MACULAR INFARCTION AFTER ENTEROCOCCUS FAECALIS ENDOPHTHALMITIS Ekta Rishi, MS, Daraius Shroff, MS, G.V.N. Rama Kumar, MD, Pukhraj Rishi, MS
Purpose: To describe a case of macular infarction occurring after Enterococcus faecalis endophthalmitis in a patient who had undergone cataract surgery. Methods: A 74-year-old woman who underwent uneventful phacoemulsification with intraocular lens implantation developed E. faecalis endophthalmitis on the second postoperative day. Management included repeated intravitreal antibiotic treatment, vitrectomy, and intraocular lens explantation. Results: One week after intraocular inflammation subsided, macular infarction was noted clinically, which was confirmed by fundus fluorescein angiography. Visual acuity did not improve beyond 1/60 by Snellen chart testing. Conclusion: Posterior segment involvement, including optic atrophy, macular hole formation, and tractional retinal detachment, has been reported clinically as a complication of E. faecalis endophthalmitis. Macular infarction could be another sight-threatening complication of endophthalmitis due to E. faecalis. RETINAL CASES & BRIEF REPORTS 3:247–250, 2009
From the Medical Research Foundation, Chennai, India.
courses of intravitreal ceftazidime (2.25 mg/0.1 mL) and vancomycin (1 mg/0.1 mL) followed by pars plana vitrectomy after 3 days. Culture of vitreous aspirate yielded E. faecalis. The patient presented to us with exacerbation of inflammation, which was unresponsive to topical treatment, 1 month after vitrectomy. Visual acuity in the right eye was light perception. At our institution, the patient underwent intraocular lens and capsular bag removal and vitrectomy and was treated with intravitreal ceftazidime (2.25 mg/0.1 mL) and vancomycin (1 mg/0.1 mL). Intraoperatively, retinal hemorrhages were noted at the posterior pole. Cultures of intraocular fluid aspirate and intraocular lens yielded E. faecalis that was susceptible only to vancomycin. She was treated again with intravitreal vancomycin (1 mg/0.1 mL) on the third postoperative day. Infection and inflammation resolved clinically after 1 week; best-corrected (Snellen) visual acuity was 1/60. Results of anterior segment examination were unremarkable, and a clear vitreous cavity permitted detailed fundus evaluation. Dot and blot retinal hemorrhages were noted at the macula with loss of the foveal reflex (Fig. 1). Fundus fluorescein angiography showed an irregular area of ⬇2 disk diameters with nonperfusion of both the capillaries and larger vessels of the retina and the choroidal vessels at the macula, suggestive of macular infarction. Areas of blocked fluorescence were seen corresponding to the retinal hemorrhages (Fig. 2). Flash electroretinogram showed a decrease in the b-wave amplitude and in the oscillatory potentials, confirming the isch-
E
nterococcus faecalis is the causative organism in ⬇1% of cases of postoperative endophthalmitis.1 Clinically, the visual outcome is usually poor, with only ⬇15% of these patients having visual acuity better than 20/200.1,2 We describe a case of macular infarction simulating aminoglycoside toxicity in a patient with E. faecalis endophthalmitis after cataract surgery. Case Report A 74-year-old woman was referred to us with a diagnosis of postoperative culture-positive E. faecalis endophthalmitis. She had undergone uneventful phacoemulsification with intraocular lens implantation in the right eye 2 months ago, with good visual recovery on the first postoperative day. This was followed by an episode of endophthalmitis that was detected on the second postoperative day. She had been treated with two
The authors have no proprietary interests in this report. Reprint requests: Pukhraj Rishi, DMSc, Sankara Nethralaya, 18 College Road, Chennai 600006, India; e-mail: [email protected]
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Fig. 1. Color fundus photography shows mild disk pallor, dot and blot hemorrhages at the macula, and loss of the foveal reflex, suggestive of macular ischemia. Hollenhorst plaques can be seen in the superotemporal branch of the central retinal artery.
emic lesion (Fig. 3). The patient was known to have hypertension that was controlled with medication. In view of the fundus findings of Hollenhorst plaques, complete cardiology evaluation, laboratory investigations, and carotid Doppler ultrasonography were performed, which did not reveal any significant abnormality.
