University of Groningen
Early prosthetic joint infection after primary total joint arthroplasty
Löwik, Claudia Aline Maria
DOI:
10.33612/diss.97641504
IMPORTANT NOTE: You are advised to consult the publisher's version (publisher's PDF) if you wish to cite from it. Please check the document version below.
Document Version
Publisher's PDF, also known as Version of record
Publication date: 2019
Link to publication in University of Groningen/UMCG research database
Citation for published version (APA):
Löwik, C. A. M. (2019). Early prosthetic joint infection after primary total joint arthroplasty: risk factors and treatment strategies. Rijksuniversiteit Groningen. https://doi.org/10.33612/diss.97641504
Copyright
Other than for strictly personal use, it is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s), unless the work is under an open content license (like Creative Commons).
Take-down policy
If you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediately and investigate your claim.
Downloaded from the University of Groningen/UMCG research database (Pure): http://www.rug.nl/research/portal. For technical reasons the number of authors shown on this cover page is limited to 10 maximum.
Early prosthetic joint infection after primary total joint
arthroplasty
Risk factors and treatment strategies
The research published in this thesis was kindly supported by a grant from ZonMw and the Nederlandse Orthopaedische Vereniging (NOV). Publication of this thesis was financially supported by kind contributions from the University of Groningen (RUG), University Medical Center Groningen (UMCG), Research Institute SHARE and Anna Fonds | NOREF.
C.A.M. Löwik
Early prosthetic joint infection after primary total joint arthroplasty: risk factors and treatment strategies
ISBN: 978-94-034-1841-4 (printed version) ISBN: 978-94-034-1840-7 (electronic version)
Cover: Ferdinand van Nispen, my-thesis.nl
Lay-out: Ferdinand van Nispen, my-thesis.nl Printing: GVO drukkers en vormgevers, Ede © 2019, Claudia Löwik, Groningen, The Netherlands
All rights reserved. No part of this publication may be reproduced or transmitted in any form by any means, electronical, or mechanical, including photocopying, recording or otherwise, without the prior written permission of the copyright owner.
Early prosthetic joint infection after
primary total joint arthroplasty
Risk factors and treatment strategies
Proefschrift
ter verkrijging van de graad van doctor aan de Rijksuniversiteit Groningen
op gezag van de
rector magnificus prof. dr. C. Wijmenga en volgens besluit van het College voor Promoties.
De openbare verdediging zal plaatsvinden op maandag 25 november 2019 om 16.15 uur
door
Claudia Aline Maria Löwik
geboren op 5 augustus 1989 te Zwolle
Promotores Prof. dr. S.K. Bulstra Dr. M. Stevens Copromotor Dr. P.C. Jutte Beoordelingscommissie
Prof. dr. A.W. Friedrich Prof. dr. R.G.H.H. Nelissen Prof. dr. ir. H.J. Busscher
Paranimfen
Marco Löwik Annet Wijnen
Contents
Chapter 1 General introduction and outline of this thesis 9
Chapter 2 Persistent wound drainage after total joint arthroplasty: a narrative review
21
Chapter 3 Periprosthetic joint infection in orthopaedic surgical oncology
39
Chapter 4 Obese patients have higher rates of polymicrobial and Gram-negative early periprosthetic joint infections of the hip than non-obese patients
53
Chapter 5 Predicting failure in early acute prosthetic joint infection treated with debridement, antibiotics, and implant retention: external validation of the KLIC score
71
Chapter 6 Use of gentamicin-impregnated beads or sponges in the treatment of early acute periprosthetic joint infection: a propensity score analysis
87
Chapter 7 Debridement, antibiotics and implant retention is a viable treatment option for early periprosthetic joint infection presenting more than four weeks after index arthroplasty
103
Chapter 8 Managing persistent wound leakage after total knee and hip arthroplasty. Results of a nationwide survey among Dutch orthopaedic surgeons
119
Chapter 9 LEAK study: design of a nationwide randomized controlled trial to find the best way to treat wound leakage after primary hip and knee arthroplasty
135
Summary 181
Nederlandse samenvatting 185
Dankwoord 190
Curriculum vitae 194
Chapter 1
General introduction and
General introduction
1
Background
Osteoarthritis (OA) is the most common joint disorder worldwide.1 It can
develop in any type of joint, although weight-bearing joints, such as the hip and knee, are most commonly affected. OA is recognized as a substantial source of disability, since it causes considerable pain and reduced mobility.2
Total hip arthroplasty (THA) and total knee arthroplasty (TKA) are highly successful surgical treatment modalities for advanced OA of the hip and knee. In 2017, 29,937 primary THAs and 26,030 primary TKAs were performed in the
Netherlands3 and over a million THAs and TKAs are performed annually in the
