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Discussion by Sanjay N. Rao, MD, Randy J. Epstein, MD
Yuhan et al 䡠 Instrument Cleaning and Maintenance in DLK
4. 5. 6. 7. 8. 9. 10. 11.
lamellar refractive surgery. Am J Ophthalmol 1999;127:129 – 36. Lyle WA, Jin GJC. Interface fluid associated with diffuse lamellar keratitis and epithelial ingrowth after laser in situ keratomileusis. J Cataract Refract Surg 1999;25:1009 –12. Smith JR, Maloney RK. Diffuse lamellar keratitis. A new syndrome in lamellar refractive surgery. Ophthalmology 1998;105:1721– 6. Holland SP. Update in cornea and external disease: solving the mystery of “sands of the Sahara” syndrome (diffuse lamellar keratitis). Can J Ophthalmol 1999;34:193– 4. Lachance A, Tremblay M. The sands of the Sahara. Can J Ophthalmol 1998;33:387– 8. Linebarger EJ, Hardten DR, Chu YR, Lindstrom RL. Understanding time course of DLK can help eliminate visual loss. Ocular Surgery News 1999;Sept 1:11–12. Mondino BJ, Rabin BS, Kessler E, et al. Corneal rings with gram-negative bacteria. Arch Ophthalmol 1977;95:2222–5. Schultz CL, Buret AG, Olson ME, et al. Lipopolysaccharide entry in the damaged cornea and specific uptake by polymorphonuclear neutrophils. Infect Immun 2000;68:1731– 4. Schultz CL, Morck DW, McKay SG, et al. Lipopolysaccha-
12.
13.
14.
15.
16.
ride induced acute red eye and corneal ulcers. Exp Eye Res 1997;64:3–9. Richburg FA, Reidy JJ, Apple DJ, Olson RJ. Sterile hypopyon secondary to ultrasonic cleaning solution. J Cataract Refract Surg 1986;12:248 –51. Kreisler KR, Martin SS, Young CW, et al. Postoperative inflammation following cataract extraction caused by bacterial contamination of the cleaning bath detergent. J Cataract Refract Surg 1992;18:106 –10. Yabuuchi E, Kosako Y, Yano I, et al. Transfer of two Burkholderia and an Alcaligenes species to Ralstonia gen. Nov.: Proposal of Ralstonia pickettii (Ralston, Palleroni and Doudoroff 1973) comb. Nov., Ralstonia solanacearum (Smith 1896) comb. Nov. and Ralstonia eutropha (Davis 1969) comb. Nov. Microbiol Immunol 1995;39:897–904. Nosocomial Ralstonia pickettii colonization associated with intrinsically contaminated saline solution —Los Angeles, California, 1998. MMWR Morb Mortal Wkly Rep 1998;47: 285– 6. Wistreich GA, Lechtman MD. Microbiology, 3rd ed. Encino, CA: Glencoe, 1980:438.
Discussion by Sanjay N. Rao, MD Randy J. Epstein, MD This study provides important information that will enhance our understanding of diffuse lamellar keratitis (DLK), a newly described, often vexing clinical problem seen most commonly after otherwise uncomplicated laser in situ keratomileusis procedures. The incidence has been estimated to be as low as 1 in 30 to as high as 1 in 400 procedures.1 The authors have demonstrated, in an excellent retrospective study, that modifying their sterilization regimen led to a statistically significant decrease in the incidence of DLK in their practice. Their data also lend support to the theory (Doane J, Sherrin R, unpublished observations, 1999; Shumer DJ, et al, Preliminary American Academy of Ophthalmology Refractory Surgery Interest Group (RSIG) presentation, 1999) that bacterial endotoxin, rather than bacterial infection per se, is important in the pathogenesis of DLK. This hypothesis is based on the finding that stagnant cleaning fluids or debris on the surface of the used instruments can harbor gram-negative bacteria that can proliferate and produce endotoxin, which then can be deposited on newly sterilized instruments and introduced into the lamellar interface. Diffuse lamellar keratitis usually is first noted between 1 and 6 days after laser in situ keratomileusis surgery.1– 4 All of the patients in the present study were identified at the time of their 1-day postoperative visit. One wonders if their results would have been different had a 1-week postoperative examination also been part of this protocol. Nonetheless, in animal studies, endotoxin-related keratitis, the subject at hand, was most pronounced between several hours and 2 days after exposure.5–7 As the authors acknowledge, no attempt was made to culture or endotoxin test the autoclave water or plastic surgical bowls, although other work has documented that bacteria can be cultured from surgical bowls and autoclave reservoirs, lending indirect support to the hypothesis that bacteria or bacterial endotoxins are
From the Cornea Service, Department of Ophthalmology, Rush-Presbyterian-St. Luke’s Medical Center, Chicago, Illinois. Address correspondence to Randy J. Epstein, MD, 1725 West Harrison Street, Suite 928, Chicago, IL 60612.