Discussion E. faecalis is a gram-positive coccus associated with virulent endophthalmitis.3 E. faecalis has been shown to localize in close proximity to retinal tissues and vitreal structures. Cytolysin-producing strains have been reported to produce fulminant and destruc-
Fig. 2. Fundus fluorescein angiography shows an irregular 2-diskdiameter area with nonperfusion of both the capillaries and larger vessels of the retina and the choroidal vessels at the macula, suggestive of macular infarction. Areas of blocked fluorescence are seen corresponding to the retinal hemorrhages.
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tive changes in retinal architecture and a decline in retinal function.4 Histopathologic examination in these cases has revealed substantial disorganization and lysis of cells in all retinal layers. A precipitous decline in the electroretinogram b-wave amplitude has also been reported in experimental models.5 In the current case, a possible cause of the macular ischemia could have been the multiple intravitreal antibiotic injections that the patient underwent, which could be retinotoxic due to high vitreous levels of the drug.6 However, there was no use of any aminoglycoside antibiotic at any stage in the reported case. To our knowledge, no retinal toxicity has been observed with intravitreal injection of ceftazidime at concentrations of 2.25 mg/0.1 mL or with intravitreal injection of vancomycin at doses up to 2 mg.7,8 Retinal toxicity has, however, been reported after repeated combinations of intravitreal injections of vancomycin and aminoglycoside and hence was part of the differential diagnosis in this case. However, in a rabbit model, the outer retina and retinal pigment epithelium were mainly affected, while in our case the electroretinogram was suggestive of inner retinal layer damage.9 The decline in the electroretinogram b-wave amplitude in the current case suggests that the causative organism was a cytolysin-expressing E. faecalis strain. It has been reported that electroretinogram loss in eyes infected by this strain is a result of toxinmediated destruction of the retina and not due to inflammatory reaction alone. The possibility of a mistaken drug being administered to the patient by the previous surgeon before the patient was referred to us cannot be completely ruled out and could have led to a similar clinical picture. The Hollenhorst plaques in our case were an incidental finding; the affected vessel was clearly patent by fundus fluorescein angiography, and the extent of macular infarction was beyond its distribution territory. Posterior segment involvement, including optic atrophy, macular hole formation, and tractional retinal detachment, has been reported clinically as a complication of E. faecalis endophthalmitis.10,11 To our knowledge, macular infarction has not been reported after E. faecalis endophthalmitis. Our case suggests that E. faecalis toxin–induced destruction of retinal architecture can lead to macular ischemia and thus poor visual outcome. In addition, delayed vitrectomy and persistence of infection because of a retained intraocular lens after vitrectomy10
MACULAR INFARCTION AFTER ENTEROCOCCUS FAECALIS ENDOPHTHALMITIS
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Fig. 3. Flash electroretinogram shows a decrease in the b-wave amplitude and in the oscillatory potentials, confirming the ischemic lesion. The decline in the electroretinogram b-wave amplitude was possibly a result of toxin-mediated retinal degeneration.
might be the cause of greater structural damage to the retina. Key words: endophthalmitis, macular infarction, Enterococcus faecalis.
References 1.
2.
Endophthalmitis Vitrectomy Study Group. Microbiologic factors and visual outcome in the Endophthalmitis Vitrectomy Study. Am J Ophthalmol 1996;122:830–846. Driebe WT, Mandelbaum S, Forster RK, et al. Pseudophakic endophthalmitis. Diagnosis and management. Ophthalmology 1986;93:442–448.
3.
4.
5.
6.
