Skip to main content

  • Noninfectious Endophthalmitis

    Retina/Vitreous
    Add to My Bookmarks

    Endophthalmitis is a potentially serious complication of any intraocular procedure. West et al. revealed that from 1994 to 2001, the incidence of presumed infectious endophthalmitis after cataract surgery rose to 2.15 per 1000 cataract surgeries.1 Although the Endophthalmitis Vitrectomy Study (EVS) provides an evidence-based approach to the management of postoperative endophthalmitis in certain cases, there are many situations in which EVS recommendations may not be easily applied.2

    In addition, while a high level of suspicion must be maintained for an infectious cause of an unusual presentation of postprocedural inflammation, there are noninfectious etiologies that should be considered in the differential diagnosis. Among these noninfectious etiologies are:

      dot Toxic anterior segment syndrome (TASS)
      dot Inflammation following intravitreal triamcinolone acetonide injection (IVTA)
      dot Inflammation secondary to retained lens material following cataract surgery

    Toxic Anterior Segment Syndrome

    TASS is a postoperative inflammatory reaction caused by a noninfectious substance that enters the anterior chamber during cataract surgery. The inflammation can be quite severe, including a hypopyon in many cases. It is always culture negative and will usually respond to topical steroids. It is often associated with diffuse endothelial cell dysfunction leading to limbus to limbus corneal edema.

    Although it can often be difficult to differentiate TASS from infectious endophthalmitis, there are some helpful features. TASS is most often limited to the anterior chamber with less posterior chamber involvement than endophthalmitis. Unlike infectious endophthalmitis, TASS presents very early, often within 12-24 hours of surgery, as opposed to the 4-7 days of acute bacterial infection.3 The absence of or presence of pain is not a helpful differentiating feature as EVS showed that 25% of patients with endophthalmitis in EVS did not have pain.2

    If the suspicion for TASS is high, one can begin frequent topical steroids along with topical antibiotics and reevaluate the patient within 2-4 hours. A patient with TASS may often improve, with decrease in hypopyon and improvement in symptoms, while a patient with infectious endophthalmitis will worsen.

    Treatment for TASS should include topical 1% prednisolone acetate every hour with close follow-up. The intraocular pressure (IOP) should also be closely followed, because while it may initially be low, it may often increase considerably as the ciliary body resumes aqueous production.

    Unfortunately, the toxic material may cause permanent damage to the trabecular meshwork, and the inflammation may lead to peripheral anterior synechia, both of which may cause chronic elevation of IOP, which may not be responsive to medical management and may require surgical intervention.3

    In addition, Breebaart et al. revealed, TASS may also lead to permanent endothelial cell loss, sometimes requiring corneal transplantation. They reported a mean endothelial cell loss of 72% in their series of 18 patients. As a result, they coined the term toxic endothelial cell destruction syndrome.4

    Noninfectious Endophthalmitis following IVTA

    As the use of IVTA has increased, there have been reports of noninfectious endophthalmitis as well as pseudohypopyon following this procedure. The incidence of endophthalmitis following IVTA is generally low, with different groups showing various rates:

      dot Westfall et al. revealed a single acute culture-negative postprocedural case out of a series of 1006 eyes (0.1%).
      dot Nelson found 0.5% incidence of bacterial endophthalmitis and a 1.6% incidence of noninfectious endophthalmitis, while Moshfeghi et al. noted a higher rate of 0.87% of culture-positive endophthalmitis.5-7
      dot Chen et al. reported a culture-negative patient with a gravity dependent pseudohypopyon composed of characteristic refractile triamcinolone crystals that would shift with change in head position.8
      dot Roth et al. described the appearance of a significant inflammatory response along with a dramatic decrease in vision in 7 patients who had undergone IVTA injection following intraocular surgery. These patients had sudden, painless loss of vision noted at the first postprocedural office visit. Of these 7 patients, 4 had a hypopyon that was not composed of triamcinolone crystals.9

    Several etiologies have been proposed to explain the inflammation seen with IVTA. Some have proposed the inflammation to be secondary to a reaction to either the drug itself, the vehicle in which the drug is suspended (Nelson), or a contaminant in the particular lot of vials used.6,9 As a result of concern about the vehicle, some physicians have moved to preservative-free triamcinolone. Others have allowed the drug to settle out of suspension, removed the supernatant, and resuspended with BSS or lactated Ringer’s solution.10 While there is a possible risk for a contaminant in a certain lot of the medicine, this seems unlikely as incidents of post-IVTA culture-negative endophthalmit is have been separated in time and geography.

    These cases may be differentiated from infection by a few characteristics

      dot Patients with the culture-negative form often notice a sudden onset of symptoms, often immediately after injection.
      dot Examination of these patients often reveals a diffuse spread of particulate matter throughout the vitreous without the usual localized deposit of medicine within the posterior chamber.11
      dot

    Some of these patients may not have ciliary injection or other external signs of inflammation, and yet still have severe media opacity from vitreous debris.

    Again, while patients with culture-negative endophthalmitis following IVTA usually do not complain of pain, this symptom should not be the determining factor for treatment of a presumed infection. Treatment for post-IVTA inflammation or pseudohypopyon involves close evaluation for improvement and clearance of debris, with some recommending the use of topical prednisolone acetate.9

    Retained lens fragments

    Retained lens fragment following cataract surgery is uncommon.12 When it does occur it may present in many ways, including inflammation, corneal edema, elevated eye pressure, and decreased vision.

