueous barrier (BAB). This inflammation reaches a peak within the first few postoperative days and then decreases over 2–3 weeks after surgery [1]. Studies of the natural history of untreated cataract surgery show a mean anterior chamber cell grade of 2+ on postoperative day 1 and of 1+ on postoperative day 15 [2,3]. In routine phacoemulsification cataract extraction and intraocular lens implantation with use of topical corticosteroids, most eyes have little inflammation after 4 weeks. However, in extracapsular cataract extraction with a large wound and manual expression of the nucleus, there may be visible inflammation for up to 8 weeks. Diabetic patients may show more prolonged postoperative inflammation due to increased compromise of the BAB [4]. Complicated cataract surgery may also have more postoperative inflammation than routine phacoemulsification. Surgical factors such as longer operative times, prior surgery, extensive procedures, intraoperative complications, and younger patient age may be associated with increased postoperative inflammation [5▪].

Box 1

Box 1

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Acute postoperative inflammation

Severe inflammation presenting in the immediate postoperative period (up to 96 h after surgery) will generally have one of four causes: acute postoperative endophthalmitis, toxic anterior segment syndrome (TASS), lens-induced uveitis, or reactivation of underlying uveitic disease.

Acute postoperative endophthalmitis, which is defined as occurring within 6 weeks after cataract surgery, should always be considered in the differential diagnosis of postoperative inflammation. In a recent retrospective observational case series by Al-Mezaine et al.[1] of patients who present with acute postoperative endophthalmitis, the 10-year incidence was 0.067%: 0.085% for phacoemulsification and 0.049% for extracapsular cataract extraction. The onset of presentation was within 2 weeks of cataract surgery in 55% and 3 or more weeks after surgery in 45%. Of the 20 patients with endophthalmitis, only one presented with visual acuity better than 20/200. In addition to poor vision, the most common presenting clinical features were ocular pain in 95%, poor red reflex in 90%, hypopyon in 70%, chemosis in 60%, lid edema in 50%, corneal edema in 40%, and vitritis and purulent discharge in 25%. Retinal periphlebitis can be the earliest sign [6]. In the Endophthalmitis Vitrectomy Study (EVS), 94.3% of patients had blurred vision, 82.1% had red eye, 74% had pain, and 34.5% had eyelid swelling. On baseline examination, 85% had hypopyon, 79% had media haze obscuring retinal vessels, and 26% had light perception only vision [2].

Acute postoperative endophthalmitis is usually diagnosed by vitreous culture, although up to 30% of cases may be culture-negative [2]. In the series by Al-Mezaine et al. [1], culture results showed that 35% of cases were positive for Staphylococcus species (Staphylococcus epidermidis and Staphylococcus aureus), 35% were positive for Streptococcus species (Streptococcus pneumonia, Streptococcus viridans, Streptococcus oralis, and Streptococcus salivarius), 15% of cases were positive for polymicrobial or mixed infections, and 5% were positive for Propionibacterium acnes. In the EVS, 94.2% of culture-confirmed cases involved Gram-positive bacteria, with 70% of isolates being Gram-positive, coagulase-negative staphylococci (CNS), 9.9% S. aureus, 9.0% Streptococcus species, and 2.2% Enterococcus species. Gram-negative species made up 5.9% of isolates. Evidence-based management of postoperative endophthalmitis is largely guided by the EVS, which demonstrated equivalent outcomes for intravitreal antibiotics or pars plana vitrectomy with antibiotics for patients with hand-motions or better presenting vision, but superior outcomes with vitrectomy for patients who were light perception or worse. Even in this latter group, 56% of patients achieved 20/100 or better vision with vitrectomy treatment [2].

