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Postoperative Endophthalmitis

  • Author: Hemang K Pandya, MD; Chief Editor: Hampton Roy, Sr, MD  more...
 
Updated: Jan 05, 2016
 

Background

Postoperative endophthalmitis is defined as severe inflammation involving both the anterior and posterior segments of the eye after intraocular surgery. Typically, postoperative endophthalmitis is caused by the perioperative introduction of microbial organisms into the eye either from the patient's normal conjunctival and skin flora or from contaminated instruments. Once organisms gain access to the vitreous cavity, overwhelming inflammation is likely to occur, making rapid recognition, diagnosis, and treatment critical in optimizing final outcomes. Although most cases of postoperative endophthalmitis occur within 6 weeks of surgery, infections seen in high-risk patients or infections caused by slow-growing organisms may occur months or years after the procedure.

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Pathophysiology

The Endophthalmitis Vitrectomy Study (EVS) demonstrated that most isolates causing clinical endophthalmitis are introduced into the eye from the patient's conjunctival flora.[1] However, contamination of sterilized instruments, disposable supplies, prepared solutions, surgical field, or the intraocular lens all have been reported. Epidemic clusters of endophthalmitis have resulted from these types of external contaminations.[2, 3]

Once bacteria are introduced into the eye, risk factors that may increase the risk of endophthalmitis include rupture of the posterior capsule, retained lens material, and surgical procedure. Published studies have demonstrated an increased risk of endophthalmitis after placement of a secondary intraocular lens, possibly due to increased surgical time or ocular manipulation.[4] Prolene haptic sutures also have been implicated as a possible risk factor for the development of endophthalmitis due to the surface properties of the material.

Once clinical infection occurs, damage to ocular tissues is believed to occur due to direct effects of bacterial replication as well as initiation of a fulminant cascade of inflammatory mediators. Endotoxins and other bacterial products appear to cause direct cellular injury while eliciting cytokines that attract neutrophils, which enhance the inflammatory effect. Thus, recent efforts in controlling the damaging effects of endophthalmitis in experimental models have focused on identifying not only appropriate antibiotics for control of the infectious agent but also on anti-inflammatory agents that might disrupt the immunologic events that occur after infection.

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Epidemiology

Frequency

United States

Postoperative endophthalmitis remains a rare complication of intraocular surgery. Of the 21,972 patients undergoing cataract extraction at the Bascom Palmer Eye Institute (BPEI) from 1995-2001, 8 (0.04%) developed endophthalmitis. During the same period at BPEI, the incidence of endophthalmitis was 0.2% after secondary intraocular lens (IOL) implantation, 0.03% after pars plana vitrectomy, 0.08% after penetrating keratoplasty, and 0.2% after glaucoma filtering surgery.[4] However, some studies have reported a potentially higher rate of acute endophthalmitis following cataract surgery in recent years, presumably secondary to the adoption of sutureless wounds.[5, 6, 7, 8]

Attention to prophylaxis appears to be the key in reducing the incidence of acute postoperative bacterial endophthalmitis. The requirement by the Bascom Palmer Eye Institute for the use of povidone-iodine prior to surgery played a major role.[9]

International

The rate of postoperative acute endophthalmitis among developed nations is similar to that of the United States.[10, 11]

Mortality/Morbidity

Fortunately, postsurgical endophthalmitis, unlike endogenous endophthalmitis, rarely causes any extraocular complications. Rarely, untreated cases can lead to late panophthalmitis and orbital cellulitis, prompting need for enucleation.

Morbidity associated with postoperative endophthalmitis can be substantial and is related not only to the acute process but also to late sequelae. In general, the risk of severe visual loss in patients with acute endophthalmitis is higher in patients who develop infections from more virulent organisms and do not seek treatment promptly.[1, 12, 13] Fortunately, 70-80% of patients with postoperative endophthalmitis have infections caused by coagulase-negative staphylococci, and the visual prognosis in these cases is usually good with rapid treatment.

Race

No racial predilection exists.

Sex

No sexual predilection exists.

Age

No age predilection exists.

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Contributor Information and Disclosures
Author

Hemang K Pandya, MD Fellow in Vitreoretinal Disease and Surgery, Dean McGee Eye Institute, University of Oklahoma College of Medicine

Hemang K Pandya, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Retina Specialists, Association for Research in Vision and Ophthalmology, Michigan State Medical Society, Michigan Society of Eye Physicians & Surgeons

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

R Christopher Walton, MD Professor, Director of Uveitis and Ocular Inflammatory Disease Service, Department of Ophthalmology, University of Tennessee College of Medicine

R Christopher Walton, MD is a member of the following medical societies: American Academy of Ophthalmology, Association for Research in Vision and Ophthalmology, Retina Society, American College of Healthcare Executives, American Uveitis Society

Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy, Sr, MD Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Hampton Roy, Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

Additional Contributors

Andrew W Lawton, MD Neuro-Ophthalmology, Ochsner Health Services

Andrew W Lawton, MD is a member of the following medical societies: American Academy of Ophthalmology, Arkansas Medical Society, Southern Medical Association

Disclosure: Nothing to disclose.

William Lloyd Clark, MD Palmetto Retina

William Lloyd Clark, MD is a member of the following medical societies: Alpha Omega Alpha, Association for Research in Vision and Ophthalmology, American Academy of Ophthalmology

Disclosure: Nothing to disclose.

William B Trattler, MD Ophthalmologist, The Center for Excellence in Eye Care; Volunteer Assistant Professor of Ophthalmology, Bascom Palmer Eye Institute

William B Trattler, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Cataract and Refractive Surgery

Disclosure: Received consulting fee from Allergan for consulting; Received consulting fee from Alcon for consulting; Received consulting fee from Bausch & Lomb for consulting; Received consulting fee from Abbott Medical Optics for consulting; Received consulting fee from CXLUSA for none; Received consulting fee from LensAR for none.

Peter K Kaiser, MD Consulting Staff, Department of Ophthalmology, Cole Eye Institute, Cleveland Clinic Foundation

Peter K Kaiser, MD is a member of the following medical societies: American Academy of Ophthalmology, Association for Research in Vision and Ophthalmology, American Medical Association, Massachusetts Medical Society, Society for Neuroscience

Disclosure: Nothing to disclose.

Acknowledgements

Mehran Taban, MD Vitreoretinal Fellow, Cole Eye Institute, Cleveland Clinic Foundation

Mehran Taban, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Ophthalmology, American Medical Association, Association for Research in Vision and Ophthalmology, and Phi Beta Kappa

Disclosure: Nothing to disclose.

References
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