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Peri-prosthetic Joint Infections (PJIs)


Traditionally, the cause of most surgical site infections (SSIs) has been either indeterminable or, as in the case of bowel contaminants, an accepted risk of surgery. It is our belief, however, that the etiology of peri-prosthetic joint infections (PJI), a specific subset of SSIs, can be determined and should not be an accepted risk of surgery.

SSI vs PJI


The term SSI commonly refers to any infection that results from surgery. Lumping the varieties of SSI’s together, however, can cause confusion. In this discussion the term “SSI” is reserved for soft-tissue infections, which are differentiated from peri-prosthetic joint infections (or deep-joint infections) that can occur after total joint replacement surgery.

The implantation of foreign material in the body fundamentally changes the pathophysiology of the infectious process. An inoculum of more than one million bacteria is required to cause an SSI, and the bacteria usually enter the wound from the adjacent skin or cut bowel.1 In sharp contrast, it has been shown that a single bacterium can cause a PJI, and it usually enters the wound as airborne contamination.2-4

Biofilms

SSIs manifest in one day to one month. PJIs manifest in one week to one year. Why the difference?

The answer is biofilm.5 In the presence of an implanted foreign material, the bacterium produces a coating of extracellular polymeric substances, also known as exopolysaccharide—a biofilm that effectively protects it from both antibodies and antibiotics. The bacterium can go dormant for up to a year and then, when the conditions are favorable, it multiplies into a deep infection.6-8

In contrast, bacteria cannot produce effective biofilm in soft tissue. Without a biofilm coating, bacteria in soft tissue are exposed to both antibodies and antibiotics. Since it takes more than a million bacteria to cause a soft tissue SSI, any airborne contamination in the operating room is virtually irrelevant for soft tissue SSIs. It is highly unlikely that the air could contain that level of biological contaminants.

Severity of a PJI

The soft tissue SSI is generally a minor and easily treatable complication. In contrast, the PJI is a catastrophic complication requiring explantation of the joint, IV antibiotics, prolonged hospitalization and, if the patient survives without amputation, re-implantation of the prosthetic joint at a later date. Even without amputation, these patients are severely and permanently debilitated. It has been shown that most of these patients never regain full capacity and frequently cannot accomplish the activities of daily living. 12% of patients rate their life after surviving a DJI as “worse than death.”9

Prevalence of PJIs

While PJIs typically occur only in about 1-2% of total joint replacement surgeries, the incidence can be much higher at any given hospital. Ironically, many of the hospitals reporting higher than “normal” deep joint infection rates are well known for their high quality care. This seems to indicate that reducing the PJI rate is not as simple as strictly following accepted operating room protocols—these high quality hospitals are already doing that. Logically, there must be a previously unrecognized causative factor that is an accepted part of the current protocol.

A Newly Discovered Possible Cause of PJIs

New studies suggest that the unrecognized causative factor may be forced-air patient warming devices, also known as forced-air warming or “FAW.”

Let’s start from the beginning…

Where do infectious agents come from?

The CDC has said that PJIs are primarily caused by Staphylococcus aureus, coagulase-negative staphylococci and gram-negative bacilli, predominantly skin bacteria.10 Most of the bacteria in the operating room are shed from the skin of the surgical staff.11-16 Dispersed airborne skin bacteria can also originate in the perineal region of the staff, including vaginal and rectal carriage.10,17-24

The average person sheds one billion skin cells per day and up to 10% of these have bacteria attached.25-28 The skin cells have been called “skin rafts” because they ride the air currents in the operating room, transporting the attached bacteria much like a flying carpet.13

Contaminated medical equipment can also spread infectious agents.29-34 One study showed that 58% of the FAW blowers tested were emitting large quantities of internally generated (grown) germ-sized particles from the hose end.29 In another study, 96% of the blowers were emitting up to 300 million germ-sized particles per hour.30

It has been shown in many studies that bacteria in the operating room can ride air currents.35-38 Since the airflow of the ventilation air is from ceiling to floor, it is not surprising that the shed skin particles and bacteria concentrate near the floor.36,37,39,40

How do infectious agents get from the contaminated floor to the sterile surgical wound?