TASS is a sterile inflammatory reaction that generally occurs within 12–48 h after surgery. TASS can be difficult to distinguish from acute bacterial endophthalmitis; however, TASS usually has an earlier onset, often within 24 h after cataract surgery, whereas endophthalmitis usually occurs approximately 4–7 days after surgery. TASS also is usually limited to the anterior chamber without substantial vitritis. Patients with TASS usually present with blurred vision without pain, but patients with endophthalmitis often have pain associated with decreased vision. Common clinical features of TASS include diffuse corneal edema from toxic injury to the corneal endothelium, a marked anterior chamber inflammatory response, often resulting in hypopyon and fibrin formation in the anterior chamber, irregularity or dilation of the pupil, iris transillumination defects, and glaucoma due to trabecular meshwork damage. Many possible causes of TASS have been identified and include endotoxin, denatured ophthalmic viscoelastic devices, preservatives, heavy-metal residue, fine-matter particulates, free radicals in intracameral preparations, and residue from cleaning and sterilization of ophthalmic instruments, and generic Trypan blue [7▪▪,8▪,9▪,10–14]. Most reports of TASS have been in adults, but Huang et al.[15▪] reported a pediatric case of TASS. TASS is typically treated with intensive topical and/or systemic corticosteroids. A recent retrospective case series of TASS cases at Aravind Eye Hospital from 2008 to 2009 showed that TASS is often associated with a good visual outcome. Of the patients with at least 6 months of follow-up following TASS, 25% of eyes had patchy iris atrophic changes with pupil distortion, 4% had cystoid macular edema (CME), 12.5% developed anterior capsular phimosis, 16.6% developed posterior capsular opacification (PCO), 16.6% had a combination of these complications, and 41.6% did not have any complications attributable to TASS. None developed corneal endothelial decompensation or secondary glaucoma [16▪]. TASS cases will often occur in clusters. Once a TASS diagnosis is made, surgery at the affected center should be suspended and a thorough investigation should be undertaken to identify the cause for the cases.

Retained nuclear or cortical fragments after phacoemulsification can be highly immunogenic. The term phacoanaphylactic uveitis has been used to describe this phenomenon although the term ‘lens-induced uveitis’ is now the preferred descriptor (as this form of uveitis is not technically anaphylactic). The level of inflammation is variable and may be dependent upon the amount of lens material left behind. An antigenic response to the lens material occurs, resulting in zonal granulomatous inflammation, with macrophages surrounding polymorphonuclear leukocyte infiltration around the lens. Symptom onset is usually within 2 weeks after surgery, although this can also be present up to a year later in the postoperative course [7▪▪]. Ultrasound biomicroscopy (UBM) can be helpful in cases where retained lens material is suspected but not easily visible. In a series evaluating chronic noninfectious pseudophakic uveitis, UBM showed that 24% of eyes had at least one lens remnant, and 11% of eyes had a number of lens remnants [14]. Gonioscopy can be invaluable in identifying nuclear material lodged in the angle of the anterior chamber. Severe lens-induced postoperative uveitis is frequently refractory to medical therapy with corticosteroids and requires surgical removal of the offending lens fragments [8▪,15▪].

Patients with preoperative uveitis are at higher risk of postoperative inflammation (both acute and chronic). Complication rates for cataract surgery in the setting of known uveitis are significantly higher than in cataract surgery for otherwise unaffected eyes. In a retrospective series of 39 eyes at the Cleveland Clinic, posterior capsule opacification occurred in 24 eyes (62%), recurrence of uveitis (41%), CME (33%), epiretinal membrane formation (15%), and posterior synechiae (8%) [17,18▪]. Control of inflammation using topical and/or systemic therapy for a minimum of 3 months preoperatively has been shown to lessen the risk of postoperative inflammation and complication in this population [19]. Generally, even in patients with controlled inflammation, it is appropriate to treat prophylactically with increased topical and systemic corticosteroids (typically 0.5–1.0 mg/kg) for several days prior to surgery, and taper medication postoperatively depending on observed inflammation.

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Chronic postoperative inflammation

The causes of chronic postoperative inflammation are broadly similar to those for acute disease, including infection and lens-related inflammation. Additionally, mechanical iritis may result in chronic inflammation following surgery.

Chronic endophthalmitis is defined as intraocular infection occurring greater than 6–12 weeks postoperatively. Infectious chronic endophthalmitis must always be considered, particularly in cases presenting with significant vitritis or visible capsular plaque. The incidence of this complication is about 0.02% after cataract surgery [20]. Common causes are: P. acnes, S. epidermidis, aerobic streptococci, Actinomyces, and fungi such as Candida parapsilosis. In one recent study, the mean time between cataract surgery and diagnosis of chronic pseudophakic endophthalmitis was 5 ± 2.48 months. Infection by P. acnes was the most common cause of delayed-onset pseudophakic endophthalmitis (41.2% of cases) and had the most favorable visual outcome, whereas fungal endophthalmitis (17.6% of cases) had worse visual prognosis [13]. Similarly, in a series by Aldave et al.[4], the average period between cataract extraction and onset of signs and symptoms of P. acnes was 18 weeks.

