Endophthalmitis


ACUTE-ONSET POSTOPERATIVE ENDOPHTHALMITIS


Endophthalmitis is characterized by marked inflammation of intraocular tissues and fluids. In a patient with endophthalmitis, the etiology and most likely infecting organisms may be predicted by the clinical setting. The largest category is acute-onset postoperative endophthalmitis, generally defined as presenting within 6 weeks of intraocular surgery.


Etiology and Epidemiology


Presents within 6 weeks of intraocular surgery


Reported incidence rates are variable. In a recent large single-center series, reported rates were 0.025% overall, 0.028% following cataract surgery, 0.2% following secondary intraocular lens (IOL) implantation, 0.108% following penetrating keratoplasty, and 0.011% following 20-gauge pars plana vitrectomy (PPV).


The Endophthalmitis Vitrectomy Study (EVS) recruited patients with acute-onset postoperative endophthalmitis following cataract surgery or secondary IOL implantation. In the EVS, 69% of patients had positive vitreous cultures. Of these, the most common etiologic organisms were coagulase-negative staphylococci.


Preoperative risk factors include immune compromise (including diabetes mellitus), active systemic infection, active blepharitis or conjunctivitis, and disease of the lacrimal drainage system.


Intraoperative risk factors include prolonged or complicated surgery, secondary IOL implantation, posterior capsular rupture, vitreous loss, iris prolapse, contaminated irrigating solutions or IOLs, and inferotemporal placement of clear corneal incisions. Some authors have suggested that a clear corneal, sutureless incision for cataract surgery is a risk factor for endophthalmitis.


Postoperative risk factors include wound leak, vitreous incarceration in the wound, and contaminated eye drops.


Symptoms


Rapid onset of visual loss, redness, and pain


Signs (Figs. 10-1 and 10-2)


Marked intraocular (anterior chamber and vitreous) inflammation with anterior chamber fibrin and hypopyon


Eyelid edema, conjunctival congestion, corneal edema, and retinal periphlebitis may occur to a variable degree.


Differential Diagnosis


Toxic anterior segment syndrome (TASS) generally occurs earlier (within 1 or 2 days) and may be associated with little or no pain, as well as little or no posterior segment inflammation.


Retained lens material


Flare-up of pre-existing uveitis


Triamcinolone acetonide particles


Long-standing (dehemoglobinized) vitreous hemorrhage


Diagnostic Evaluation


Acute-onset postoperative endophthalmitis is a clinical diagnosis, followed by laboratory confirmation.


If the posterior segment cannot be visualized, B-scan ultrasonography may be helpful to rule out retinal detachment, suprachoroidal hemorrhage, or retained lens fragment.


Aqueous and vitreous cultures. Vitreous samples are more likely to yield a positive culture than aqueous samples. Vitreous cultures may be obtained either with a needle (tap) or with PPV instrumentation.


Commonly used culture media include 5% blood agar (most common organisms), chocolate agar (fastidious organisms, such as N. gonorrhoeae and H. influenzae), Sabouraud agar (fungi), thioglycollate broth (anaerobes), and anaerobic blood agar (anaerobes).


Blood culture bottles may also be used and are helpful in after-hours cases.


Treatment


The EVS reported that for patients with acute-onset postoperative endophthalmitis following cataract surgery or secondary IOL implantation and presenting visual acuity of light perception, PPV was associated with improved visual outcomes when compared to vitreous tap. For patients with hand motion vision or better, the results of intravitreal tap with injection of antibiotics were similar to PPV. In diabetic patients with presenting visual acuity of hand motions or better, there was a trend toward better visual outcomes in patients treated with PPV, but this was not statistically significant.


The EVS treated all patients with intravitreal vancomycin (1 mg in 0.1 mL) and amikacin (0.4 mg in 0.1 mL). However, to reduce the risk of aminoglycoside toxicity, either ceftazidime (2.25 mg in 0.1 mL) or ceftriaxone (2 mg in 0.1 mL) may be considered.


The EVS reported no additional visual benefit associated with the adjunctive use of systemic amikacin and ceftazidime. However, fourth-generation systemic fluoroquinolones such as moxifloxacin achieve intraocular penetration and may be considered for adjunctive use, although supporting evidence of efficacy is lacking.