The answer: forced-air patient warming. FAW produces significant amounts of waste heat. The nearly 1000 watts of waste heat from a lower body or underbody FAW blanket escapes from under the surgical drapes at their lower edge near the floor,41 warming the floor air that has the highest concentration of airborne contaminants. The heated floor air rises alongside the surgical table, directly into the downward ventilation airflow and into the sterile surgical field above the wound.42-44

“...forced-air warming established convection currents that mobilized resident air from non-sterile areas such as the floor and under the anaesthesia/surgery drape into the surgical site.” McGovern et al42

Alternatively, the waste heat from an upper body blanket has been shown to both rise along the anesthesia screen and to radiate through the drapes. If a surgical light is positioned in the typical location over the chest of the patient, the rising warm waste air crosses over the anesthesia screen into the “dead zone” under the light and then into the sterile field.45 Contaminants from the anesthesia provider as well as the patient’s head and arms have been shown to ride the convection current of waste heated air into the sterile surgical field.42,44

The radiant waste heat has been shown to increase the temperature at the surgical site by 5˚C. That heat radiating through the drapes interacts with the downward-flowing ventilation air to form vortexes above the sterile field. The rapidly spinning air can suck contaminants from the floor and deposit them at the surgical wound. One study found 2,000 times more contaminant particles in the air over the wound with Bair Hugger (FAW) than with air-free HotDog® conductive fabric patient warming. With HotDog, only 1,000 particles per cubic meter of air were present. With Bair Hugger warming, the particle count was 2,174,000 per cubic meter, an increase of 217,300%.46

With five peer-reviewed, published studies documenting this effect, it is now irrefutable that the massive amount of waste heat from FAW venting near the floor grossly disrupts the protection of the surgical ventilation system.42-46 The waste heat has been clearly shown to mobilize contaminants from the floor and head end of the patient into the sterile surgical field.

Is there proof of infection?

If the standard of proof requires a multi-center, prospective, randomized controlled trial, the answer is “no.” Given the cost involved, that study is unlikely to ever be done. The exercise of basic logic, however, reveals ample proof.

It has been shown that the concentration of airborne contaminants in the surgical field is directly proportional to the concentration of contaminants in the wound.47-57 The waste heat from FAW clearly increases the airborne contamination in the sterile surgical field.42-46,58,59 Contaminating the air in the surgical field with contaminated air from the floor inevitably leads to increased contamination of the wound.

Viewed as a logical formula, it looks like this:

Greater contamination over the wound = larger numbers of PJI’s

Forced-air warming = greater contamination over the wound

…therefore…

Forced-air warming = larger numbers of PJI’s

As mentioned earlier, the total joint arthroplasty patient is susceptible to even small numbers of airborne contaminants because of the implanted foreign materials. In the presence of a foreign body, a single bacterium can cause a PJI, and it is usually from airborne contamination.2-4

McGovern et al effectively tested this hypothesis by removing the FAW link in the chain. They discontinued the use of Bair Hugger FAW and reported that their PJI rate fell by 74% (3.1% ==> 0.8%) p=0.024, 1437 patients, 2.5 years.42 They switched to HotDog (air-free) conductive fabric patient warming and maintained the lower infection rate.