Propionibacterium acnes endophthalmitis after cataract extraction can be difficult to diagnose because it presents as a low-grade uveitis with latent onset, initially responds to topical steroids, and often lacks typical endophthalmitis signs and symptoms, such as pain, conjunctival chemosis, and injection. Because the P. acnes organisms are sequestered in the capsular bag (may be visible as a white intracapsular plaque), this endophthalmitis is often associated with recurrence after standard endophthalmitis treatment, and may be triggered following laser capsulotomy. In the series by Aldave et al.[4], the most common presenting features of P. acnes endophthalmitis were decreased vision (100%), anterior chamber reaction (80%), vitreous cells (52%), a white intracapsular plaque (40%), hypopyon (36%), and pain (33%). In a study by Clark et al. [3], 89% of cases presented with a white intracapsular plaque, and the remaining 11% had chronic granulomatous inflammation. All patients demonstrated conjunctival injection and vitreous inflammation, and the majority had keratic precipitates (81%). Hypopyon was only present in only 31% of patients.

Chronic pseudophakic endophthalmitis is often diagnosed by aqueous and/or vitreous cultures; however, there can be culture-negative cases which are responsive to antibiotic therapy, and these are also presumed to be infectious in etiology. PCR diagnostics have higher sensitivity for detection of P. acnes than does traditional culture, but are not widely available [21]. Laser flare photometry may be helpful in determining when chronic postoperative inflammation is infectious in cause. Notably, eyes that were treated with systemic antibiotics showed a significant decrease in mean flare values after 2 weeks of treatment, whereas topical treatment of the inflammation was ineffective in reducing the flare values [12].

Treatment of chronic P. acnes endophthalmitis with intravitreal antibiotics has a high failure rate; definitive treatment frequently requires explanation of lens and capsule along with intraocular antibiotic therapy [22]. Similarly, delayed onset fungal endophthalmitis may fail medical therapy and require surgical debridement and removal of lens and capsule [23].

Mechanical lens-related causes may be the most common reason for postoperative chronic inflammation. In one series [12], 69% of eyes with chronic postoperative uveitis had misplaced intraocular lens haptics touching the iris/iris root, ciliary body, or the ciliary body/iris junction. Of posterior chamber intraocular lenses (IOLs) with misplaced haptics, most were placed in the sulcus rather than in the capsular bag. Of those eyes with chronic pseudophakic uveitis with an anterior chamber intraocular lens, 63% had misplaced lens haptics [14].

Classically, uveitis–glaucoma–hyphema (UGH) syndrome was described as anterior chamber lens causing inflammation or hyphema from abnormal contact of the angle structures or folding of the iris, and was particularly associated with closed-loop haptics which are no longer in use. With declining utilization of anterior chamber lenses, most cases of UGH syndrome are associated with posterior chamber lenses placed in the ciliary sulcus. Usually three piece IOLs are well tolerated in the sulcus, but these can cause inflammation and hemorrhage if the haptics rub on the iris or ciliary body [9▪,24–26]. Single piece acrylic IOLs should not be placed in the sulcus. When these IOLs are placed in the sulcus, the sharp optic edges and thick haptics can chafe the posterior iris pigment [27▪]. Capture of the lens optic in the pupil may also be associated with inflammation due to mechanical contact. Other mechanical issues such as the iris or vitreous to the wound are likely to induce inflammation and CME. In a small series of nine eyes with complete or incomplete UGH syndrome, UBM showed that all patients had malpositioned IOLs, with contact between the intraocular lens haptic or optic with uveal tissue [28]. Therefore, UBM should be performed in patients with chronic pseudophakic uveitis to determine whether or not there is retained lens material and to assess for intraocular lens malposition.

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Foldable IOL placement into the capsular bag through a small incision at the time of surgery is standard of care in adults, and is being used increasingly in pediatric cataract extraction. Although advances in microsurgical techniques and materials have reduced the incidence of lens-related complications, efforts should still be made to choose an IOL material and design with optimal biocompatibility to ensure the best visual outcome. This topic has been reviewed recently [29,30]. Biomaterials (silicone or a variety of acrylics) and surface characteristics determine uveal and capsular biocompatibility of the IOL, measured clinically by anterior chamber reaction/inflammatory cell deposition and PCO, respectively.