In patients with acute-onset postoperative endophthalmitis with suspected bacterial etiology, intravitreal dexamethasone (0.4 mg in 0.1 mL) may be considered.


The EVS treated all patients with subconjunctival vancomycin (25 mg in 0.5 mL), ceftazidime (100 mg in 0.5 mL), and dexamethasone (6 mg in 0.25 mL). However, subsequent clinical trials have demonstrated that there may be no additional benefit associated with subconjunctival antibiotics.


The EVS treated all patients with systemic prednisone (30 mg b.i.d. for 5 to 10 days). However, systemic corticosteroids should be used with caution in certain at-risk patients, including diabetics and the elderly.


The EVS treated all patients with fortified topical vancomycin (50 mg/cc) and fortified topical amikacin (20 mg/cc), up to every hour. As a substitute, commercially available topical antibiotics (such as fourth-generation fluoroquinolones) may be considered. In addition, the EVS treated all patients with topical corticosteroids and cycloplegics.


If the clinical status appears to be worsening at 48 to 72 hours, consideration should be given to reculturing and reinjection of anti­biotics based on the initial culture results. If the initial culture was a needle tap, PPV can be considered for the subsequent procedure.


Prognosis


The strongest predictor of final visual outcome in the EVS was presenting visual acuity. Therefore, prompt initiation of treatment is more important than any other factor, including vitreous tap versus PPV.


Other predictors of less favorable outcomes in the EVS included older age, diabetes mellitus, corneal infiltrate, abnormal intraocular pressure, anterior segment neovascularization, absent red reflex, and open posterior capsule.


REFERENCES


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.


Lalwani GA, Flynn HW Jr, Scott IU, et al. Acute-onset endophthalmitis after clear corneal cataract surgery (1996–2005). Clinical features, causative organisms, and visual acuity outcomes. Ophthalmology. 2008;115:473–476.


Schwartz SG, Flynn HW Jr, Scott IU. Endophthalmitis: classification and current management. Exp Rev Ophthalmol. 2007;2:385–396.


Wykoff CC, Parrott MB, Flynn HW Jr., et al. Nosocomial acute-onset postoperative endophthalmitis at a university teaching hospital (2002–2009). Am J Ophthalmol. 2010 Jul 7 [Epub ahead of print].



Figure 10-1. This person has conjunctival chemosis, injection, hypopyon, and fibrin in the anterior chamber, all indicative of acute-onset postoperative endophthalmitis.


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Figure 10-2. The patient has acute post­operative endophthalmitis. In this case, there is a profuse amount of purulent material with an opaque cornea, suggestive of an organism such as Pseudomonas aeruginosa.


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DELAYED-ONSET (CHRONIC) POSTOPERATIVE ENDOPHTHALMITIS


Endophthalmitis is characterized by marked inflammation of intraocular tissues and fluids. Delayed-onset (chronic) postoperative endophthalmitis is defined as endophthalmitis presenting more than 6 weeks after intraocular surgery.


Etiology and Epidemiology


Presents more than 6 weeks following intraocular surgery


In one single-center series, the reported rate of delayed-onset postoperative endophthalmitis following cataract surgery was 0.017%.


Common causative organisms in cases of chronic postoperative endophthalmitis include P. acnes, fungi, and various less virulent gram-positive and gram-negative organisms.


Symptoms


Insidious onset of visual loss, redness, photophobia, and pain. Symptoms are typically less severe than in patients with acute-onset postoperative endophthalmitis.


Signs (Fig. 10-3)


Slowly progressive intraocular inflammation with variable occurrence of hypopyon and keratic precipitates. A white intracapsular plaque may be present and may be indicative of P. acnes infection. Signs are typically less severe than in patients with acute-onset postoperative endophthalmitis.


Eyelid edema, conjunctival congestion, corneal edema, and aqueous and vitreous inflammation may occur, but generally to a lesser degree than in acute-onset postoperative endophthalmitis.


Differential Diagnosis


Noninfectious uveitis


Retained lens material


Triamcinolone acetonide particles


Longstanding (dehemoglobinized) vitreous hemorrhage


Diagnostic Evaluation


Delayed-onset (chronic) postoperative endophthalmitis is a clinical diagnosis, confirmed with laboratory testing.