References
1. Elek SD, Cohen PE. The virulence of Staphylococcus pyogenes for man. A study of the problem of wound infection. Br J Exp Path. 1957;38:573-586.
2. Lidwell OM et al. Bacteria isolated from deep joint sepsis after operation for total hip or knee replacement and the sources of the infections with Staphylococcus aureus. J Hosp Infect 1983;4:19-29.
3. Whyte W, Hodgson R, Tinkler J. the importance of airborne bacterial contamination of wounds. J Hosp Infect 1982;3:123-135.
4. Petty W, Spanier S, Shuster JJ. The influence of skeletal implants on incidence of infection. J Bone and Joint Surg 1985;67A:1236-1244.
5. Galanakos SP, et al. Biofilm and orthopaedic practice: the world of microbes in a world of implants. Orthopaedics and Trauma 2009;23(3):175-179.
6. Davis SC, et al. Microscopic and physiologic evidence for biofilm-associated wound colonization in vivo. Wound Repair and Regeneration 2008;16(1):23–9.
7. Lewis K. Riddle of Biofilm Resistance. Antimicrobial Agents and Chemotherapy 2001;45(4): 999–1007.
8. Parsek MR, et al. Bacterial biofilms: an emerging link to disease pathogenesis. Annual Review of Microbiology 2003;57:677–701.
9. Cahill JL et al. Quality of life after infection in total joint replacement. J Orthopaedic Surg 2008;16(1):58-65.
10. Mangram A, et al. CDC -- Guideline for Prevention of surgical site infection, 1999. AJIC 1999;27:97-132.
11. Lidwell, OM et al. Infection and sepsis after operations for total hip or knee replacement: influence of ultraclean air, prophylactic antibiotics and other factors. J. Hyg (Camb.) 1984;93:505.
12. Ayliffe GA et al. Role of the environment of the operating suite in surgical wound infection. Rev Infect Dis 1991;13(Suppl 10):S800-4.
13. Doig CM. The effect of clothing on the dissemination of bacteria in operating theaters. Br J Surg 1972;59:878-881.
14. Whyte W et al. Bacterial dispersion in relation to operating room clothing. J Hyg (Camb) 1976;76:367-378.
15. Burke JF. Identification of sources of staphylococci contamination of the surgical wound during operation. Ann Surg 1963; 158:898-904.
16. Favero MS, et al. Comparative levels and types of microbial contamination detected in industrial clean rooms. Appl Microb 1966;14:539-551.
17. Bethune D. W., et al. Dispersal of Staphylococcus aureus by patients and surgical staff. Lancet 1965;285:480–483.
18. Berkelman RL, et al. Streptococcal wound infection caused by a vaginal carrier. JAMA1982;247:2680-2.
19. Schaffner W, et al. Hospital outbreak of infections with group A streptococci traced to an asymptomatic anal carrier. N Eng J Med 1969;280:1224-5.
20. Stamm W, et al. Wound infection due to group A streptococcus traced to a vaginal carrier. J Infect Dis 1978;138:287-92.
21. McIntyre DM. An epidemic of Streptococcus pyogenes puerperal and postoperative sepsis with an unusual carrier site- the anus. Am J Obstet Gyn 1968; 101:308-14.
22. May KR, et al. Bacterial dispersion from the body surface. In: Airborne Transmission and Airborne Infection (Ed. By JF Hers and KC Winkler), p-426.l Oosthoek, Utrecht.
23. Hill J, et al. Effect of clothing on dispersal of Staphylococcus aureus by males and females. Lancet 1974;ii:1131.
24. Mitchell NJ, et al. Clothing design for operating room personnel. Lancet 1974;ii:1133.
25. Jansen LH, et al. Improved fluorescence staining technique for estimating turnover of the human stratum corneum. Br J Derm 1974;90:9-12.
26. MacIntosh CA, et al. The dimensions of skin fragments dispersed into the air during activity. J Hyg (Camb) 1978;81:471-479.
27. Noble WC, et al. The size distribution of airborne particles carrying micro-organisms. J Hyg (Camb) 1963;66:385-391.
28. Noble WC, et al. Dispersal of skin microorganisms. Br J Derm 1975;93:447-485.
29. Albrecht M, Leaper D et al. Forced-air warming blowers: An evaluation of filtration adequacy and airborne contamination emissions in the operating room. Am J Infect Control 2011;39:321-8.