All modern IOLs generally have good clinical uveal biocompatibility [31]. Indeed, even in uveitic eyes with pre-existing BAB compromise, a recent long-term follow-up study showed that hydrophilic or hydrophobic acrylic, and second generation silicone IOLs generally have good biocompatibility [32▪▪]. Several studies have shown clinically insignificant trends toward higher late foreign body giant cell reaction in hydrophobic acrylic IOLs compared with hydrophilic IOLs [32▪▪,33–38]. However, at least one study has shown the opposite, with lowest foreign body giant cells on hydrophobic acrylics [39]. Stronger initial small cell inflammatory response has been seen in silicone lenses, and some authors suggest avoiding these lenses in eyes with pre-existing BAB compromise [33,35,39]. If a rigid polymethylmethacrylate (PMMA) lens must be used, multiple studies have shown that heparin surface modification improves biocompatibility in uveitic eyes [30].

Lens epithelial cell migration plays an important role in the pathogenesis of PCO. Because these cells can induce a late inflammatory process, some authors consider PCO to be a form of postoperative inflammation [36]. Also, capsulotomy itself is pro-inflammatory, which is of special concern in uveitic eyes. A 2010 Cochrane review of PCO prevention found that sharp posterior optic edges, small capsulorrhexis, and in-bag IOL placement reduce PCO rates. The review found no significant difference in the PCO scores between different IOL materials [40▪]. However, many studies have shown trends toward increased lens epithelial cell migration and/or PCO rates in hydrophilic acrylic IOLs compared with hydrophobic IOLs [33,34,36,41–43]. This finding was confirmed recently in two 2011 studies showing statistically significant higher rates of visually important PCO at 2–3 years in the hydrophilic compared with hydrophobic acrylic IOLs [44,45]. This difference was also seen in hydrophilic vs. hydrophobic acrylic multifocal IOLs [46]. Similar results were found in prevalence of anterior capsule contraction rates, with the hydrophilic group having more contraction [47]. Some authors caution interpretation of these studies, as certain hydrophilic acrylic IOLs marketed as having sharp edges are rounder than sharp-edged hydrophobic acrylic and silicone IOLs [48,49]. Late postoperative mineral-deposit opacification of hydrophilic acrylic IOLs, requiring lens explanation, has been reported widely in the literature [50]. Various mechanisms explaining these opacities have been suggested, including pre-existing BAB compromise, and silicone contamination in commercial packaging.

The use of IOL implantation in the pediatric population is evolving, with recent increases in IOL use in the traditionally vulnerable groups of infant and uveitic eyes. This topic has been reviewed recently [51,52]. A few studies have shown good results in IOL implantation in pediatric uveitis, but success in this group is linked to careful patient selection and strict management of perioperative inflammation [51]. Favorable outcomes were shown recently in a 2011 retrospective review of 16 patients with juvenile idiopathic arthritis who underwent pars plana vitrectomy with lensectomy, intravitreal triamcinolone, and intraocular lens implantation [53▪]. A large-scale randomized multicenter trial recently showed no difference in visual acuity between aphakic and pseudophakic infants under 6 months of age, but higher rates of re-operation in the pseudophakic group [54].

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The incidence of pseudophakic CME in uveitic patients has been reported to be between 4 and 21% [27▪,55▪▪]. Those with preoperative macular lesions, such as epiretinal membrane or macular edema, are especially at risk for poor visual outcome after cataract surgery [55▪▪]. The use of perioperative oral steroid and control of uveitis for 3 or more months prior to cataract surgery decreases the risk of postoperative CME in uveitic eyes [19].

The treatment strategies commonly utilized for uveitic CME and pseudophakic CME, including periocular corticosteroids, topical nonsteroidal medication, systemic corticosteroids, intravitreal vascular endothelial growth factor (VEGF) antagonists, and local and systemic carbonic anhydrase inhibitors, can be applied to pseudophakic uveitic CME. There are few studies specifically addressing pseudophakic uveitic CME; however, Roesel et al.[24] recently compared intraoperative intravitreal triamcinolone injection, intraoperative orbital floor triamcinolone injection, and a 4-week course of postoperative oral prednisolone in this patient population. These studies showed that the CME improvement and anti-inflammatory effect after intravitreal triamcinolone were better than after orbital floor triamcinolone injection, but that the single intraoperative orbital floor injection of triamcinolone is as effective on postoperative inflammation, macular edema, and visual outcome as a 4-week course of postoperative oral prednisolone [56▪].

