Clinical Infectious Diseases Advance Access published January 1, 2015
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Correspondence Surgical Site Infections and Postoperative Factors
and the dressing left until the wound is dry and sealed. Unfortunately, most surgeons seem to derive pleasure from taking the dressing off within 24 hours to admire the incision, and there are no conclusive data in humans to support either my practice or the early removal. However, leaving the dressing on has no potential adverse consequences that I can think of. An area not mentioned by Manian is the issue of perioperative glucose control. A growing body of literature ties perioperative hyperglycemia to a dramatically increased risk for SSI both in diabetic and nondiabetic patients, and most publications in this field demonstrate an increased risk associated with hyperglycemia for at least 2 days after the operation as well as, of course, for hyperglycemia in the operating room [11–20]. However, at this time, the precise level of perioperative glucose control that should be achieved and the optimal method for doing that remain controversial. Finally, I would like to caution readers regarding the interpretation of the article by Murphy et al [21], cited by Manian as possible acquisition of methicillinresistant Staphylococcus aureus (MRSA) infection in the postoperative period. In that article, patients scheduled for orthopedic surgery were screened for MRSA and, if it was found, decolonized. They were then scheduled for surgery after decolonization was confirmed, and there was a higher rate of MRSA infection in these “decolonized” patients. However, the interval between decolonization and surgery was as long as 3 months, they were not screened again, and they received a cephalosporin for prophylaxis. We know that many patients colonized by S. aureus tend to remain colonized or become recolonized after decolonization,
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Downloaded from http://cid.oxfordjournals.org/ at Columbia University Libraries on February 16, 2015
TO THE EDITOR—I read with interest the article by Farrin Manian regarding the role of postoperative factors in surgical site infections (SSIs) [1]. I agree with Dr Manian that, although the majority of SSIs are almost certainly determined during surgery, there are definitely factors after the patient leaves the operating room that can lead to infection. Dr Manian cites several references regarding the risk of infection when surgical drains are left after an operation. It would be astounding if this were not the case. The drain crosses the epidermal barrier to microorganisms and provides a ready route to the surgical site just as a central line directs bacteria into the bloodstream. Although not well studied, the same principles that reduce the risk of central line–associated bloodstream infection (CLABSI) should reduce the risk of drain-associated SSI, including not using drains whenever possible, removing them as soon as possible, and using strict sterile management and dressings, perhaps including chlorhexidine gluconate–impregnated dressings. More studies, such as the one by Degnim et al [2], are definitely needed. In my own practice I have seen a dramatic decline in the use of drains for many surgical procedures compared with their use in the 1970s, but we still have a long way to go in this area. Dr Manian also cites the association between bacteremia and SSI. This connection was demonstrated in animal models many years ago, showing conclusively that in that setting the surgical incision was at risk for infection from bacteremia [3–5]. Of the studies cited by Manian, that by Le Guillou et al [6] is the most convincing; in their study, 9% of the SSIs observed followed a central line–
associated bacteremia with the same organism. This, combined with the strong animal evidence, suggests that the association is real, and provides yet another reason to redouble our efforts to prevent CLABSI. Another article that suggests this association is an interesting report by Ehrenkranz and Pfaff [7] from 1991, when they observed that a cardiac surgical practice that operated in 2 hospitals had a significantly higher mediastinitis rate in one hospital than in the other. Investigation found no difference in processes in the operating rooms, but quite different infection control practices in the intensive care units (ICUs) of the 2 hospitals. When the poorly performing ICU was corrected, the infection rate decreased without any change in other patient care practices. Manian cites the association of skin closure techniques and anticoagulation and hematomas with SSI. Interestingly, there are also animal models that show conclusively that recent incisions are susceptible to infection from the outside after the conclusion of surgery for several days until the incisions are sealed [8, 9]. In addition, work by Olsen et al [10] that demonstrates a higher rate of SSI after spinal surgery in patients with postoperative fecal incontinence also suggests infection from external sources after leaving the operating room. In my own practice, when I perform a clean operation, especially one with placement of a prosthetic device, I seal the incision and place an impermeable sterile dressing on in the operating room, which I leave on for a minimum of 5 days. If wound seepage requires dressing change, this is done in a sterile manner as if we were back in the operating room, and the area is reprepped and redressed in the same manner
and thus the most likely explanation for these patients is that they went into surgery colonized with MRSA and received inappropriate prophylaxis. I thank Dr Manian for bringing up this topic, and I hope that the readers will take this into account as they work in their own institutions to try to minimize the morbidity of SSI. Note
E. Patchen Dellinger Division of General Surgery, University of Washington, Seattle
References 1. Manian FA. The role of postoperative factors in surgical site infections: time to take notice. Clin Infect Dis 2014; 59:1272–6. 2. Degnim AC, Scow JS, Hoskin TL, et al. Randomized controlled trial to reduce bacterial colonization of surgical drains after breast and axillary operations. Ann Surg 2013; 258:240–7. 3. Howe CW. Experimental wound sepsis from transient bacteremia. Surg Gynecol Obstet 1968; 126:1066–70. 4. Howe CW. Experimental wound sepsis from transient Escherichia coli bacteremia. Surgery 1969; 66:570–4. 5. Howe CW. Experimental wound sepsis from transient Klebsiella pneumoniae bacteraemia. Br J Exp Pathol 1969; 50:456–60.