USA.4 Due to general ageing of the population and increasing levels of obesity,
the incidence of OA continues to rise. Because of this increasing incidence and changing thresholds for arthroplasty surgery, the demand for THA and TKA continues to rise too and is expected to keep rising in the coming decades.5
Although most patients experience good results after THA and TKA, some patients develop postoperative complications. One of the most serious complications after joint arthroplasty and an important cause for revision arthroplasty is prosthetic joint infection (PJI), developing in approximately
1-2% of primary arthroplasties and up to 10% of revision arthroplasties.6,7
Although this percentage is relatively low, the absolute number of patients with PJI is substantial, given the large and still-increasing number of patients who undergo total joint arthroplasty surgery. Prevention of PJI is therefore an important issue, especially given the significant burden it poses on patients and society: PJI is associated with high morbidity and mortality, as well as high socioeconomic costs due to prolonged hospital stay, additional surgical
procedures and antimicrobial treatment.8
Classification of PJI
PJI can develop at any time point after surgery. Several classification systems for PJI have been composed over the years.9-14 Most systems divide PJI into early,
late and hematogenous PJI, depending on the time from joint arthroplasty to development of PJI and duration of symptoms. A large proportion of PJIs occur within the first three months after implantation and are defined as early PJIs.15,16
Early PJIs are typically acquired at the time of surgery through intraoperative contamination and are caused by relatively virulent microorganisms, such as
Chapter 1
have an acute presentation with a warm, swollen, painful, erythematous joint, often with features of sepsis. Late PJIs can also present acutely but usually have more subtle signs, such as chronic pain, a sinus tract with chronic drainage and sometimes prosthetic loosening at the bone-cement interface. Late PJIs present more than three months after index surgery. Just as early PJIs, they are also typically acquired at the time of index surgery but are caused by less virulent or indolent microorganisms, such as coagulase negative staphylococci. Some patients develop hematogenous PJI, in which the prosthetic joint gets infected after a longstanding infection-free period. These infections are typically secondary to an infection at a different site in the body, such as dental infections. Patients with hematogenous PJI usually present with the same acute symptoms as patients with early PJI.
Risk factors for PJI
Minimizing the risk of PJI after THA and TKA requires elimination of two types of risk factors: 1) factors that increase the risk of exposure of the hip or knee joint to microorganisms, and 2) factors that limit a patient’s ability to eliminate intra-articular microorganisms. One of the most important type-1 risk factors is prolonged wound leakage,17,18 a difficult complication as it could be a symptom
of an already existing PJI as well as a risk factor for developing PJI. Moreover, surgical wounds may show prolonged wound leakage for reasons other than infection (such as hematoma, seroma or fatty necrosis) and take longer to heal without development of an infection. As leaking wounds increase the risk of exposure to microorganisms by providing a porte d’entrée, prolonged wound leakage should be considered as potentially imminent PJI.19 Identified type-2 risk
factors include obesity, diabetes mellitus, immunodeficiency and rheumatoid arthritis.20,21 Literature indicates that the risk of PJI increases exponentially with
body mass index.20,22 Patients with an oncological condition requiring tumor
resection are often immunodeficient due to their need for chemotherapy or radiotherapy.23,24 Further, patients with rheumatoid arthritis are at increased
risk due to their immunosuppressive therapy and susceptibility to infectious
disorders of bone, joint and soft tissue.25 The number of comorbidities also
limits a patient’s ability to eliminate intra-articular microorganisms, thus increasing the risk of PJI.26
General introduction
1
Treatment strategies for PJIThere are several surgical and non-surgical treatment strategies for PJI, such as debridement, antibiotics and implant retention (DAIR), revision surgery and suppressive antibiotic therapy. The aim of performing a DAIR is to reduce the infective load of intra-articular microorganisms, provide extensive debridement and start antibiotic therapy in order to retain the prosthesis and avoid more invasive surgery (such as revision arthroplasty). During DAIR the pre-existing wound is opened and the joint cavity is debrided and thoroughly lavaged. If possible, modular components are exchanged. Multiple deep-tissue biopsies are subsequently obtained for culturing, broad-spectrum intravenous antibiotic treatment is started, and the wound is meticulously closed. DAIR is the recommended treatment for patients with early PJI, and is most successful for early acute PJI, in which symptoms exist for less than three weeks.27,28