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The algorithm for management of postsurgical inflammation is different depending on whether the inflammation is acute or chronic (Fig. 1). Patients with acute, severe postoperative inflammation should be worked up for possibilities of endophthalmitis, TASS, retained less fragments, or exacerbation of known uveitic disease. Workup should include ultrasonography, including UBM if lens material is suspected and B-scan if view to posterior pole is clouded. If the cause is unclear, it is generally appropriate to treat as presumptive endophthalmitis and perform vitreous tap and injection of intravitreal antibiotics or pars plana vitrectomy depending on vision. For retained lens fragments, high-dose topical and systemic corticosteroids may be used to temporize inflammation, but definitive treatment often requires surgical debridement of the offending lens material.



For chronic inflammation, workup generally includes UBM, B-scan if posterior view is poor, and occasionally vitreous tap with cultures and PCR to evaluate for fungal or indolent chronic endophthalmitis. As new onset uveitis can occur in pseudophakic individuals, a workup for typical uveitic diseases is also warranted. As intraocular lymphoma occurs in patients of similar age to those needing cataract surgery, an index of suspicion for this masquerade syndrome should be maintained, particularly in patients presenting with bilateral inflammation. Management of chronic inflammation is dependent on cause, including aggressive intraocular antibiotics with potential surgical explanation of IOL in cases of delayed endophthalmitis, explanation or repositioning of IOL in cases of severe mechanical uveitis, limited or complete vitrectomy for inflammation associated with vitreous disorder (such as incarceration in wound), and potentially chronic local steroids for patients with mild mechanical postoperative uveitis.

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Conflicts of interest

Supported in part by an unrestricted research grant from Research to Prevent Blindness.

There are no conflicts of interest.

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Papers of particular interest, published within the annual period of review, have been highlighted as:

  • ▪ of special interest
  • ▪▪ of outstanding interest

Additional references related to this topic can also be found in the Current World Literature section in this issue (p. 73).

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1. Al-Mezaine HS, Kangave D, Al-Assiri A, Al-Rajhi AA. Acute-onset nosocomial endophthalmitis after cataract surgery: incidence, clinical features, causative organisms, and visual outcomes. J Cataract Refract Surg 2009; 35:643–649.
2. Endophthalmitis Vitrectomy Study Group. Results of the Endophthalmitis Vitrectomy Study. A randomized trial of immediate vitrectomy and of intravenous antibiotics for the treatment of postoperative bacterial endophthalmitis. Arch Ophthalmol 1995; 113:1479–1496.
3. Clark WL, Kaiser PK, Flynn HW Jr, et al. Treatment strategies and visual acuity outcomes in chronic postoperative Propionibacterium acnes endophthalmitis. Ophthalmology 1999; 106:1665–1670.
4. Aldave AJ, Stein JD, Deramo VA, et al. Treatment strategies for postoperative Propionibacterium acnes endophthalmitis. Ophthalmology 1999; 106:2395–2401.
Habot-Wilner Z, Sallam A, Pacheco PA, et al. Intravitreal triamcinolone acetonide as adjunctive treatment with systemic therapy for uveitic macular edema. Eur J Ophthalmol 2010; 21 (Suppl 6):56–61.

This study shows that a single intravitreal injection of triamcinolone acetonide is effective as an adjunctive treatment to systemic immune suppression in refractory uveitic CME, resulting in resolution of CME and improvement of visual acuity in most patients. This is allowed for the dosage of the systemic immune suppressives to be reduced or stopped in most cases.

6. Packer AJ, Weingeist TA, Abrams GW. Retinal periphlebitis as an early sign of bacterial endophthalmitis. Am J Ophthalmol 1983; 96:66–71.
Cutler Peck CM, Brubaker J, Clouser S, et al. Toxic anterior segment syndrome: common causes. J Cataract Refract Surg 2010; 36:1073–1080.