Choi S, Hahn TW, Osterhout G, O’Brien TP. Comparative intravitreal antibiotic therapy for experimental Enterococcus faecalis endophthalmitis. Arch Ophthalmol 1996;114: 61–65. Callegan MC, Engelbert M, Parke DW 2nd, et al. Bacterial endophthalmitis: epidemiology, therapeutics, and bacteriumhost interactions. Clin Microbiol Rev 2002;15:111–124. Jett BD, Jensen HG, Atkuri RV, Gilmore MS. Evaluation of therapeutic measures for treating endophthalmitis caused by isogenic toxin-producing and toxin-nonproducing Enterococcus faecalis strains. Invest Ophthalmol Vis Sci 1995;36:9–15. Haider S. Intraocular vancomycin levels after intravitreal injection in post– cataract extraction endophthalmitis. Retina 2001;21:210–213.
250 7.
8.
9.
RETINAL CASES & BRIEF REPORTSℜ Campochiaro PA, Green WR. Toxicity of intravitreous ceftazidime in primate retina. Arch Ophthalmol 1992;110:1625– 1629. Pflugfelder SC, Hernandez E, Fliesler SJ, et al. Intravitreal vancomycin. Retinal toxicity, clearance, and interaction with gentamicin. Arch Ophthalmol 1987;105:831– 837. Oum BS, D’Amico DJ, Kwak HW, Wong KW. Intravitreal antibiotic therapy with vancomycin and aminoglycoside: examination of the retinal toxicity of repetitive injections after
10.
11.
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vitreous and lens surgery. Graefes Arch Clin Exp Ophthalmol 1992;230:56–61. Scott IU, Loo RH, Flynn HW Jr, Miller D. Endophthalmitis caused by Enterococcus faecalis: antibiotic selection and treatment outcomes. Ophthalmology 2003;110:1573– 1577. Teoh SC, Lee JJ, Chee CK, Au Eong KG. Recurrent Enterococcus faecalis endophthalmitis after phacoemulsification. J Cataract Refract Surg 2005;31:622–666.
Purpose: To describe a case of macular infarction occurring after Enterococcus faecalis endophthalmitis in a patient who had undergone cataract surgery. Methods: A 74-year-old woman who underwent uneventful phacoemulsification with intraocular lens implantation developed E. faecalis endophthalmitis on the second postoperative day. Management included repeated intravitreal antibiotic treatment, vitrectomy, and intraocular lens explantation. Results: One week after intraocular inflammation subsided, macular infarction was noted clinically, which was confirmed by fundus fluorescein angiography. Visual acuity did not improve beyond 1/60 by Snellen chart testing. Conclusion: Posterior segment involvement, including optic atrophy, macular hole formation, and tractional retinal detachment, has been reported clinically as a complication of E. faecalis endophthalmitis. Macular infarction could be another sight-threatening complication of endophthalmitis due to E. faecalis. RETINAL CASES & BRIEF REPORTS 3:247–250, 2009
From the Medical Research Foundation, Chennai, India.