The higher effectiveness of DAIR in early acute PJI compared with late PJI is due to biofilm formation, a highly complex process in which microorganisms attach to a surface and proliferate into a mature biofilm (Figure 1). Nearly all microorganisms are capable of forming a biofilm, although some types of microorganisms are more potent than others. In vitro studies showed that a biofilm already starts to form within hours of inoculation of bacteria,29 but
these experiments are performed under optimal circumstances for bacterial growth and do not include the complexity of the host’s environment and the
protective effect of its immune system.30 Recent in vivo models showed that
a biofilm is evident after two weeks, but extends and is covered by fibrinous tissue and multiple host cells after six weeks.31 The process of biofilm formation
does vary widely between bacterial species, size of inoculum and hosts.32,33
Due to multiple phenotypic and genotypic changes in the process of biofilm formation, embedded microorganisms become unresponsive to almost any antibiotic treatment once a mature biofilm is formed.35,36 As a consequence, a
PJI cannot be cured with DAIR without removal of the implant. In that case a different surgical treatment option for PJI is revision arthroplasty, which involves replacing the primary prosthesis with a new prosthesis. The prosthesis, including the mature biofilm, is removed, achieving infection control in approximately 90% of patients.37,38 However, benefits of DAIR over revision arthroplasty include
retention of the prosthesis, preservation of bone stock, shorter duration of the surgical procedure, decreased risk of intraoperative fractures (caused by removal of components and implantation of cement spacers) and faster postoperative
Chapter 1
37% to 88%.41-44 This variation in infection control after DAIR stresses the need
for careful selection of eligible patients, especially since performing a DAIR
procedure could reduce the effectiveness of subsequent revision surgery.45-48
Moreover, this indicates that surgical techniques of a DAIR procedure should be optimized to improve infection control after DAIR.
Aims and outline of this thesis
The studies described in this thesis aim to examine and evaluate the risk factors and treatment strategies for early PJI. The first part of the thesis focuses on patient groups at risk for PJI, such as obese patients, oncology patients and patients with prolonged wound leakage after THA and TKA. The second part of this thesis strives to provide insights on factors that can influence the treatment success of DAIR, such as patient selection, use of local antibiotics during DAIR and optimization of the timing of DAIR.
Part 1: Evaluation of patients at risk for early PJI
Chapter 2 presents a review of the available literature on the diagnosis and treatment of prolonged wound leakage after THA and TKA. As patients
Figure 1. Description of various stages involved in the development of a biofilm. 1) Bacterial adhesion to the surface, 2) cell-to-cell adhesion, 3) attached cell monolayer, 4) maturation of a biofilm and
General introduction
1
with prolonged wound leakage are at increased risk for developing PJI, it is important to optimally diagnose and treat these patients. Remarkably, there are no evidence-based guidelines on this topic that can guide orthopaedic surgeons in their decision-making process. The lack of scientific consensus motivated this review of the available literature.
Chapter 3 provides a review of the available literature on PJI in orthopaedic oncology patients. PJI rates among these patients are high due to local and systemic immunodeficiency caused by chemotherapy or radiotherapy. Moreover, these patients usually require large implants because of the need for extensive tumor resections. Even though this patient category is clearly different than regular patients receiving THA or TKA, literature on oncologic PJI is scarce. Hence information on regular PJI is usually applied to oncology patients too. To outline the topics that need future research, conducted specifically on oncology patients, this review describes the current evidence on the definition, diagnosis and treatment of oncologic PJI.
Obese patients are another well-known patient category with an increased risk of PJI. Chapter 4 describes the clinical and microbiological characteristics of obese patients with early PJI, aiming to identify characteristics that contribute to this increased risk and to ultimately improve preventive measures for this specific patient category.