30. Reed M et al. Forced Air Warming Design: An Evaluation of Intake Filtration, Internal Microbial Build-Up, and Airborne-Contamination Emissions. AANA Journal 2012: in press.
31. Leaper D et al. Forced-air warming: a source of airborne contamination in the operating room? Orthopedic Rev. 2009;1(2):e28.
32. Avidan MS, et al. Convection warmers--not just hot air. Anaesthesia. 1997;52(11):1073-107.
33. Baker N, et al. Infection control hazards of intraoperative forced air warming. Hosp. Infect. 2002;51(2):153-154
34. Bernards AT,et al. Persistent Acinetobacter baumannii? Look inside your medical equipment. Infect.Control Hosp. Epidemiol. 2004;25(11):1002-1004.
35. Clark RP, et al. The generation of aerosols from the human body. In Airborne transmission and airborne infection (eds Hers J. F. P. H., Winkler K. C., editors.). 1973. Utrecht, The Netherlands: Oosthoek Publishing Co.
36. Clark RP, et al. Some aspects of the airborne transmission of infection. J Royal Soc Interface 2009;6 (Suppl 6):S767-782.
37. Eames I, et al. Movement of airborne contaminants in a hospital isolation room. J Royal Soc Interface 2009;6 (Suppl 6):S757-766.
38. Davies RR, et al. Dispersal of bacteria on desquamated skin. Lancet. 1962;ii:1295.
39. Hambraeus A, et al. Bacterial contamination in a modern operating suite. 3. Importance of floor contamination as a source of airborne bacteria. J Hyg (Camb.) 1978;80:169-174.
40. Pasquarella C, et al. The index of microbial air contamination. J Hosp Infect 2000;46:241-256.
41. Heat-rises.blogspot.com
42. McGovern et al. Forced-air warming and ultra-clean ventilation do not mix. J Bone and Joint Surg-Br. 2011;93(11):1537-1544.
43. Legg et al. Do forced air patient-warming devices disrupt unidirectional downward airflow? J Bone and Joint Surg-Br. 2012;94-B:254-6.
44. Belani et al. Patient warming excess heat: The effects on orthopedic operating room ventilation performance. Anesthesia & Analgesia 2012;X:X (prepublished online).
45. Dasari et al. Effect of forced air warming on the performance of operating theatre laminar flow ventilation. Anaesthesia 2012;67:244-249.
46. Legg, A.J. and Hamer, A.J. Forced-air patient warming blankets disrupt unidirectional airflow. Bone and Joint Journal, March 2013 vol. 95-B no. 3 407-410
47. Lidwell OM. Air, antibiotics and sepsis in replacement joints. J. Hosp Infect. 1988; 11 Suppl C:18-40.
48. Friberg B, et al. Correlation between surface and air counts of particles carrying aerobic bacteria in operating rooms with turbulent ventilation: an experimental study. J Hosp Infect 1999;42(1):61-8.
49. Lidwell OM. Clean air at the operation and subsequent sepsis in the joint. Clin Orthop 1986; 211: 91-102.
50. Lidwell OM, et al. Airborne contamination of wounds in joint replacement operations: the relationship to sepsis rates. J Hosp Infect 1983;4:111.
51. Ritter MA. Operating room environment. Clin Orthop 1999; 369:103.
52. Whyte W. The role of clothing and drapes in the operating room. J Hosp Infect 1988;11(C):2-17.
53. Gosden PE, et al. Importance of air quality and related factors in the prevention of infection in orthopaedic implant surgery. J Hosp Infect 1998; 39(3):173-80.
54. Stocks GW, et al. Predicting bacterial populations based on airborne particulates: a study performed in nonlaminar flow operating rooms during joint arthroplasty surgery. Am J Infect Control 2010;38(3):199-204.
55. Howorth H. Prevention of airborne infection in operating room. J Med Sci & Tech 1987;11(5):263-66.
56. Lidwell OM, et al. Effects of ultraclean air in operating room on deep sepsis in the joint after total hip or knee replacement: A randomized study. Br Med J 1982;285:10-14.
57. Nelson JP. The operating room environment and its influence on deep wound infection in the hip. Proceedings of the 5th Scientific Meetings of Hip Society. CV Mosby, St. Louis.
58. Tumia N, et al. Convection warmners—a possible source of contamination in laminar airflow operating theatre? J Hosp Infection 2002;52:171-4.
59. Scherrer M. Hygiene and room climate in the operating room. Min Invas Ther & Allied Tech 2003;12(6);293-299.