“An ounce of prevention is worth a pound of cure.”
Cataract surgery and laser in situ keratomileusis (LASIK) are the most commonly performed intraocular and refractive surgical procedures, respectively. Thankfully, with the advent of microincision cataract surgery and the use of intracameral antibiotics, the incidence of post-surgical endophthalmitis is low. The global reported incidence of post-cataract surgery endophthalmitis ranges from 0.02% to 0.26%.1,2 The incidence of infectious keratitis after surface ablation and LASIK varies widely depending on the data source and has been reported to be 0.2% (1 case in 500) after surface ablation and 0.035% after LASIK.3
Sterile, noninfectious, postoperative anterior segment inflammation is not uncommon in clinical practice. First described in 1992, toxic anterior segment syndrome (TASS) is characterized by sterile postoperative inflammation of the anterior segment after cataract surgery.4 A variety of substances have been implicated as causes of TASS. These can be broadly divided into extraocular substances that inadvertently enter the anterior chamber during or after surgery (eg, talc from gloves, ophthalmic ointments), products that are introduced into the anterior chamber as part of the surgical procedure (eg, intracameral anaesthetics, antibiotics), and irritants on the surface of intraocular surgical instruments that have accumulated as a consequence of inadequate or inappropriate cleaning (eg, detergents, heat-stable endotoxins, biofilms, and impurities in autoclave steam).
Diffuse lamellar keratitis (DLK) is a recently recognised condition primarily associated with LASIK. First described by Smith and Maloney in 1998, it is characterized by diffuse infiltrate in the interface, progressively increasing in extent and density before resolving.5 DLK usually responds to intensive topical steroids, however, lifting of the flap and irrigation may be required in more advanced cases. Untreated or severe cases may progress to melting of the flap with the potential for significant vision loss.
In nature bacteria exists as either planktonic, free-floating individual organisms or as a biofilm conglomerate, which are bacteria that produce and live in a polysaccharide biofilm.6 A biofilm is an assemblage of microbial cells that is irreversibly associated with a surface and enclosed in a matrix of primarily polysaccharide material. Noncellular materials such as corrosion particles or blood components, depending on the environment in which the biofilm has developed, may also be found in the biofilm matrix. Biofilm-associated organisms also differ from their planktonic, freely suspended, counterparts with respect to the genes that are transcribed. Biofilms may form on a wide variety of surfaces, including living tissues, indwelling medical devices, potable water system piping, or natural aquatic systems.
The durability of microbial biofilms during infections after contamination of medical equipment, growth on medical devices, and growth in the environment is well established.7–9 Although the etiology can be multifactorial, biofilms/endotoxins are strongly associated in causing sterile, acute post-surgical ocular inflammation clinically identified as DLK and/or TASS. Simon et al. in 2000 reported on a large cluster outbreak of DLK in 52 eyes related to endotoxins released from gram-negative biofilms in sterilizer reservoirs.10 Epidemiologic investigation showed that biofilm control in the sterilizer reservoirs was associated with a significant reduction in the development of DLK. Sorenson et al. in 2016 very eloquently demonstrated the causal relationship between TASS (following uncomplicated cataract surgery) and bacterial biofilm contamination of autoclave reservoirs. Their data suggests widespread prevalence of bacterial biofilms on fluid-reservoir walls, despite adherence to manufacturer guidelines for cleaning and maintenance.11
In this issue, Sorenson et al. (page 340) report on a cluster of DLK associated with tabletop autoclaves and resulting biofilms. As healthcare providers both clinicians and the paramedical staff has to be vigilant on the issues around safe and adequate sterilization of instruments so we can all provide the best outcomes for the patients we care for.
1. Day AC, Donachie PH, Sparrow JM, Johnston RL; Royal College of Ophthalmologists' National Ophthalmology Database. The Royal College of Ophthalmologists' National Ophthalmology Database study of cataract surgery: report 1, visual outcomes and complications. Eye (Lond) 2015;29:552–560
2. Katz G, Blum S, Leeva O, Axer-Siegel R, Moisseiev J, Esler G, Ehrlic R. Intracameral cefuroxime and the incidence of post-cataract endophthalmitis: an Israeli experience. Graefes Arch Clin Exp Ophthalmol 2015;253:1729–1733
3. Llovet F, de Rojas V, Interlandi E, Martín C, Cobo-Soriano R, Ortega-Usobiaga J, Baviera J. Infectious keratitis in 204 586 LASIK procedures. Ophthalmology 2010;117:232–238
4. Monson MC, Mamalis N, Olson RJ. Toxic anterior segment inflammation following cataract surgery. J Cataract Refract Surg 1992;18:184–189
5. Smith RJ, Maloney RK. Diffuse lamellar keratitis. A new syndrome in lamellar refractive surgery. Ophthalmology 1998;105:1721–1726
6. Christersson LA, Zambon JJ, Genco RJ. Dental bacterial plaques. Nature and role in periodontal disease. J Clin Periodontol 1991;18:441–446
7. Dunne WM Jr. Bacterial adhesion: seen any good biofilms lately? Clin Microbiol Rev 2002;15:155–166
8. Percival SL, Suleman L, Vuotto C, Donelli G. Healthcare-associated infections, medical devices and biofilms: risk, tolerance and control. J Med Microbiol 2015;64:323–334
9. Gupta P, Sarkar S, Das B, Bhattacharjee S, Tribedi P. Biofilm, pathogenesis and preventionda journey to break the wall: a review. Arch Microbiol 2016;198:1–15
10. Holland SP, Mathias RG, Morck DW, Chiu J, Slade SG. Diffuse lamellar keratitis related to endotoxins released from sterilizer reservoir biofilms. Ophthalmology 2000;107:1227–1233
11. Sorenson AL, Sorenson RL, Evans DJ. Toxic anterior segment syndrome caused by autoclave reservoir wall biofilms and their residual toxins. J Cataract Refract Surg 2016;42:1602–1614