This retrospective review identifies common etiologies of TASS, allowing surgical centers to change their practices as needed to prevent TASS. The most common causes of TASS were inadequate cleaning and flushing of ophthalmic instruments and hand pieces. The use of intraocular medications with preservatives or additives was also associated with TASS in a significant number of cases.

Lockington D, Macdonald EC, Young D, et al. Presence of free radicals in intracameral agents commonly used during cataract surgery. Br J Ophthalmol 2010; 94:1674–1677.

This study highlights the risk of endothelial damage and TASS when multiple intracameral preparations are used in complicated cataract surgery. It shows that free radicals are present in intracameral preparations.

Buzard K, Zhang JR, Thumann G, et al. Two cases of toxic anterior segment syndrome from generic trypan blue. J Cataract Refract Surg 2010; 36:2195–2199.

This case report indicates that trypan blue, which is commonly used to stain the anterior lens capsule during the phacoemulsification of dense cataracts, can be toxic to the corneal endothelium in its generic form and has been associated with TASS.

10. Lemley CA, Han DP. Endophthalmitis: a review of current evaluation and management. Retina 2007; 27:662–680.
11. Mardelli PG, Mehanna CJ. Phacoanaphylactic endophthalmitis secondary to capsular block syndrome. J Cataract Refract Surg 2007; 33:921–922.
12. Fardeau C, Herbort CP, Nghiem S, et al. Laser flare photometry in the therapeutic management of bacterial chronic pseudophakic endophthalmitis. J Cataract Refract Surg 2009; 35:98–104.
13. Al-Mezaine HS, Al-Assiri A, Al-Rajhi AA. Incidence, clinical features, causative organisms, and visual outcomes of delayed-onset pseudophakic endophthalmitis. Eur J Ophthalmol 2009; 19:804–811.
14. Ozdal PC, Mansour M, Deschenes J. Ultrasound biomicroscopy of pseudophakic eyes with chronic postoperative inflammation. J Cataract Refract Surg 2003; 29:1185–1191.
Huang Y, Dai Y, Wu X, et al. Toxic anterior segment syndrome after pediatric cataract surgery. J AAPOS 2010; 14:444–446.

This case report is a reminder that acute postoperative inflammation following pediatric cataract surgery can be due to TASS.

Sengupta S, Chang DF, Gandhi R, et al. Incidence and long-term outcomes of toxic anterior segment syndrome at Aravind Eye Hospital. J Cataract Refract Surg 2011; 37:1673–1678.

This study indicates that TASS is often associated with a good visual outcome.

17. Androudi S, Tsironi E, Kalogeropoulos C, et al. Intravitreal adalimumab for refractory uveitis-related macular edema. Ophthalmology 2010; 117:1612–1616.
Soheilian M, Rabbanikhah Z, Ramezani A, et al. Intravitreal bevacizumab versus triamcinolone acetonide for refractory uveitic cystoid macular edema: a randomized pilot study. J Ocul Pharmacol Ther 2010; 26:199–206.

This paper describes the first randomized pilot trial comparing the effect of intravitreal bevacizumab and intravitreal triamcinolone in the treatment of refractory uveitic CME.

19. Belair ML, Kim SJ, Thorne JE, et al. Incidence of cystoid macular edema after cataract surgery in patients with and without uveitis using optical coherence tomography. Am J Ophthalmol 2009; 148:128e2–135e2.
20. Weiss K, Steinbrugger I, Weger M, et al. Intravitreal VEGF levels in uveitis patients and treatment of uveitic macular oedema with intravitreal bevacizumab. Eye (Lond) 2009; 23:1812–1818.
21. Lohmann CP, Linde HJ, Reischl U. Improved detection of microorganisms by polymerase chain reaction in delayed endophthalmitis after cataract surgery. Ophthalmology 2000; 107:1047–1051.discussion 1051–2.
22. Winward KE, Pflugfelder SC, Flynn HW Jr, et al. Postoperative Propionibacterium endophthalmitis. Treatment strategies and long-term results. Ophthalmology 1993; 100:447–451.
23. Gregori NZ, Flynn HW Jr, Miller D, et al. Clinical features, management strategies, and visual acuity outcomes of Candida endophthalmitis following cataract surgery. Ophthalmic Surg Lasers Imaging 2007; 38:378–385.
24. Roesel M, Tappeiner C, Heinz C, et al. Comparison between intravitreal and orbital floor triamcinolone acetonide after phacoemulsification in patients with endogenous uveitis. Am J Ophthalmol 2009; 147:406–412.
25. Guex-Crosier Y. The pathogenesis and clinical presentation of macular edema in inflammatory diseases. Doc Ophthalmol 1999; 97:297–309.
26. Schilling H, Heiligenhaus A, Laube T, et al. Long-term effect of acetazolamide treatment of patients with uveitic chronic cystoid macular edema is limited by persisting inflammation. Retina 2005; 25:182–188.
Ram J, Gupta A, Kumar S, et al. Phacoemulsification with intraocular lens implantation in patients with uveitis. J Cataract Refract Surg 2010; 36:1283–1288.