Part 2: Improving treatment strategies for early PJI
Chapter 5 shows the results of the external validation of a preoperative risk score for DAIR failure. As success rates of DAIR vary widely, it is important to select the right patients for this procedure: rates of infection control by DAIR could be optimized and the number of more extensive revision surgeries reduced. To estimate the risk of DAIR failure prior to surgery, thereby selecting the right patients for DAIR, Tornero et al. developed the KLIC score.49 This score
preoperatively calculates the risk of DAIR failure by evaluating five patient-related factors: 1) chronic renal failure (Kidney), 2) Liver cirrhosis, 3) Index surgery, 4) Cemented prosthesis and 5) CRP >115 mg/L (KLIC). Before the KLIC score can be implemented as a standard tool in clinical practice, it has to be validated in an external cohort.
In addition to selecting the right patients for DAIR, infection control after DAIR can also be improved by optimizing surgical techniques and antibiotic treatment. Chapter 6 provides results on the efficacy of
gentamicin-Chapter 1
impregnated beads and sponges in patients with early PJI treated with DAIR. In the Netherlands, gentamicin-impregnated beads and sponges are routinely applied to achieve higher rates of infection control. However, the beneficial effects of applying these local antibiotic carriers have never been demonstrated.
Moreover, it is important to perform DAIR at the right time point. To this end, Chapter 7 describes the rate of infection control after DAIR according to the interval between index surgery and DAIR. As the success rate of DAIR is dependent on the time needed for bacteria to form a mature biofilm at the surface of the prosthesis, PJI can no longer be cured by DAIR once embedded bacteria in the biofilm become unresponsive to antibiotic treatment. So far, the time interval until formation of this mature biofilm is unknown. Hence it cannot be estimated whether it is useful to perform a DAIR procedure at a certain time point after joint arthroplasty.
While Chapter 7 describes the optimal timing of DAIR in patients with early PJI in general, Chapters 8 and 9 focus on the optimal timing of DAIR in patients with prolonged wound leakage after THA and TKA. As there are no evidence-based guidelines on the best treatment for prolonged wound leakage, the Dutch orthopaedic community stated in 2015 that this topic constitutes an important knowledge gap. To address this gap, Consortium Orthopaedic Research (CORE) assembled the LEakage After primary Knee and hip arthroplasty (LEAK) study group. Chapter 8 provides the results of a survey the LEAK study group conducted among Dutch orthopaedic surgeons on the definition, diagnosis and treatment of prolonged wound leakage, to assess current clinical practice in the Netherlands.
Based on the results of this survey and the literature review in Chapter 2, the LEAK study group designed the LEAK study, which is described in Chapter 9. This nationwide multicenter randomized controlled trial compares the revision rates, clinical effectiveness and cost effectiveness of DAIR and non-surgical treatment. It is hypothesized that performing DAIR at an early time point is helpful in preventing and treating PJI and salvaging the implant in patients with prolonged wound leakage after THA and TKA.
Chapter 10 presents a general discussion on the main findings of the studies described in this thesis. It also provides future perspectives and implications for clinical practice.
General introduction
1
References
1. Hiligsmann M, Cooper C, Arden N, Boers M, Branco JC, Luisa Brandi M, et al. Health economics in the field of osteoarthritis: an expert’s consensus paper from the European Society for Clinical and Economic Aspects of Osteoporosis and Osteoarthritis (ESCEO). Semin Arthritis Rheum 2013; 43(3): 303-13.
2. Moskowitz RW. The burden of osteoarthritis: clinical and quality-of-life issues. Am J Manag Care 2009; 15(8 Suppl): S223-9.
3. LROI. Online LROI annual report 2017: 10 years of registration, a wealth of information.
4. Centers for Disease Control and Prevention. Number of all listed procedures for discharges from short-stay hospitals, by procedure category and age: United States, 2010. www.cdc.gov.
5. Kurtz SM, Lau E, Schmier J, Ong KL, Zhao K, Parvizi J. Infection burden for hip and knee arthroplasty in the United States. J Arthroplasty 2008; 23(7): 984-91.
6. Kurtz SM, Ong KL, Lau E, Bozic KJ, Berry D, Parvizi J. Prosthetic joint infection risk after TKA in the medicare population. Clin Orthop Relat Res 2010; 468(1): 52-6.
7. Kunutsor SK, Whitehouse MR, Blom AW, Beswick AD, INFORM Team. Re-infection outcomes following one- and two-stage surgical revision of infected hip prosthesis: a systematic review and meta-analysis. PLoS One 2015; 10(9): 1-15.
8. Kallala RF, Vanhegan IS, Ibrahim MS, Sarmah S, Haddad FS. Financial analysis of revision knee surgery based on NHS tariffs and hospital costs: does it pay to provide a revision service? Bone Joint J 2015; 97-B(2): 197-201.
