Postoperative endophthalmitis is a rare complication of cataract surgery with intraocular lens (IOL) placement, which can present acutely or chronically. Chronic postoperative endophthalmitis (CPOE) is characterized by a delayed onset of inflammatory symptoms weeks to years postoperatively. CPOE typically involves worsening vision and low-grade inflammation, which may be treated with topical corticosteroids but recurs or flares on tapering. Its incidence is unclear.1 It may be caused by a number of bacterial or fungal organisms such as Staphylococcus aureus and Cutibacterium acnes, formerly known as Propionibacterium acnes. Key characteristics of C acnes endophthalmitis include white intracapsular plaques and anterior segment inflammation.2
Cutibacterium acnes is an anaerobic, gram-positive bacterium that can be found in the normal body flora, including in normal, noninfectious conjunctival cultures.3,4 As such, it is important to consider the possibility of C acnes as the causative organism of a postoperative infection. Owing to its indolent nature and often initial response to topical corticosteroids, the diagnosis of CPOE is typically delayed, with average diagnosis made about 4 months after cataract surgery.5 The longest reported case, to our knowledge, is 21 years. Here, we report 2 cases of CPOE secondary to C acnes, which were diagnosed 4 and 7 years from the time of cataract surgery. We also discuss the management of 1 case that necessitated endolaser photocoagulation destruction of an infectious nidus to resolve the chronic infection.
Patient Consent Statement
Patients 1 and 2 have provided written informed consent for their information to be used in a deidentified manner.
An 88-year-old man underwent uneventful phacoemulsification and posterior chamber IOL insertion of the left eye in April 2010. In the ensuing months, the patient had a rhegmatogenous retinal detachment and underwent pars plana vitrectomy (PPV) with gas tamponade, epiretinal membrane peel, and capsulectomy. In 2011, the patient developed a granulomatous uveitis and presented to our institution with an initial concerning for an intraocular manifestation of the patient's long-standing systemic follicular lymphoma. Infectious and inflammatory serum laboratory workup was negative. PPV with vitreous biopsy was performed, and cytology and flow cytometry were negative for malignant cells. IOL subluxation was then thought to be the cause of the patient's recurrent intraocular inflammation. A successful IOL exchange was performed, and after tapering his topical corticosteroids at postoperative month 1, the patient's vision worsened with recurrent anterior chamber inflammation and keratic precipitates. On increasing topical corticosteroids, his inflammation improved, and intravitreal triamcinolone acetonide was administered with complete resolution of the patient's anterior uveitis. However, a few months later, inflammation recurred and an anterior chamber tap and intravitreal injection of vancomycin and ceftazidime were performed. The aqueous tap was negative for bacterial or fungal growth. A second intravitreal triamcinolone acetonide injection was administered with good response. Two months later, there was a moderate anterior chamber cell recurrence, and an intravitreal dexamethasone implant (Ozurdex) was given. Two months later, the patient's inflammation significantly worsened, and a diagnostic PPV with repeat vitreous biopsy and capsulectomy was performed because of the concern of possible CPOE, and intravitreal vancomycin and ceftazidime were administered. Vitreous culture was positive for C acnes, now 4 years after the initial cataract surgery. The patient's inflammation and keratic precipitates resolved postoperatively. At 6-year follow-up, there have been no inflammatory recurrences; however, the patient's vision has declined to 20/500 because of geographic atrophy from nonexudative age-related macular degeneration and an episode of giant cell arteritis.
A 79-year-old woman underwent uneventful phacoemulsification and Crystalens placement in July 2013 in the left eye, followed by a YAG capsulotomy 5 months later. She developed postoperative anterior uveitis, and an infectious and inflammatory serum workup was negative at an outside institution. Per outside reports, the inflammation responded to topical corticosteroid medications but would recur on taper. The patient preferred nontopical treatment options and received 3 intravitreal dexamethasone implants (Ozurdex) over the course of the following year. After the third Ozurdex implant, a significant increase in anterior chamber inflammation and keratic precipitates appeared. PPV with IOL explantation and total capsulectomy was performed, and the patient was left aphakic. No aqueous or vitreous culture was obtained, and to our knowledge, no intravitreal antibiotics were administered. The inflammation temporarily resolved postoperatively. In 2017, the patient presented to our institution for a secondary IOL. Her previous anterior uveitis was controlled on daily topical difluprednate, and she had minimal cystoid macular edema. She remained quiet for a few months, and in September 2017, an anterior chamber IOL was implanted. Intraoperatively, no remnant capsule was visualized. The patient was maintained on daily topical difluprednate in the postoperative period with good response. About 1 year later, in October 2018, the patient's inflammation significantly recurred and responded to topical corticosteroid treatment. Her intraocular pressures remained normal. Two years later, in August 2020, the patient had a significant inflammatory recurrence with diffuse keratic precipitates and dense endothelial corneal plaques (Figure 1, A). Visual acuity fell to 20/300. An anterior chamber tap was performed, which was positive for C acnes. The patient was then given an intravitreal vancomycin injection. Visual acuity improved to 20/60. Shortly after, she developed recurrent iritis, and PPV was performed with careful anterior scleral depression looking for the residual capsule. Again, no remnant capsule was seen, but 3 areas of white plaques along the ciliary body were visualized and thought to be areas of infectious nidus as the cause of her chronic endophthalmitis (Figure 2, A). The white ciliary body plaques were very adherent, and aggressive manipulation was deferred to avoid choroidal hemorrhage and iatrogenic cyclodialysis cleft. The plaques were therefore treated with endolaser photocoagulation (Figure 2, B). In January 2021, keratic precipitates and corneal edema had resolved (Figure 1, B). At the patient's most recent visit in February 2021, over 7 years after the initial cataract surgery, the left eye was doing well clinically, and visual acuity was 20/60.