This study shows that phacoemulsification with IOL implantation improves vision in most patients with coexisting cataract and uveitis. It also highlights the common postoperative complications that lead to decreased vision.

28. Piette S, Canlas OA, Tran HV, et al. Ultrasound biomicroscopy in uveitis-glaucoma-hyphema syndrome. Am J Ophthalmol 2002; 133:839–841.
29. Werner L. Biocompatibility of intraocular lens materials. Curr Opin Ophthalmol 2008; 19:41–49.
30. Perry LJ, Papaliodis GN. Selection of intraocular lenses in patients with uveitis. Int Ophthalmol Clin 2010; 50:61–70.
31. Teichman JC, Ahmed II. Intraocular lens choices for patients with glaucoma. Curr Opin Ophthalmol 2010; 21:135–143.
Abela-Formanek C, Amon M, Kahraman G, et al. Biocompatibility of hydrophilic acrylic, hydrophobic acrylic, and silicone intraocular lenses in eyes with uveitis having cataract surgery: long-term follow-up. J Cataract Refract Surg 2011; 37:104–112.

This study follows the long-term results of patients with uveitis who underwent cataract surgery and indicates that there is an overall benefit to cataract surgery in this patient population. The results show that sharp-edged hydrophilic and hydrophobic IOLs perform well in eyes with uveitis. There is also higher uveal biocompatibility with the modern hydrophilic acrylic IOLs than with the hydrophobic acrylic IOL.

33. Abela-Formanek C, Amon M, Schauersberger J, et al. Results of hydrophilic acrylic, hydrophobic acrylic, and silicone intraocular lenses in uveitic eyes with cataract: comparison to a control group. J Cataract Refract Surg 2002; 28:1141–1152.
34. Abela-Formanek C, Amon M, Schild G, et al. Uveal and capsular biocompatibility of hydrophilic acrylic, hydrophobic acrylic, and silicone intraocular lenses. J Cataract Refract Surg 2002; 28:50–61.
35. Abela-Formanek C, Amon M, Schild G, et al. Inflammation after implantation of hydrophilic acrylic, hydrophobic acrylic, or silicone intraocular lenses in eyes with cataract and uveitis: comparison to a control group. J Cataract Refract Surg 2002; 28:1153–1159.
36. Mullner-Eidenbock A, Amon M, Schauersberger J, et al. Cellular reaction on the anterior surface of 4 types of intraocular lenses. J Cataract Refract Surg 2001; 27:734–740.
37. Richter-Mueksch S, Kahraman G, Amon M, et al. Uveal and capsular biocompatibility after implantation of sharp-edged hydrophilic acrylic, hydrophobic acrylic, and silicone intraocular lenses in eyes with pseudoexfoliation syndrome. J Cataract Refract Surg 2007; 33:1414–1418.
38. Roesel M, Heinz C, Heimes B, et al. Uveal and capsular biocompatibility of two foldable acrylic intraocular lenses in patients with endogenous uveitis: a prospective randomized study. Graefes Arch Clin Exp Ophthalmol 2008; 246:1609–1615.
39. Hollick EJ, Spalton DJ, Ursell PG, Pande MV. Biocompatibility of poly(methyl methacrylate), silicone, and AcrySof intraocular lenses: randomized comparison of the cellular reaction on the anterior lens surface. J Cataract Refract Surg 1998; 24:361–366.
Findl O, Buehl W, Bauer P, Sycha T. Interventions for preventing posterior capsule opacification. Cochrane Database Syst Rev 2010:CD003738.

This review summarizes the effects of different interventions to inhibit posterior capsular opacification, including modifications of surgical technique and intraocular lens design, implantation of additional devices and pharmacological interventions.