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with postoperative hyperglycemia. J Gastrointest Surg 2009; 13:508–15. Olsen MA, Nepple JJ, Riew KD, et al. Risk factors for surgical site infection following orthopaedic spinal operations. J Bone Joint Surg Am 2008; 90:62–9. Ramos M, Khalpey Z, Lipsitz S, et al. Relationship of perioperative hyperglycemia and postoperative infections in patients who undergo general and vascular surgery. Ann Surg 2008; 248:585–91. Umpierrez GE, Smiley D, Jacobs S, et al. Randomized study of basal-bolus insulin therapy in the inpatient management of patients with type 2 diabetes undergoing general surgery (RABBIT 2 surgery). Diabetes Care 2011; 34:256–61. Vilar-Compte D, Alvarez de Iturbe I, MartinOnraet A, Perez-Amador M, SanchezHernandez C, Volkow P. Hyperglycemia as a risk factor for surgical site infections in patients undergoing mastectomy. Am J Infect Control 2008; 36:192–8. Vriesendorp TM, Morelis QJ, Devries JH, Legemate DA, Hoekstra JB. Early postoperative glucose levels are an independent risk factor for infection after peripheral vascular surgery. A retrospective study. Eur J Vasc Endovasc Surg 2004; 28:520–5. Murphy E, Spencer SJ, Young D, Jones B, Blyth MJ. MRSA colonisation and subsequent risk of infection despite effective eradication in orthopaedic elective surgery. J Bone Joint Surg Br 2011; 93:548–51.
Correspondence: E. Patchen Dellinger, MD, FIDSA, FSHEA, FACS, Division of General Surgery, University of Washington, Box 356410, 1959 NE Pacific St, Seattle, WA 98195-6410 ( [email protected]). Clinical Infectious Diseases® © The Author 2014. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals. [email protected]. DOI: 10.1093/cid/ciu1141
Downloaded from http://cid.oxfordjournals.org/ at Columbia University Libraries on February 16, 2015
Potential conflict of interest. Author certifies no potential conflicts of interest. The author has submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest. Conflicts that the editors consider relevant to the content of the manuscript have been disclosed.
6. Le Guillou V, Tavolacci MP, Baste JM, et al. Surgical site infection after central venous catheter-related infection in cardiac surgery. Analysis of a cohort of 7557 patients. J Hosp Infect 2011; 79:236–41. 7. Ehrenkranz NJ, Pfaff SJ. Mediastinitis complicating cardiac operations: evidence of postoperative causation. Rev Infect Dis 1991; 13:803–14. 8. DuMortier JJ. The resistance of healing wounds to infection. Surg Gynecol Obstet 1963; 56:762–6. 9. Schauerhamer RA, Edlich RF, Panek P, Thul J, Prusak M, Wangensteen OH. Studies in the management of the contaminated wound: VII. Susceptibility of surgical wounds to postoperative surface contamination. Am J Surg 1971; 122:74–7. 10. Olsen MA, Mayfield J, Lauryssen C, et al. Risk factors for surgical site infection in spinal surgery. J Neurosurg 2003; 98:149–55. 11. Ambiru S, Kato A, Kimura F, et al. Poor postoperative blood glucose control increases surgical site infections after surgery for hepato-biliary-pancreatic cancer: a prospective study in a high-volume institute in Japan. J Hosp Infect 2008; 68:230–3. 12. Ata A, Lee J, Bestle SL, Desemone J, Stain SC. Postoperative hyperglycemia and surgical site infection in general surgery patients. Arch Surg 2010; 145:858–64. 13. Kwon S, Thompson R, Dellinger P, Yanez D, Farrohki E, Flum D. Importance of perioperative glycemic control in general surgery: a report from the surgical care and outcomes assessment program. Ann Surg 2013; 257:8–14. 14. Latham R, Lancaster AD, Covington JF, Pirolo JS, Thomas CS. The association of diabetes and glucose control with surgicalsite infections among cardiothoracic surgery patients. Infect Control Hosp Epidemiol 2001; 22:607–12. 15. McConnell YJ, Johnson PM, Porter GA. Surgical site infections following colorectal surgery in patients with diabetes: association
0 JANUARY
Correspondence Surgical Site Infections and Postoperative Factors
and the dressing left until the wound is dry and sealed. Unfortunately, most surgeons seem to derive pleasure from taking the dressing off within 24 hours to admire the incision, and there are no conclusive data in humans to support either my practice or the early removal. However, leaving the dressing on has no potential adverse consequences that I can think of. An area not mentioned by Manian is the issue of perioperative glucose control. A growing body of literature ties perioperative hyperglycemia to a dramatically increased risk for SSI both in diabetic and nondiabetic patients, and most publications in this field demonstrate an increased risk associated with hyperglycemia for at least 2 days after the operation as well as, of course, for hyperglycemia in the operating room [11–20]. However, at this time, the precise level of perioperative glucose control that should be achieved and the optimal method for doing that remain controversial. Finally, I would like to caution readers regarding the interpretation of the article by Murphy et al [21], cited by Manian as possible acquisition of methicillinresistant Staphylococcus aureus (MRSA) infection in the postoperative period. In that article, patients scheduled for orthopedic surgery were screened for MRSA and, if it was found, decolonized. They were then scheduled for surgery after decolonization was confirmed, and there was a higher rate of MRSA infection in these “decolonized” patients. However, the interval between decolonization and surgery was as long as 3 months, they were not screened again, and they received a cephalosporin for prophylaxis. We know that many patients colonized by S. aureus tend to remain colonized or become recolonized after decolonization,
