Introduction
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.
See related CME at Cataract and Refractive Surgery.
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.
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
International
The rate of postoperative acute endophthalmitis among developed nations is similar to that of the United States.8,9
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.1,10,11 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.
Clinical
History
Patients with acute postoperative endophthalmitis typically present within 6 weeks of intraocular surgery with moderate to severe eye pain and decreased vision.
Physical
- The hallmark findings on ophthalmic examination are posterior and anterior chamber inflammation.10,11,12
- Hypopyon is present in most cases.10,11,12
- Other important findings include conjunctival hyperemia and chemosis, corneal edema, wound abnormalities, and associated eyelid or orbital inflammation.
- In rare circumstances, patients may develop chronic, infectious endophthalmitis months to years after intraocular surgery. These patients exhibit indolent inflammation, which is initially responsive to corticosteroids, but over time, become refractory to therapy. Although conjunctival hyperemia, corneal edema, and anterior and posterior chamber inflammation are often present, rapid deterioration of vision and hypopyon are not seen frequently.13,14
Causes
- Risk factors for development of postoperative endophthalmitis may include the following:
- Increased operative time, low volume (experienced) surgeon15
- Posterior capsule rupture/vitreous loss11,12
- Retained lens fragments
- Inadequate sterilization of the operative field
- Contamination of surgical instruments
- Inadequate wounds (eg, leaky), as in some cases of sutureless clear corneal cataract incisions and sutureless sclerotomies5,6,16,17
- In the EVS, a prospective randomized clinical trial that evaluated the management of acute postoperative (cataract extraction or secondary IOL implantation) endophthalmitis, the most common organisms isolated were coagulase-negative staphylococci (70%), Staphylococcus aureus (9.9%), and streptococci species (9.0%). Infections caused by gram-negative organisms were seen in 6% of cases.1,18
- Endophthalmitis following other types of intraocular surgery has a similar microbiological profile with the following exceptions:
- In filtering bleb-associated cases, the most common offending species is Streptococcus, followed by Haemophilus influenzae and coagulase-negative staphylococci.11,19
- In chronic postoperative endophthalmitis, an important causative organism is Propionibacterium acnes, a slow-growing, gram-positive bacillus that is associated with a characteristic white, intracapsular plaque that develops weeks to months and years after cataract surgery.13,14
- Coagulase-negative staphylococci, fungal species, and unusual gram-negative organisms also have been reported to cause chronic postoperative endophthalmitis.11
More on Endophthalmitis, Postoperative |
 Overview: Endophthalmitis, Postoperative |
| Differential Diagnoses & Workup: Endophthalmitis, Postoperative |
| Treatment & Medication: Endophthalmitis, Postoperative |
| Follow-up: Endophthalmitis, Postoperative |
| References |
| Next Page » |
References
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Kunimoto DY, Kaiser RS. Incidence of endophthalmitis after 20- and 25-gauge vitrectomy. Ophthalmology. Dec 2007;114(12):2133-7. [Medline].
Johnson MW, Doft BH, Kelsey SF, et al. The Endophthalmitis Vitrectomy Study. Relationship between clinical presentation and microbiologic spectrum. Ophthalmology. Feb 1997;104(2):261-72. [Medline].
Busbee BG, Recchia FM, Kaiser R, et al. Bleb-associated endophthalmitis: clinical characteristics and visual outcomes. Ophthalmology. Aug 2004;111(8):1495-503; discussion 1503. [Medline].
Doft BH, Kelsey SF, Wisniewski SR. Additional procedures after the initial vitrectomy or tap-biopsy in the Endophthalmitis Vitrectomy Study. Ophthalmology. Apr 1998;105(4):707-16. [Medline].
Park SS, Vallar RV, Hong CH, et al. Intravitreal dexamethasone effect on intravitreal vancomycin elimination in endophthalmitis. Arch Ophthalmol. Aug 1999;117(8):1058-62. [Medline].
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Further Reading
Keywords
postoperative endophthalmitis, eye infection, vitritis, hypopyon, bacterial infection