9. Tsukayama DT, Estrada R, Gustilo RB. Infection after total hip arthroplasty: a study of the treatment of one hundred and six infections. J Bone Joint Surg Am 1996; 78(4): 512-23.
10. Fitzgerald RH Jr, Nolan DR, Ilstrup DM, van Scoy RE, Washington JA 2nd, Coventry MB. Deep wound sepsis following total hip arthroplasty. J Bone Joint Surg Am 1977; 59(7): 847-55.
11. McPherson EJ, Woodson C, Holtom P, Roidis N, Shufelt C, Patzakis M. Periprosthetic total hip infection: outcomes using a staging system. Clin Orthop Relat Res 2002; 403: 8-15.
12. Romanò CL, Romanò D, Logoluso N, Drago L. Bone and joint infections in adults: a comprehensive classification proposal. Eur Orthop Traumatol 2011; 1(6): 207-17.
13. Zimmerli W, Trampuz A, Ochsner PE. Prosthetic-joint infections. N Engl J Med 2004; 351(16): 1645-54.
14. Giulieri SG, Graber P, Ochsner PE, Zimmerli W. Management of infection associated with total hip arthroplasty according to a treatment algorithm. Infection 2004; 32(4): 222-8.
15. Yokoe DS, Avery TR, Platt R, Huang SS. Reporting surgical site infections following total hip and knee arthroplasty: impact of limiting surveillance to the operative hospital. Clin Infect Dis 2013; 57(9): 1282-8.
16. Barrett L, Atkins B. The clinical presentation of prosthetic joint infection. J Antimicrob Chemother 2014; 69(Suppl 1): 25-8.
17. Surin VV, Sundholm K, Bäckman L. Infection after total hip replacement: with special reference to a discharge from the wound. J Bone Joint Surg Br 1983; 65(4): 412-8.
18. Saleh K, Olson M, Resig S, Bershadsky B, Kuskowski M, Gioe T, et al. Predictors of wound infection in hip and knee joint replacement: results from a 20 year surveillance program. J Orthop Res 2002; 20(3): 506-15.
19. Weiss AP, Krackow KA. Persistent wound drainage after primary total knee arthroplasty. J Arthroplasty 1993; 8(3): 285-9.
20. Chen J, Cui Y, Li X, Miao X, Wen Z, Xue Y, et al. Risk factors for deep infection after total knee arthroplasty: a meta-analysis. Arch Orthop Trauma Surg 2013; 133(5): 675-87.
21. Eka A, Chen AF. Patient-related medical risk factors for periprosthetic joint infection of the hip and knee. Ann Transl Med 2015; 3(16): 233.
22. Smith JO, Framptom CMA, Hooper GJ, Young SW. The impact of patient and surgical factors on the rate of postoperative infection after total hip arthroplasty – a New Zealand joint registry study. J Arthroplasty 2018; 33(6): 1884-90.
Chapter 1
23. Jeys LM, Luscombe JS, Grimer RJ, Abudu A, Tillman RM, Carter SR. The risks and benefits of radiotherapy with massive endoprosthetic replacement. J Bone Joint Surg Br 2007; 89-B(10): 1352-5.
24. Wafa H, Grimer RJ, Reddy K, Jeys LM, Abudu A, Carter SR, et al. Retrospective evaluation of the incidence of early periprosthetic infection with silver-treated endoprostheses in high-risk patients: case-control study. Bone Joint J 2015; 97-B(2): 252-7.
25. Doran MF, Crowson CS, Pond GR, O’Fallon WM, Gabriel SE. Frequency of infection in patients with rheumatoid arthritis compared with controls: a population-based study. Arthritis Rheum 2002; 46(9): 2287-93.
26. Lai K, Bohm ER, Burnell C, Hedden DR. Presence of medical comorbidities in patients with infected primary hip or knee arthroplasties. J Arthroplasty 2007; 22(5): 651-6.
27. Parvizi J, Gehrke T, Chen AF. Proceedings of the international consensus on periprosthetic joint infection. Bone Joint J 2013; 95-B(11): 1450-2.
28. Osmon DR, Berbari ER, Berendt AR, Lew D, Zimmerli W, Steckelberg JM, et al. Diagnosis and management of prosthetic joint infection: clinical practice guidelines by the Infectious Diseases Society of America. Clin Infect Dis 2013; 56(1): 1-25.