CORRESPONDENCE
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Downloaded from http://cid.oxfordjournals.org/ at Columbia University Libraries on February 16, 2015
TO THE EDITOR—I read with interest the article by Farrin Manian regarding the role of postoperative factors in surgical site infections (SSIs) [1]. I agree with Dr Manian that, although the majority of SSIs are almost certainly determined during surgery, there are definitely factors after the patient leaves the operating room that can lead to infection. Dr Manian cites several references regarding the risk of infection when surgical drains are left after an operation. It would be astounding if this were not the case. The drain crosses the epidermal barrier to microorganisms and provides a ready route to the surgical site just as a central line directs bacteria into the bloodstream. Although not well studied, the same principles that reduce the risk of central line–associated bloodstream infection (CLABSI) should reduce the risk of drain-associated SSI, including not using drains whenever possible, removing them as soon as possible, and using strict sterile management and dressings, perhaps including chlorhexidine gluconate–impregnated dressings. More studies, such as the one by Degnim et al [2], are definitely needed. In my own practice I have seen a dramatic decline in the use of drains for many surgical procedures compared with their use in the 1970s, but we still have a long way to go in this area. Dr Manian also cites the association between bacteremia and SSI. This connection was demonstrated in animal models many years ago, showing conclusively that in that setting the surgical incision was at risk for infection from bacteremia [3–5]. Of the studies cited by Manian, that by Le Guillou et al [6] is the most convincing; in their study, 9% of the SSIs observed followed a central line–
associated bacteremia with the same organism. This, combined with the strong animal evidence, suggests that the association is real, and provides yet another reason to redouble our efforts to prevent CLABSI. Another article that suggests this association is an interesting report by Ehrenkranz and Pfaff [7] from 1991, when they observed that a cardiac surgical practice that operated in 2 hospitals had a significantly higher mediastinitis rate in one hospital than in the other. Investigation found no difference in processes in the operating rooms, but quite different infection control practices in the intensive care units (ICUs) of the 2 hospitals. When the poorly performing ICU was corrected, the infection rate decreased without any change in other patient care practices. Manian cites the association of skin closure techniques and anticoagulation and hematomas with SSI. Interestingly, there are also animal models that show conclusively that recent incisions are susceptible to infection from the outside after the conclusion of surgery for several days until the incisions are sealed [8, 9]. In addition, work by Olsen et al [10] that demonstrates a higher rate of SSI after spinal surgery in patients with postoperative fecal incontinence also suggests infection from external sources after leaving the operating room. In my own practice, when I perform a clean operation, especially one with placement of a prosthetic device, I seal the incision and place an impermeable sterile dressing on in the operating room, which I leave on for a minimum of 5 days. If wound seepage requires dressing change, this is done in a sterile manner as if we were back in the operating room, and the area is reprepped and redressed in the same manner
and thus the most likely explanation for these patients is that they went into surgery colonized with MRSA and received inappropriate prophylaxis. I thank Dr Manian for bringing up this topic, and I hope that the readers will take this into account as they work in their own institutions to try to minimize the morbidity of SSI. Note
E. Patchen Dellinger Division of General Surgery, University of Washington, Seattle
References 1. Manian FA. The role of postoperative factors in surgical site infections: time to take notice. Clin Infect Dis 2014; 59:1272–6. 2. Degnim AC, Scow JS, Hoskin TL, et al. Randomized controlled trial to reduce bacterial colonization of surgical drains after breast and axillary operations. Ann Surg 2013; 258:240–7. 3. Howe CW. Experimental wound sepsis from transient bacteremia. Surg Gynecol Obstet 1968; 126:1066–70. 4. Howe CW. Experimental wound sepsis from transient Escherichia coli bacteremia. Surgery 1969; 66:570–4. 5. Howe CW. Experimental wound sepsis from transient Klebsiella pneumoniae bacteraemia. Br J Exp Pathol 1969; 50:456–60.
