Endophthalmitis: Epidemiology, Causing Agents, Therapy and Visual Outcome with Special Focus on Glaucoma Patients

Abstract

Background Endophthalmitis is one of the most serious emergencies in ophthalmology. In order to reduce its prevalence, it is important to have a proper understanding of potential risk. Surgical therapy with targeted, pathogen-specific medication and an intact immune system are fundamental for preserving visual acuity. As it is unclear whether an unfavourable course is more likely in the presence of underlying ocular disease, a comparison was made between glaucoma patients (G) and non-glaucoma patients (NG) in terms of causative factors, pathogens, treatment and visual acuity. Since a potential alteration of the local immune system in glaucoma has been described, it is of interest to determine whether the clinical course of endophthalmitis in glaucoma patients differ from that of non-glaucoma patients.

Patients and Methods A retrospective analysis of 75 eyes (13 G, 62 NG) who underwent treatment and surgery following a diagnosis of endophthalmitis in the Department of Ophthalmology, University of Erlangen-Nuremberg has been evaluated over a period of 5 years. Clinical characteristics, surgical treatment, microbial spectrum and visual acuity in glaucoma and non-glaucoma eyes were investigated.

Results Severe visual impairment (44%) with inflammation of the anterior chamber (62.7%), hypopyon (52%) and reduced (40%) or absent view (26.7%) of the fundus were predominantly present at first diagnosis in all patients. Previous eye surgery was observed in a total of 53%, primarily cataract surgery. Gram-positive cocci were seen as the most common causative agent in both groups, (G: 23.1%; NG: 38.7%), whereas other rare pathogens were present only in glaucomatous eyes. Pars plana vitrectomy was performed in 76% and enucleations in 20% of all patients, with the latter significantly more common in glaucomatous eyes (p = 0.01). A significant postoperative improvement in visual acuity was achieved in non-glaucoma patients (p < 0.001); visual acuity was worse in glaucomatous eyes.

Conclusion Although rare, early diagnosis and treatment of endophthalmitis is crucial in terms of prognosis. In the present cohort, worse visual acuity outcomes were obtained in glaucoma patients in comparison to non-glaucoma patients.

Fazitbox

Bereits bekannt:

• Trotz intensiver Therapien sind Endophthalmitiden primär mit einem schlechten visuellen Outcome verbunden.

• Da dies bislang nicht beschrieben war, wurde ein Vergleich der klinischen Verläufe zwischen Glaukom- und Nichtglaukompatienten gezogen.

Neu beschrieben:

• Das visuelle Outcome nach Endophthalmitis bei Glaukompatienten war schlechter als bei nicht glaukomatös vorerkrankter Augen.

• Ursächlich hierfür könnten neben dem Vorkommen seltener, aggressiver Erreger auch vorbestehende Ulcera corneae sein, weshalb Glaukompatienten signifikant häufiger einer Enukleation unterzogen wurden.

• Auch pathologische Veränderungen des Immunsystems könnten bei Glaukompatienten eine Rolle spielen.

Conclusion Box

Already known:

• Despite intensive treatment, endophthalmitis is usually associated with poor visual outcomes.

• Since this has not been described previously, a comparison was made between the clinical courses of glaucoma and non-glaucoma patients.

New findings:

• Visual outcomes after endophthalmitis in glaucoma patients was worse than in non-glaucoma patients.

• This could be due to the presence of rare, aggressive pathogens as well as pre-existing corneal ulcers, which is why glaucoma patients underwent enucleation significantly more often.

• Pathologic changes in the immune system may also play a role in glaucoma patients.