29. Veerachamy S, Yarlagadda T, Manivasagam G, Yarlagadda PK. Bacterial adherence and biofilm formation on medical implants: a review. Proc Inst Mech Eng H 2014; 228(10): 1083-99.
30. Bandyk DF, Kinney EV, Riefsnyder TI, Kelly H, Towne JB. Treatment of bacteria-biofilm graft infection by in situ replacement in normal and immune-deficient states. J Vasc Surg 1993; 18(3): 398-405. 31. Carli AV, Bhimani S, Yang X, Shirley MB, de Mesy Bentley KL, Ross FP, et al. Quantification of
peri-implant bacterial load and in vivo biofilm formation in an innovative, clinically representative mouse model of periprosthetic joint infection. J Bone Joint Surg Am 2017; 99(6): e25.
32. Lovati AB, Bottagisio M, de Vecchi E, Gallazzi E, Drago L. Animal models of implant-related lowgrade infections: a twenty year review. Adv Exp Med Biol 2017; 971: 29-50.
33. Vidlak D, Kielian T. Infectious dose dictates the host response during Staphylococcus aureus orthopedic-implant biofilm infection. Infect Immun 2016; 84(7): 1957-65.
34. Tshikantwa TS, Ullah MW, He F, Yang G. Current trends and potential applications of microbial interactions for human welfare. Front Microbiol 2018; 9: 1156. Available from: https://www. researchgate.net/figure/Description-of-various-stages-involved-in-the-development-of-a-biofilm-1-Bacterial_fig2_325258657.
35. Lebeaux D, Ghigo JM, Beloin C. Biofilm-related infections: bridging the gap between clinical management and fundamental aspects of recalcitrance toward antibiotics. Microbiol Mol Biol Rev 2014; 78(3): 510-43.
36. Davies D. Understanding biofilm resistance to antibacterial agents. Nat Rev Drug Discov 2003; 2(2): 114-22.
37. Haleem AA, Berry DJ, Hanssen AD. Mid-term to long-term follow-up of two-stage reimplantation for infected total knee arthroplasty. Clin Orthop Relat Res 2004; 428: 35-9.
38. Hirakawa K, Stulberg BN, Wilde AH, Bauer TW, Secic M. Results of 2-stage reimplantation for infected total knee arthroplasty. J Arthroplasty 1998; 13(1): 22-8.
39. Choi HR, von Knoch F, Zurakowski D, Nelson SB, Malchau H. Can implant retention be recommended for treatment of infected TKA? Clin Orthop Relat Res 2011; 469(4): 961-9.
40. Fisman DN, Reilly DT, Karchmer AW, Goldie SJ. Clinical effectiveness and cost-effectiveness of 2 management strategies for infected total hip arthroplasty in the elderly. Clin Infect Dis 2001; 32(3): 419-30.
41. Sukeik M, Patel S, Haddad FS. Aggressive early débridement for treatment of acutely infected cemented total hip arthroplasty. Clin Orthop Relat Res 2012; 470(11): 3164-70.
42. Cobo J, Garcia San Miguel L, Euba G, Rodríguez D, García-Lechuz JM, Riera M, et al. Early prosthetic joint infection: outcomes with debridement and implant retention followed by antibiotic therapy. Clin Microbiol Infect 2011; 17(11): 1632-7.
43. Duque AF, Post ZD, Lutz RW, Orozco FR, Pulido SH, Ong AC. Is there still a role for irrigation and debridement with liner exchange in acute periprosthetic total knee infection? J Arthroplasty 2017; 32(4): 1280-4.
General introduction
1
44. Fehring TK, Odum SM, Berend KR, Jiranek WA, Parvizi J, Bozic KJ, et al. Failure of irrigation and débridement for early postoperative periprosthetic infection. Clin Orthop Relat Res 2013; 471(1): 250-7.
45. Sherrell JC, Fehring TK, Odum S, Hansen E, Zmistowski B, Dennos A, et al. Fate of two-stage reimplantation after failed irrigation and débridement for periprosthetic knee infection. Clin Orthop Relat Res 2011; 469(1): 18-25.
46. Gardner J, Gioe TJ, Tatman P. Can this prosthesis be saved? Implant salvage attempts in infected primary TKA. Clin Orthop Relat Res 2011; 469(4): 970-6.