Diagnosis of CPOE with C acnes as the causative organism is often challenging. Because of its clinical appearance, CPOE is easily confused with granulomatous uveitis or chronic iridocyclitis.2 Initial flares may be controlled by topical, intraocular, or periocular corticosteroids for an extended period of time and mask the indolent underlying infection. When testing for C acnes, aqueous and/or vitreous specimens may result in negative cultures because the organism can be sequestered in the capsular bag. Even polymerase chain reaction may be unsuccessful in detection.6 In addition, if the microbiology laboratory is not instructed to incubate the sample for up to 2 weeks, the yield of identifying C acnes decreases.7
Treatments for C acnes endophthalmitis include intraocular antibiotic (IOAB) injections and/or PPV plus or minus IOL explantation and capsulectomy.5,8 The patient in our first case experienced recurrent inflammation despite PPV, IOL exchange, and IOAB injections and repeated negative aqueous and vitreous cultures until a second vitreous biopsy confirmed the diagnosis of C acnes CPOE. Inflammatory control was not achieved until capsulectomy was performed. In our second case, the patient experienced recurrent inflammation despite prior PPV, IOL explantation, and capsulectomy due to white ciliary body plaques felt to be an infectious nidus source for recurrent inflammation. The patient required endolaser photocoagulation of ciliary body plaques to resolve C acnes CPOE. Localized destruction of an infectious nidus has been rarely reported and is an uncommon but useful treatment modality to control recalcitrant infectious uveitis. The use of external scleral cryotherapy has been described to treat resistant endophthalmitis caused by localized peripheral lesions, and the use of endophotocoagulation to an infectious nidus adjacent to ciliary processes has also been described.9,10 Although we used scleral depression and a posterior segment endolaser photocoagulation probe to visualize and target the ciliary processes, endoscopic cyclophotocoagulation techniques more familiar to anterior segment and glaucoma surgeons could be used in appropriate circumstances.
CPOE secondary to C acnes is rare, with most cases diagnosed within 6 months to 1 year after the initial surgery. Cases diagnosed years after extracapsular cataract surgery are even more rarely described in the literature. Clark et al. describe 36 patients with a mean time to initial treatment of 36 weeks and 3 cases that presented at 133 weeks, 160 weeks, and 172 weeks after the initial surgery.11 Al-Mezaine et al. reported 17 patients with a mean time of 5 months between cataract surgery and endophthalmitis diagnosis, with C acnes being the most common cause.12 One report highlights a case diagnosed 5 years after the initial surgery, but this was after intracapsular cataract surgery.13 Recently, a case of suspected C acnes endophthalmitis was described 21 years after cataract surgery.14 This case had an initial negative aqueous tap and vitreous culture with subsequent positive aqueous C acnes culture. The patient then underwent IOL explantation and capsulectomy from which culture grew Staphylococcus epidermidis, but this was felt to be a contaminant rather than a source of the infection. This report also states that no recurrence occurred, but in this patient with multiple recurrent inflammatory events, the authors do not offer a timeframe for recurrence-free follow-up. The cases represented here, diagnosed 4 years and 7 years after initial extracapsular cataract surgery, describe some of the longest delayed diagnosed C acnes CPOE cases. One case persisted after IOAB, complete PPV, IOL explantation, and capsulectomy, highlighting the importance of careful intraoperative examination of the ciliary body for plaques in recalcitrant cases or even at the time of initial surgery. We also describe a unique therapeutic technique of endolaser photocoagulation to an infectious nidus to prevent recurrent inflammation. Despite the delayed diagnosis, long-term follow-up in both of these cases demonstrates that inflammatory control is still achievable with appropriate treatment. Excellent visual outcomes can also be achieved as demonstrated in our second case.
WHAT WAS KNOWN
- Chronic postoperative endophthalmitis can present several months after uneventful cataract surgery.
- It is often difficult to identify Cutibacterium acnes as the causative organism of chronic postoperative endophthalmitis.
WHAT THIS PAPER ADDS
- The cases represented here, diagnosed 4 years and 7 years after initial extracapsular cataract surgery, describe some of the longest delayed diagnosed C acnes chronic postoperative endophthalmitis cases.
- Endolaser photocoagulation can be used on intracapsular or ciliary body plaques to treat an active infectious nidus.
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