If the posterior segment cannot be visualized, B-scan ultrasonography may be helpful to rule out retinal detachment, suprachoroidal hemorrhage, and retained lens fragment.


Cultures: Vitreous samples are more likely to yield a positive culture than are aqueous samples.


Vitreous cultures may be obtained either with a needle (tap) or with PPV instrumentation.


Commonly used culture media include 5% blood agar (most common organisms), chocolate agar (fastidious organisms, such as N. gonorrhoeae and H. influenzae), Sabouraud agar (fungi), thioglycollate broth (anaerobes), and anaerobic blood agar (anaerobes). If delayed-onset (chronic) postoperative endophthalmitis is suspected, the laboratory should be instructed to hold the cultures for at least 2 weeks to allow isolation of fastidious organisms.


Blood culture bottles may also be used.


Treatment


Many authors recommend initial PPV with capsulectomy in cases of chronic postoperative endophthalmitis. Alternatively, one may consider initial tap and inject, followed by more invasive surgery if the clinical examination does not improve. The Endophthalmitis Vitrectomy Study (EVS) did not enroll patients with delayed-onset (chronic) postoperative endophthalmitis, so its findings regarding vitreous tap versus PPV are not necessarily applicable to these patients. If PPV with capsulotomy or capsulectomy is not successful, explantation of the IOL and removal of the capsular bag may be necessary.


Similar to acute-onset postoperative endophthalmitis, a reasonable initial treatment would include intravitreal vancomycin (1 mg in 0.1 mL) and amikacin (0.4 mg in 0.1 mL). However, to reduce the risk of aminoglycoside toxicity, either ceftazidime (2.25 mg in 0.1 mL) or ceftriaxone (2 mg in 0.1 mL) may be considered.


If fungal endophthalmitis is suspected, either intravitreal amphotericin B (0.005 mg in 0.1 mL) or intravitreal voriconazole (0.1 mg in 0.1 mL) may be used. Adjunctive systemic antifungals may be used, typically in consultation with an internist or infectious disease specialist.


In patients with suspected bacterial etiology, intravitreal dexamethasone (0.4 mg in 0.1 mL) may be considered. However, fungal infections are relatively more common in patients with delayed-onset (chronic) postoperative endophthalmitis, so intravitreal dexamethasone should be used with caution in these patients.


Similar to acute-onset postoperative endophthalmitis, subconjunctival vancomycin (25 mg in 0.5 mL), ceftazidime (100 mg in 0.5 mL), and dexamethasone (6 mg in 0.25 mL) can be given.


Similar to acute-onset postoperative endophthalmitis, systemic corticosteroids should be used with caution in certain at-risk patients, including diabetics and the elderly. In addition, fungal infections are relatively more common in these patients, so systemic corticosteroids should be used with caution if fungal infection is suspected.


Fortified topical vancomycin (50 mg/cc) and fortified topical amikacin (20 mg/cc) may be beneficial. However, fortified topical antibiotics may require access to a compounding pharmacy, which may not be available in all locations. As a substitute, commercially available topical antibiotics (such as fourth-generation fluoroquinolones) may be considered. In addition, topical corticosteroids and cycloplegics are suggested.


Prognosis


Because delayed-onset (chronic) postoperative endophthalmitis is frequently caused by indolent organisms, the prognosis may be slightly more favorable than for patients with acute-onset postoperative endophthalmitis caused by more virulent species.


REFERENCES


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.


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.


Doshi RR, Arevalo JF, Flynn HW Jr, et al. Evaluating exaggerated, prolonged, or delayed postoperative intraocular inflammation. Am J Ophthalmol. 2010 July 12 [Epub ahead of print].


Schwartz SG, Flynn HW Jr, Scott IU. Endophthalmitis: classification and current management. Exp Rev Ophthalmol. 2007;2:385–396.



Figure 10-3. This eye had delayed-onset postoperative endophthalmitis. Externally, the eye is not injected, and no anterior chamber keratic precipitates or hypopyon is noted. The white plaque within the capsular bag is suggestive of P. acnes, which was the organism eventually isolated on cultures.


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Nov 5, 2016 | Posted by in OPHTHALMOLOGY | Comments Off on Endophthalmitis
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