courses of intravitreal ceftazidime (2.25 mg/0.1 mL) and vancomycin (1 mg/0.1 mL) followed by pars plana vitrectomy after 3 days. Culture of vitreous aspirate yielded E. faecalis. The patient presented to us with exacerbation of inflammation, which was unresponsive to topical treatment, 1 month after vitrectomy. Visual acuity in the right eye was light perception. At our institution, the patient underwent intraocular lens and capsular bag removal and vitrectomy and was treated with intravitreal ceftazidime (2.25 mg/0.1 mL) and vancomycin (1 mg/0.1 mL). Intraoperatively, retinal hemorrhages were noted at the posterior pole. Cultures of intraocular fluid aspirate and intraocular lens yielded E. faecalis that was susceptible only to vancomycin. She was treated again with intravitreal vancomycin (1 mg/0.1 mL) on the third postoperative day. Infection and inflammation resolved clinically after 1 week; best-corrected (Snellen) visual acuity was 1/60. Results of anterior segment examination were unremarkable, and a clear vitreous cavity permitted detailed fundus evaluation. Dot and blot retinal hemorrhages were noted at the macula with loss of the foveal reflex (Fig. 1). Fundus fluorescein angiography showed an irregular area of ⬇2 disk diameters with nonperfusion of both the capillaries and larger vessels of the retina and the choroidal vessels at the macula, suggestive of macular infarction. Areas of blocked fluorescence were seen corresponding to the retinal hemorrhages (Fig. 2). Flash electroretinogram showed a decrease in the b-wave amplitude and in the oscillatory potentials, confirming the isch-
E
nterococcus faecalis is the causative organism in ⬇1% of cases of postoperative endophthalmitis.1 Clinically, the visual outcome is usually poor, with only ⬇15% of these patients having visual acuity better than 20/200.1,2 We describe a case of macular infarction simulating aminoglycoside toxicity in a patient with E. faecalis endophthalmitis after cataract surgery. Case Report A 74-year-old woman was referred to us with a diagnosis of postoperative culture-positive E. faecalis endophthalmitis. She had undergone uneventful phacoemulsification with intraocular lens implantation in the right eye 2 months ago, with good visual recovery on the first postoperative day. This was followed by an episode of endophthalmitis that was detected on the second postoperative day. She had been treated with two
The authors have no proprietary interests in this report. Reprint requests: Pukhraj Rishi, DMSc, Sankara Nethralaya, 18 College Road, Chennai 600006, India; e-mail: [email protected]
247
RETINAL CASES & BRIEF REPORTSℜ
248
Fig. 1. Color fundus photography shows mild disk pallor, dot and blot hemorrhages at the macula, and loss of the foveal reflex, suggestive of macular ischemia. Hollenhorst plaques can be seen in the superotemporal branch of the central retinal artery.
emic lesion (Fig. 3). The patient was known to have hypertension that was controlled with medication. In view of the fundus findings of Hollenhorst plaques, complete cardiology evaluation, laboratory investigations, and carotid Doppler ultrasonography were performed, which did not reveal any significant abnormality.
Discussion E. faecalis is a gram-positive coccus associated with virulent endophthalmitis.3 E. faecalis has been shown to localize in close proximity to retinal tissues and vitreal structures. Cytolysin-producing strains have been reported to produce fulminant and destruc-
Fig. 2. Fundus fluorescein angiography shows an irregular 2-diskdiameter area with nonperfusion of both the capillaries and larger vessels of the retina and the choroidal vessels at the macula, suggestive of macular infarction. Areas of blocked fluorescence are seen corresponding to the retinal hemorrhages.