47. Brimmo O, Ramanathan D, Schiltz NK, Pillai AL, Klika AK, Barsoum WK. Irrigation and debridement before a 2-stage revision total knee arthroplasty does not increase risk of failure. J Arthroplasty 2016; 31(2): 461-4.
48. Nodzo SR, Boyle KK, Nocon AA, Henry MW, Mayman DJ, Westrich GH. The influence of a failed irrigation and debridement on the outcomes of a subsequent 2-stage revision knee arthroplasty. J Arthroplasty 2017; 32(8): 2508-12.
49. Tornero E, Morata L, Martínez-Pastor JC, Bori G, Climent C, García-Velez DM, et al. KLIC-score for predicting early failure in prosthetic joint infections treated with debridement, implant retention and antibiotics. Clin Microbiol Infect 2015; 21(8): 9-17.
Chapter 2
Persistent wound drainage
after total joint arthroplasty: a
narrative review
Frank-Christiaan B.M. Wagenaar, Claudia A.M. Löwik, Akos Zahar, Paul C. Jutte, Thorsten Gehrke, Javad Parvizi
Chapter 2
Abstract
Background
Persistent wound drainage after total joint arthroplasty (TJA) is an important complication with potential substantial adverse consequences, in particular periprosthetic joint infection.
Methods
This review evaluated the available literature regarding several issues in the field of persistent wound drainage after TJA and offers a classification of persistent wound drainage and an algorithmic approach to the decision-making process.
Results
Available literature addressing the diagnosis and treatment of persistent wound drainage after TJA is scarce and an evidence-based clinical guideline is lacking. This is partially caused by the absence of a universally accepted definition of persistent wound drainage. In patients with persistent wound drainage, clinical signs and serological tests can be helpful in the diagnosis of a developing infection. Regarding the treatment of persistent wound drainage, non-surgical treatment consists of absorbent dressings, pressure bandages, and temporary joint immobilization. Surgical treatment is advised when wound drainage persists for more than five to seven days and consists of open debridement with irrigation and exchange of modular components and antimicrobial treatment.
Conclusion
Based on this literature review, we proposed a classification and algorithmic approach for the management of patients with persistent wound drainage after TJA. Hopefully, this offers the orthopaedic surgeon a practical clinical guideline by finding the right balance between overtreatment and undertreatment, weighing the risks and benefits. However, this classification and algorithmic approach should first be evaluated in a prospective trial.
Review on persistent wound drainage
2
Introduction
Persistent wound drainage (PWD) after total joint arthroplasty (TJA) is an important problem because of its potential adverse influence on the outcome following TJA, in particular development of a periprosthetic joint infection (PJI).1-8 PJI is associated with high morbidity and mortality, and a high
socio-economic burden due to prolonged hospital stay, surgical procedure(s), antimicrobial treatment, and wound care.
Remarkably, PWD is rarely reported in literature and thereby literature fails to provide conclusive scientific evidence on many issues related to PWD after TJA, including the definition and treatment of PWD. This lack of evidence results in wide variation in diagnosis and treatment in daily practice, often only founded by the surgeon’s opinion. The absence of scientific consensus prompted this review of the available literature.
We performed a literature search and included all papers relevant to the subject of PWD (Table 1). Articles that were not written in English or did not have full text available were excluded. We included all relevant papers, regardless of the level of evidence.14 Although most articles were of low level of
evidence, we included these articles because of the small number of available papers on the subject of PWD and due to the lack of articles with a higher level of evidence. Based on this literature review, we developed a classification of PWD and an algorithmic approach to PWD after TJA that may guide clinicians in their decision-making process to select the appropriate treatment for PWD.
Incidence and relevance
The reported incidence of PWD after TJA varies between 0.2% and 21%,3-5,8,9,13
with higher incidences after revision TJA.8 This wide range in incidence is
mainly caused by the variation in definitions of PWD (Table 1), illustrating the lack of consensus regarding the definition of PWD. Moreover, higher awareness results in higher incidences of PWD, as demonstrated by Maathuis et al. who found a 21% incidence of PWD when protocol-based surveillance was used to detect wound drainage after TJA.13
Chapter 2
Table 1. Overview of literature addressing wound drainage after total joint arthroplasty Author Study type and
sample size Level of evidence Definition Incidence of wound
drainage
Results Duration of drainage Amount of drainage
Adelani 9 Retrospective
N = 2221 TKAs
3 N/A N/A 0.2% 17 patients had non-infectious wound complications (including persistent wound
drainage) and 12 patients had deep infection. Patients with complications had lower Knee Society function scores and a higher incidence of mild or greater pain.