Key words

endophthalmitis - glaucoma - infection

Publication History

Received: 17 April 2022

Accepted: 24 May 2022

Accepted Manuscript online:
08 July 2022

Article published online:
30 September 2022

• References/Literatur

• 1 Sheu SJ. Endophthalmitis. Korean J Ophthalmol 2017; 31: 283-289
• 2 Lemley CA, Han DP. Endophthalmitis: a review of current evaluation and management. Retina 2007; 27: 662-680
• 3 Novosad BD, Callegan MC. Severe bacterial endophthalmitis: towards improving clinical outcomes. Expert Rev Ophthalmol 2010; 5: 689-698
• 4 Cunningham C, Widder J, Raiji V. Endophthalmitis. Dis Mon 2017; 63: 45-48
• 5 Durand ML. Endophthalmitis. Clin Microbiol Infect 2013; 19: 227-234
• 6 Callegan MC, Engelbert M, Parke 2nd DW. et al. Bacterial endophthalmitis: epidemiology, therapeutics, and bacterium-host interactions. Clin Microbiol Rev 2002; 15: 111-124
• 7 Kernt M, Kampik A. Endophthalmitis: pathogenesis, clinical presentation, management, and perspectives. Clin Ophthalmol 2010; 4: 121-135
• 8 [Anonymous] Results of the endophthalmitis vitrectomy study. A randomized trial of immediate vitrectomy and of intravenous antibiotics for the treatment of postoperative bacterial endophthalmitis. Endophthalmitis Vitrectomy Study Group. Arch Ophthalmol 1995; 113: 1479-1496
• 9 Kaul K, Tarr JM, Ahmad SI. et al. Introduction to diabetes mellitus. Adv Exp Med Biol 2012; 771: 1-11
• 10 Rieck J. The pathogenesis of glaucoma in the interplay with the immune system. Invest Ophthalmol Vis Sci 2013; 54: 2393-2409
• 11 Hohberger B, Kunze R, Wallukat G. et al. Autoantibodies activating the beta2-adrenergic receptor characterize patients with primary and secondary glaucoma. Front Immunol 2019; 10: 2112
• 12 Von Thun und Hohenstein-Blaul N, Bell K, Pfeiffer N. et al. Autoimmune aspects in glaucoma. Eur J Pharmacol 2016; 787: 105-118
• 13 Joachim SC, Bruns K, Lackner KJ. et al. Antibodies to alpha B-crystallin, vimentin, and heat shock protein 70 in aqueous humor of patients with normal tension glaucoma and IgG antibody patterns against retinal antigen in aqueous humor. Curr Eye Res 2007; 32: 501-509
• 14 Joachim SC, Wuenschig D, Pfeiffer N. et al. IgG antibody patterns in aqueous humor of patients with primary open angle glaucoma and pseudoexfoliation glaucoma. Mol Vis 2007; 13: 1573-1579
• 15 Joachim SC, Reinehr S, Kuehn S. et al. Immune response against ocular tissues after immunization with optic nerve antigens in a model of autoimmune glaucoma. Mol Vis 2013; 19: 1804-1814
• 16 Lu X, Ng DS, Zheng K. et al. Risk factors for endophthalmitis requiring evisceration or enucleation. Sci Rep 2016; 6: 28100
• 17 Kiss S, Dugel PU, Khanani AM. et al. Endophthalmitis rates among patients receiving intravitreal anti-VEGF injections: a USA claims analysis. Clin Ophthalmol 2018; 12: 1625-1635
• 18 Li T, Sun J, Min J. et al. Safety of receiving anti-vascular endothelial growth factor intravitreal injection in office-based vs. operating room settings: a meta-analysis. JAMA Ophthalmol 2021; 139: 1080-1088
• 19 Wong JS, Chan TK, Lee HM. et al. Endogenous bacterial endophthalmitis: an East Asian experience and a reappraisal of a severe ocular affliction. Ophthalmology 2000; 107: 1483-1491
• 20 Callegan MC, Gilmore MS, Gregory M. et al. Bacterial endophthalmitis: therapeutic challenges and host-pathogen interactions. Prog Retin Eye Res 2007; 26: 189-203
• 21 Sudhalkar A, Majji AB, Chhablani J. et al. Pantoea agglomerans endophthalmitis: clinical features and outcomes. Retina 2014; 34: 1702-1706
• 22 Chen H, Cho KS, Vu THK. et al. Commensal microflora-induced T cell responses mediate progressive neurodegeneration in glaucoma. Nat Commun 2018; 9: 3209
• 23 Wax MB. The case for autoimmunity in glaucoma. Exp Eye Res 2011; 93: 187-190
• 24 Boehm N, Beck S, Lossbrand U. et al. Analysis of complement proteins in retina and sera of glaucoma patients. ARVO Annual Meeting Abstract. Invest Ophthalmol Vis Sci 2010; 51: 5221
• 25 Baudouin C, Kolko M, Melik-Parsadaniantz S. et al. Inflammation in Glaucoma: From the back to the front of the eye, and beyond. Prog Retin Eye Res 2021; 83: 100916
• 26 Wax MB, Tezel G, Yang J. et al. Induced autoimmunity to heat shock proteins elicits glaucomatous loss of retinal ganglion cell neurons via activated T-cell-derived fas-ligand. J Neurosci 2008; 28: 12085-12096
• 27 Tezel G, Edward DP, Wax MB. Serum autoantibodies to optic nerve head glycosaminoglycans in patients with glaucoma. Arch Ophthalmol 1999; 117: 917-924
• 28 Yang J, Patil RV, Yu H. et al. T cell subsets and sIL-2R/IL-2 levels in patients with glaucoma. Am J Ophthalmol 2001; 131: 421-426
• 29 Wax MB, Barrett DA, Pestronk A. Increased incidence of paraproteinemia and autoantibodies in patients with normal-pressure glaucoma. Am J Ophthalmol 1994; 117: 561-568
• 30 Hohberger B, Hosari S, Wallukat G. et al. Agonistic autoantibodies against β2-adrenergic receptor influence retinal microcirculation in glaucoma suspects and patients. PLoS One 2021; 16: e0249202