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tive changes in retinal architecture and a decline in retinal function.4 Histopathologic examination in these cases has revealed substantial disorganization and lysis of cells in all retinal layers. A precipitous decline in the electroretinogram b-wave amplitude has also been reported in experimental models.5 In the current case, a possible cause of the macular ischemia could have been the multiple intravitreal antibiotic injections that the patient underwent, which could be retinotoxic due to high vitreous levels of the drug.6 However, there was no use of any aminoglycoside antibiotic at any stage in the reported case. To our knowledge, no retinal toxicity has been observed with intravitreal injection of ceftazidime at concentrations of 2.25 mg/0.1 mL or with intravitreal injection of vancomycin at doses up to 2 mg.7,8 Retinal toxicity has, however, been reported after repeated combinations of intravitreal injections of vancomycin and aminoglycoside and hence was part of the differential diagnosis in this case. However, in a rabbit model, the outer retina and retinal pigment epithelium were mainly affected, while in our case the electroretinogram was suggestive of inner retinal layer damage.9 The decline in the electroretinogram b-wave amplitude in the current case suggests that the causative organism was a cytolysin-expressing E. faecalis strain. It has been reported that electroretinogram loss in eyes infected by this strain is a result of toxinmediated destruction of the retina and not due to inflammatory reaction alone. The possibility of a mistaken drug being administered to the patient by the previous surgeon before the patient was referred to us cannot be completely ruled out and could have led to a similar clinical picture. The Hollenhorst plaques in our case were an incidental finding; the affected vessel was clearly patent by fundus fluorescein angiography, and the extent of macular infarction was beyond its distribution territory. Posterior segment involvement, including optic atrophy, macular hole formation, and tractional retinal detachment, has been reported clinically as a complication of E. faecalis endophthalmitis.10,11 To our knowledge, macular infarction has not been reported after E. faecalis endophthalmitis. Our case suggests that E. faecalis toxin–induced destruction of retinal architecture can lead to macular ischemia and thus poor visual outcome. In addition, delayed vitrectomy and persistence of infection because of a retained intraocular lens after vitrectomy10
MACULAR INFARCTION AFTER ENTEROCOCCUS FAECALIS ENDOPHTHALMITIS
249
Fig. 3. Flash electroretinogram shows a decrease in the b-wave amplitude and in the oscillatory potentials, confirming the ischemic lesion. The decline in the electroretinogram b-wave amplitude was possibly a result of toxin-mediated retinal degeneration.
might be the cause of greater structural damage to the retina. Key words: endophthalmitis, macular infarction, Enterococcus faecalis.
References 1.
2.
Endophthalmitis Vitrectomy Study Group. Microbiologic factors and visual outcome in the Endophthalmitis Vitrectomy Study. Am J Ophthalmol 1996;122:830–846. Driebe WT, Mandelbaum S, Forster RK, et al. Pseudophakic endophthalmitis. Diagnosis and management. Ophthalmology 1986;93:442–448.
3.
4.
5.
6.
Choi S, Hahn TW, Osterhout G, O’Brien TP. Comparative intravitreal antibiotic therapy for experimental Enterococcus faecalis endophthalmitis. Arch Ophthalmol 1996;114: 61–65. Callegan MC, Engelbert M, Parke DW 2nd, et al. Bacterial endophthalmitis: epidemiology, therapeutics, and bacteriumhost interactions. Clin Microbiol Rev 2002;15:111–124. Jett BD, Jensen HG, Atkuri RV, Gilmore MS. Evaluation of therapeutic measures for treating endophthalmitis caused by isogenic toxin-producing and toxin-nonproducing Enterococcus faecalis strains. Invest Ophthalmol Vis Sci 1995;36:9–15. Haider S. Intraocular vancomycin levels after intravitreal injection in post– cataract extraction endophthalmitis. Retina 2001;21:210–213.
250 7.
8.
9.
RETINAL CASES & BRIEF REPORTSℜ Campochiaro PA, Green WR. Toxicity of intravitreous ceftazidime in primate retina. Arch Ophthalmol 1992;110:1625– 1629. Pflugfelder SC, Hernandez E, Fliesler SJ, et al. Intravitreal vancomycin. Retinal toxicity, clearance, and interaction with gentamicin. Arch Ophthalmol 1987;105:831– 837. Oum BS, D’Amico DJ, Kwak HW, Wong KW. Intravitreal antibiotic therapy with vancomycin and aminoglycoside: examination of the retinal toxicity of repetitive injections after
10.
11.
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vitreous and lens surgery. Graefes Arch Clin Exp Ophthalmol 1992;230:56–61. Scott IU, Loo RH, Flynn HW Jr, Miller D. Endophthalmitis caused by Enterococcus faecalis: antibiotic selection and treatment outcomes. Ophthalmology 2003;110:1573– 1577. Teoh SC, Lee JJ, Chee CK, Au Eong KG. Recurrent Enterococcus faecalis endophthalmitis after phacoemulsification. J Cataract Refract Surg 2005;31:622–666.