    The amount of inflammation and percentage of patients who are affected may vary. In their series of 65 patients, Gilliland et al. revealed that 32 patients (57%) had some inflammation.13 In their series of 54 patients, however, Kim et al. reported uveitis in 47 patients (87%). However, severe inflammation may be less common. Of the patients that Kim et al. described only 4 (7%) were found to have hypopyon.14 These patients may also have significant vitreous debris.15

    It may be difficult to differentiate retained lens material from infectious endophthalmitis. Irvine et al., in their series of 4 patients, revealed that intraocular inflammation was generally delayed, with none occurring within the first week after surgery.

    In cases where severe inflammation results in media opacity, retained lens material in the posterior chamber appears highly reflective with ophthalmic ultrasound.15 However, even with clinical history, it may be difficult to differentiate inflammation from retained lens fragments from that of superimposed acute infectious endophthalmitis. As a result, it may be useful in these cases to send a vitrectomy specimen for microbiological evaluation when the patient undergoes surgery to remove retained lens material.

    In addition to vitrectomy, it is important to treat any inflammation with topical prednisolone acetate, and any elevation of eye pressure should also be closely monitored and treated. As patients these may also develop macular edema, some physicians have treated them with topical nonsteroidal anti-inflammatory medications as well.15

    Conclusion

    While ophthalmologists should remain vigilant against postprocedural infectious endophthalmitis, noninfectious causes of intraocular inflammation should also be remembered and managed appropriately.

    1. West ES, Behrens A, McDonnell PJ, Tielsch JM, Schein OD. The incidence of endophthalmitis after cataract surgery among the U.S. Medicare population increased between 1994 and 2001.Ophthalmology. 2005;112(8):1388-1394.
    2. The Endophthlmitis Vitrectomy Study Group: Results of the Endophthlmitis Vitrectomy Study: A randomized trial of immediate vitrectomy and of intravenous antibiotics for the treatment of postoperative bacterial endophthalmitis.Arch Ophthalmol. 1995;113(12):1479-1496.
    3. Mamalis N, Edelhauser HF, Dawson DG, Chew J, LeBoyer RM, Werner L. Toxic anterior segment syndrome.J Cataract Refract Surg.2006;32(2):324-333.
    4. Breebaart AC, Nuyts RMMA, Pels E, Edelhauser HF, Verbraak FD. Toxic endothelial cell destruction of the cornea after routine extracapsular cataract surgery.Arch Ophthalmol. 1990;108(8):1121-1125.
    5. Westfall AC, Osborn A, Kuhl D, Benz MS, Mieler WF, Holz ER. Acute Endophthalmitis incidence: intravitreal triamcinolone.Arch Ophthalmol. 2005;123(8):1075-1077.
    6. Nelson ML, Tennant MT, Sivalingam A, Regillo CD, Belmont JB, Martidis A. Infectious and presumed noninfectious endophthalmitis after intravitreal triamcinolone acetonide injection.Retina. 2003;23(5):686–691.
    7. Moshfeghi DM, Kaiser PK, Scott IU, et al. Acute endophthalmitis following intravitreal triamcinolone acetonide injection.Am J Ophthalmol. 2003;136(5):791-796.
    8. Chen SDM, Lochhead J, McDonald B, Patel CK. Pseudohypopyon after intravitreal triamcinolone injection for the treatment of pseudophakic cystoid macular oedema.Br J Ophthalmol. 2004;88(6):843-844.
    9. Roth DB, Chieh J, Spirn MJ, et al. Noninfectious endophthalmitis associated with intravitreal triamcinolone injection.Arch Ophthalmol. 2003;121(9):1279–1282.
    10. Jonas JB, Hayler JK, Panda-Jones S. Intravitreal injection of crystalline cortisone as an adjunctive treatment of proliferative vitreoretinopathy.Br J Ophthalmol. 2000;84(9):1064-1067.
    11. Sutter FK, Gillies MC. Pseudo-endophthalmitis after intravitreal injection of triamcinolone.Br J Ophthalmol. 2003;87(8):972-974.
    12. Blodi BA, Flynn HW, Blodi CF, Folk JC, Daily MJ. Retained nuclei after cataract surgery.Ophthalmology. 1992;99(1):41-44.
    13. Gilliland GD, Hutton WL, Fuller DG. Retained intravitreal lens fragments after cataract surgery.Ophthalmology. 1992;99(8):1263-1269.
    14. Kim JE, Flynn HW, Smiddy WE, Murray TG, Rubsamen PE, Davis JL, Nicholson DH. Retained lens fragments after phacoemulsification.Ophthalmology. 1994;101(11):1827-1832.
    15. Irvine WD, Flynn HW, Murray TG, Rubsamen PE. Retained lens fragments after phacoemulsification manifesting as marked intraocular inflammation with hypopyon.Am J Ophthalmology. 1992;114(5):610-614.

    Author Disclosure

    The authors state that they have no proprietary interest in any of the practices or medications discussed in this article. Although Oregon Health and Science University receives some support from outside sources in Dr. Flaxel’s name, she herself does not receive any direct support or funding from outside the university.