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with postoperative hyperglycemia. J Gastrointest Surg 2009; 13:508–15. Olsen MA, Nepple JJ, Riew KD, et al. Risk factors for surgical site infection following orthopaedic spinal operations. J Bone Joint Surg Am 2008; 90:62–9. Ramos M, Khalpey Z, Lipsitz S, et al. Relationship of perioperative hyperglycemia and postoperative infections in patients who undergo general and vascular surgery. Ann Surg 2008; 248:585–91. Umpierrez GE, Smiley D, Jacobs S, et al. Randomized study of basal-bolus insulin therapy in the inpatient management of patients with type 2 diabetes undergoing general surgery (RABBIT 2 surgery). Diabetes Care 2011; 34:256–61. Vilar-Compte D, Alvarez de Iturbe I, MartinOnraet A, Perez-Amador M, SanchezHernandez C, Volkow P. Hyperglycemia as a risk factor for surgical site infections in patients undergoing mastectomy. Am J Infect Control 2008; 36:192–8. Vriesendorp TM, Morelis QJ, Devries JH, Legemate DA, Hoekstra JB. Early postoperative glucose levels are an independent risk factor for infection after peripheral vascular surgery. A retrospective study. Eur J Vasc Endovasc Surg 2004; 28:520–5. Murphy E, Spencer SJ, Young D, Jones B, Blyth MJ. MRSA colonisation and subsequent risk of infection despite effective eradication in orthopaedic elective surgery. J Bone Joint Surg Br 2011; 93:548–51.
Correspondence: E. Patchen Dellinger, MD, FIDSA, FSHEA, FACS, Division of General Surgery, University of Washington, Box 356410, 1959 NE Pacific St, Seattle, WA 98195-6410 ( [email protected]). Clinical Infectious Diseases® © The Author 2014. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals. [email protected]. DOI: 10.1093/cid/ciu1141
Downloaded from http://cid.oxfordjournals.org/ at Columbia University Libraries on February 16, 2015
Potential conflict of interest. Author certifies no potential conflicts of interest. The author has submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest. Conflicts that the editors consider relevant to the content of the manuscript have been disclosed.
6. Le Guillou V, Tavolacci MP, Baste JM, et al. Surgical site infection after central venous catheter-related infection in cardiac surgery. Analysis of a cohort of 7557 patients. J Hosp Infect 2011; 79:236–41. 7. Ehrenkranz NJ, Pfaff SJ. Mediastinitis complicating cardiac operations: evidence of postoperative causation. Rev Infect Dis 1991; 13:803–14. 8. DuMortier JJ. The resistance of healing wounds to infection. Surg Gynecol Obstet 1963; 56:762–6. 9. Schauerhamer RA, Edlich RF, Panek P, Thul J, Prusak M, Wangensteen OH. Studies in the management of the contaminated wound: VII. Susceptibility of surgical wounds to postoperative surface contamination. Am J Surg 1971; 122:74–7. 10. Olsen MA, Mayfield J, Lauryssen C, et al. Risk factors for surgical site infection in spinal surgery. J Neurosurg 2003; 98:149–55. 11. Ambiru S, Kato A, Kimura F, et al. Poor postoperative blood glucose control increases surgical site infections after surgery for hepato-biliary-pancreatic cancer: a prospective study in a high-volume institute in Japan. J Hosp Infect 2008; 68:230–3. 12. Ata A, Lee J, Bestle SL, Desemone J, Stain SC. Postoperative hyperglycemia and surgical site infection in general surgery patients. Arch Surg 2010; 145:858–64. 13. Kwon S, Thompson R, Dellinger P, Yanez D, Farrohki E, Flum D. Importance of perioperative glycemic control in general surgery: a report from the surgical care and outcomes assessment program. Ann Surg 2013; 257:8–14. 14. Latham R, Lancaster AD, Covington JF, Pirolo JS, Thomas CS. The association of diabetes and glucose control with surgicalsite infections among cardiothoracic surgery patients. Infect Control Hosp Epidemiol 2001; 22:607–12. 15. McConnell YJ, Johnson PM, Porter GA. Surgical site infections following colorectal surgery in patients with diabetes: association