involved in the pathogenesis of DLK.8,9 Because this study was retrospective, it is difficult to determine which of the changes in the cleaning and sterilization protocol were most responsible for reducing the incidence of DLK. Emptying the autoclave water reservoir tank at the end of the day alone could have decreased profoundly the incidence of DLK. In conclusion, this study provides convincing evidence that improving cleaning and sterilization protocols can decrease the incidence of DLK. Laser in situ keratomileusis surgeons who encounter a cluster of DLK cases would be well advised to evaluate systematically all of their instrument cleaning and sterilization protocols. Surgeons using autoclaves with reservoirs should make certain that these reservoirs are emptied, cleaned, and dried at the end of the surgical day so as to eliminate the possibility of endotoxin contamination. References 1. Lin RT, Maloney RK. Flap complications associated with lamellar refractive surgery. Am J Ophthalmol 1999;127:129 –36. 2. Alio JL, Perez-Santonja JJ, Tervo T, et al. Postoperative inflammation, microbial complications, and wound healing following laser in situ keratomileusis. J Refract Surg 2000;16: 523–38. 3. Lyle WA, Jin GJC. Interface fluid associated with diffuse lamellar keratitis and epithelial ingrowth after laser in situ keratomileusis. J Cataract Refract Surg 1999;25:1009 –12. 4. Smith JR, Maloney RK. Diffuse lamellar keratitis. A new syndrome in lamellar refractive surgery. Ophthalmology 1998; 105:1721– 6. 5. Mondino BJ, Rabin BS, Kessler E, et al. Corneal rings with gram-negative bacteria. Arch Ophthalmol 1977;95:2222–5. 6. Schultz CL, Buret AG, Olson ME, et al. Lipopolysaccharide entry in the damaged cornea and specific uptake by polymorphonuclear neutrophils. Infect Immun 2000;68:1731– 4. 7. Schultz CL, Morck DW, McKay SG, et al. Lipopolysaccharide induced acute red eye and corneal uclers. Exp Eye Res 1997; 64:3–9.
403
Ophthalmology Volume 109, Number 2, February 2002 8. Holland SP, Mathias RG, Morck DW, et al. Diffuse lamellar keratitis related to endotoxins released from sterilizer reservoir biofilms. Ophthalmology 2000;107:1227–33; discussion 1233– 4.
404
9. Doane JF. Diffuse intralamellar keratitis: sands of Sahara syndrome. In: Buratto L, Brint S, eds. Lasik: Surgical Technique and Complications. New Jersey: Slack, Inc., 2000; chap. 35.
4. 5. 6. 7. 8. 9. 10. 11.
lamellar refractive surgery. Am J Ophthalmol 1999;127:129 – 36. Lyle WA, Jin GJC. Interface fluid associated with diffuse lamellar keratitis and epithelial ingrowth after laser in situ keratomileusis. J Cataract Refract Surg 1999;25:1009 –12. Smith JR, Maloney RK. Diffuse lamellar keratitis. A new syndrome in lamellar refractive surgery. Ophthalmology 1998;105:1721– 6. Holland SP. Update in cornea and external disease: solving the mystery of “sands of the Sahara” syndrome (diffuse lamellar keratitis). Can J Ophthalmol 1999;34:193– 4. Lachance A, Tremblay M. The sands of the Sahara. Can J Ophthalmol 1998;33:387– 8. Linebarger EJ, Hardten DR, Chu YR, Lindstrom RL. Understanding time course of DLK can help eliminate visual loss. Ocular Surgery News 1999;Sept 1:11–12. Mondino BJ, Rabin BS, Kessler E, et al. Corneal rings with gram-negative bacteria. Arch Ophthalmol 1977;95:2222–5. Schultz CL, Buret AG, Olson ME, et al. Lipopolysaccharide entry in the damaged cornea and specific uptake by polymorphonuclear neutrophils. Infect Immun 2000;68:1731– 4. Schultz CL, Morck DW, McKay SG, et al. Lipopolysaccha-
12.
13.
14.
15.
16.
ride induced acute red eye and corneal ulcers. Exp Eye Res 1997;64:3–9. Richburg FA, Reidy JJ, Apple DJ, Olson RJ. Sterile hypopyon secondary to ultrasonic cleaning solution. J Cataract Refract Surg 1986;12:248 –51. Kreisler KR, Martin SS, Young CW, et al. Postoperative inflammation following cataract extraction caused by bacterial contamination of the cleaning bath detergent. J Cataract Refract Surg 1992;18:106 –10. Yabuuchi E, Kosako Y, Yano I, et al. Transfer of two Burkholderia and an Alcaligenes species to Ralstonia gen. Nov.: Proposal of Ralstonia pickettii (Ralston, Palleroni and Doudoroff 1973) comb. Nov., Ralstonia solanacearum (Smith 1896) comb. Nov. and Ralstonia eutropha (Davis 1969) comb. Nov. Microbiol Immunol 1995;39:897–904. Nosocomial Ralstonia pickettii colonization associated with intrinsically contaminated saline solution —Los Angeles, California, 1998. MMWR Morb Mortal Wkly Rep 1998;47: 285– 6. Wistreich GA, Lechtman MD. Microbiology, 3rd ed. Encino, CA: Glencoe, 1980:438.