41. Hollick EJ, Spalton DJ, Ursell PG. Surface cytologic features on intraocular lenses: can increased biocompatibility have disadvantages? Arch Ophthalmol 1999; 117:872–878.
42. Kugelberg M, Wejde G, Jayaram H, Zetterstrom C. Two-year follow-up of posterior capsule opacification after implantation of a hydrophilic or hydrophobic acrylic intraocular lens. Acta Ophthalmol 2008; 86:533–536.
43. Johansson B. Clinical consequences of acrylic intraocular lens material and design: Nd:YAG-laser capsulotomy rates in 3 × 300 eyes 5 years after phacoemulsification. Br J Ophthalmol 2010; 94:450–455.
44. Iwase T, Nishi Y, Oveson BC, Jo YJ. Hydrophobic versus double-square-edged hydrophilic foldable acrylic intraocular lens: effect on posterior capsule opacification. J Cataract Refract Surg 2011; 37:1060–1068.
45. Vasavada AR, Raj SM, Shah A, et al. Comparison of posterior capsule opacification with hydrophobic acrylic and hydrophilic acrylic intraocular lenses. J Cataract Refract Surg 2011; 37:1050–1059.
46. Gauthier L, Lafuma A, Laurendeau C, Berdeaux G. Neodymium:YAG laser rates after bilateral implantation of hydrophobic or hydrophilic multifocal intraocular lenses: twenty-four month retrospective comparative study. J Cataract Refract Surg 2010; 36:1195–1200.
47. Tsinopoulos IT, Tsaousis KT, Kymionis GD, et al. Comparison of anterior capsule contraction between hydrophobic and hydrophilic intraocular lens models. Graefes Arch Clin Exp Ophthalmol 2010; 248:1155–1158.
48. Nanavaty MA, Spalton DJ, Boyce J, et al. Edge profile of commercially available square-edged intraocular lenses. J Cataract Refract Surg 2008; 34:677–686.
49. Werner L, Tetz M, Feldmann I, Bucker M. Evaluating and defining the sharpness of intraocular lenses: microedge structure of commercially available square-edged hydrophilic intraocular lenses. J Cataract Refract Surg 2009; 35:556–566.
50. Huang Y, Xie L. Delayed postoperative opacification of foldable hydrophilic acrylic intraocular lenses. J Biomed Mater Res B Appl Biomater 2011; 96:386–391.
51. Hug D. Update on pediatric cataracts and cataract surgery. Int Ophthalmol Clin 2010; 50:107–113.
52. Lin AA, Buckley EG. Update on pediatric cataract surgery and intraocular lens implantation. Curr Opin Ophthalmol 2010; 21:55–59.
Grajewski RS, Zurek-Imhoff B, Roesel M, et al. Favourable outcome after cataract surgery with IOL implantation in uveitis associated with juvenile idiopathic arthritis. Acta Ophthalmol 2011.

This study analyzes the controversy of IOL implantation in patients with juvenile idiopathic arthritis (JIA). It shows that phacoemulsification and in-the-bag IOL implantation may improve visual outcome in JIA-associated uveitis with minimally invasive surgical technique and intravitreal triamcinolone acetonide injection.

54. Lambert SR, Buckley EG, Drews-Botsch C, et al. A randomized clinical trial comparing contact lens with intraocular lens correction of monocular aphakia during infancy: grating acuity and adverse events at age 1 year. Arch Ophthalmol 2010; 128:810–818.
Yoeruek E, Deuter C, Gieselmann S, et al. Long-term visual acuity and its predictors after cataract surgery in patients with uveitis. Eur J Ophthalmol 2010; 20:694–701.

This retrospective study of uveitic patients undergoing cataract surgery identifies predictors of long-term visual acuity. It shows that preoperatively observed macular lesions are independently associated with poor visual outcome. However, sex, age at cataract surgery, preoperative vision, cause of uveitis, and preoperative anterior segment disorders are not associated with failure of vision improvement.

Roesel M, Heinz C, Koch JM, Heiligenhaus A. Comparison of orbital floor triamcinolone acetonide and oral prednisolone for cataract surgery management in patients with noninfectious uveitis. Graefes Arch Clin Exp Ophthalmol 2010; 248:715–720.

cataract; inflammation; phacoemulsification; uveitis

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