Discussion by Sanjay N. Rao, MD Randy J. Epstein, MD This study provides important information that will enhance our understanding of diffuse lamellar keratitis (DLK), a newly described, often vexing clinical problem seen most commonly after otherwise uncomplicated laser in situ keratomileusis procedures. The incidence has been estimated to be as low as 1 in 30 to as high as 1 in 400 procedures.1 The authors have demonstrated, in an excellent retrospective study, that modifying their sterilization regimen led to a statistically significant decrease in the incidence of DLK in their practice. Their data also lend support to the theory (Doane J, Sherrin R, unpublished observations, 1999; Shumer DJ, et al, Preliminary American Academy of Ophthalmology Refractory Surgery Interest Group (RSIG) presentation, 1999) that bacterial endotoxin, rather than bacterial infection per se, is important in the pathogenesis of DLK. This hypothesis is based on the finding that stagnant cleaning fluids or debris on the surface of the used instruments can harbor gram-negative bacteria that can proliferate and produce endotoxin, which then can be deposited on newly sterilized instruments and introduced into the lamellar interface. Diffuse lamellar keratitis usually is first noted between 1 and 6 days after laser in situ keratomileusis surgery.1– 4 All of the patients in the present study were identified at the time of their 1-day postoperative visit. One wonders if their results would have been different had a 1-week postoperative examination also been part of this protocol. Nonetheless, in animal studies, endotoxin-related keratitis, the subject at hand, was most pronounced between several hours and 2 days after exposure.5–7 As the authors acknowledge, no attempt was made to culture or endotoxin test the autoclave water or plastic surgical bowls, although other work has documented that bacteria can be cultured from surgical bowls and autoclave reservoirs, lending indirect support to the hypothesis that bacteria or bacterial endotoxins are
From the Cornea Service, Department of Ophthalmology, Rush-Presbyterian-St. Luke’s Medical Center, Chicago, Illinois. Address correspondence to Randy J. Epstein, MD, 1725 West Harrison Street, Suite 928, Chicago, IL 60612.
involved in the pathogenesis of DLK.8,9 Because this study was retrospective, it is difficult to determine which of the changes in the cleaning and sterilization protocol were most responsible for reducing the incidence of DLK. Emptying the autoclave water reservoir tank at the end of the day alone could have decreased profoundly the incidence of DLK. In conclusion, this study provides convincing evidence that improving cleaning and sterilization protocols can decrease the incidence of DLK. Laser in situ keratomileusis surgeons who encounter a cluster of DLK cases would be well advised to evaluate systematically all of their instrument cleaning and sterilization protocols. Surgeons using autoclaves with reservoirs should make certain that these reservoirs are emptied, cleaned, and dried at the end of the surgical day so as to eliminate the possibility of endotoxin contamination. References 1. Lin RT, Maloney RK. Flap complications associated with lamellar refractive surgery. Am J Ophthalmol 1999;127:129 –36. 2. Alio JL, Perez-Santonja JJ, Tervo T, et al. Postoperative inflammation, microbial complications, and wound healing following laser in situ keratomileusis. J Refract Surg 2000;16: 523–38. 3. Lyle WA, Jin GJC. Interface fluid associated with diffuse lamellar keratitis and epithelial ingrowth after laser in situ keratomileusis. J Cataract Refract Surg 1999;25:1009 –12. 4. Smith JR, Maloney RK. Diffuse lamellar keratitis. A new syndrome in lamellar refractive surgery. Ophthalmology 1998; 105:1721– 6. 5. Mondino BJ, Rabin BS, Kessler E, et al. Corneal rings with gram-negative bacteria. Arch Ophthalmol 1977;95:2222–5. 6. Schultz CL, Buret AG, Olson ME, et al. Lipopolysaccharide entry in the damaged cornea and specific uptake by polymorphonuclear neutrophils. Infect Immun 2000;68:1731– 4. 7. Schultz CL, Morck DW, McKay SG, et al. Lipopolysaccharide induced acute red eye and corneal uclers. Exp Eye Res 1997; 64:3–9.
403
Ophthalmology Volume 109, Number 2, February 2002 8. Holland SP, Mathias RG, Morck DW, et al. Diffuse lamellar keratitis related to endotoxins released from sterilizer reservoir biofilms. Ophthalmology 2000;107:1227–33; discussion 1233– 4.
404
9. Doane JF. Diffuse intralamellar keratitis: sands of Sahara syndrome. In: Buratto L, Brint S, eds. Lasik: Surgical Technique and Complications. New Jersey: Slack, Inc., 2000; chap. 35.