Dennis 10 Opinion N/A >7 days after TJA N/A N/A Persistent wound drainage (not associated with erythema or purulence) can be
managed with wound care and immobilization. If wound drainage persists beyond 5 to 7 days, spontaneous cessation of drainage is unlikely and surgical debridement is indicated.
Hansen 11 Prospective
N = 5627 THAs
4 >3-4 days after TJA Drainage that has soaked
through the postoperative dressings
2.0% NPWT was started after 3-4 days of wound drainage in 109 patients and applied for
2 days. 76% did not need additional surgery, 10% needed superficial debridement, 11% needed deep debridement, and 3% required component removal. Predictors for additional surgery were INR >2, previous hip surgery and NPWT >48 hours.
Jaberi 3 Retrospective
N = 11,785 TKAs / THAs
3 >2 days after TJA Drainage that has soaked
through the postoperative dressings
2.9% 300 patients with wound drainage >48 hours were treated with local wound
care and oral antibiotics. Wound drainage stopped between 2-4 days in 72%. The remaining patients underwent single debridement (76%) or additional treatment (repeat debridement, resection arthroplasty or long-term antibiotics). Timing of surgery and malnutrition predicted failure of the first debridement.
Lonner 12 Opinion N/A Several days after TJA N/A N/A Wound drainage beyond several days after surgery may increase the risk of
infection. Drainage will usually stop after 24-48 hours of immobilization. If not, open debridement should be performed, including obtaining cultures, irrigation and meticulous wound closure. Exercises may be resumed once the wound is stable.
Maathuis 13 Retrospective
N = 558 TKAs / THAs
3 >5 days after TJA N/A 16.5% Comparison of an algorithmic approach to an ad hoc approach. In the algorithmic
approach, registration of persistent wound drainage was two-fold (21% vs 11%), but the number of open debridements was lower (17% vs 30%) and the salvage rate higher (94% vs 85%)
Patel 4 Retrospective
N = 2437 TKAs / THAs
2 >5 days after TJA ≥2x2cm area of gauze covering
the wound is wet or when fluid is noted to be originating from the surgical wound
20.1% Persistent wound drainage results in longer hospital stay. Each day of wound
drainage after day 5 increased the risk of wound infection by 42% following THA (p<.001) and by 29% following TKA (not significant after correction for BMI).
Saleh 7 Prospective
N = 2305 TKAs / THAs
3 Wound drainage N/A N/A 33 patients developed a superficial wound infection. Hematoma formation and
days of wound drainage were significant predictors of superficial wound infection. 58% developed a prosthetic joint infection, patients with >5 days of wound drainage had 12.7 times more risk of developing a prosthetic joint infection.
Surin 5 Retrospective
N = 803 THAs
3 N/A N/A 12.6% 115 patients had superficial wound drainage and cultures were positive in 70
wounds. 34 patients developed prosthetic joint infection. Patients with superficial wound drainage had a 3.2 times higher risk of developing a prosthetic joint infection. The risk was further influenced by the character of the exudate and the use of prophylactic antibiotics.
Vince 1 Review / opinion N/A Limited amount of
time N/A N/A Persistent wound drainage should be treated by wound care and immobilization. If drainage does not stop after 3 to 7 days, open debridement should be performed.
Aggressive surgery may prevent sepsis. Drainage that starts in the late postoperative phase is a great concern as it usually results from a prosthetic joint infection.
Weiss 8 Retrospective
N = 597 TKAs
4 ≥4 consecutive days
beyond day 5 after TJA
≥2x2cm area of gauze covering the wound is wet or when fluid is noted to be originating from the surgical wound
1.3% 8 patients with persistent wound drainage. Open debridement was performed at
an average of 12.5 days after index surgery. 25% of patients had positive tissue cultures. All patients were successfully treated with adjuvant antibiotics.
BMI: body mass index; INR: international normalized ratio; N/A: not applicable or not described; NPWT: negative pressure wound therapy; THA: total hip arthroplasty; TJA: total joint arthroplasty; TKA: total knee arthroplasty.
Review on persistent wound drainage
2
Table 1. Overview of literature addressing wound drainage after total joint arthroplasty Author Study type and
sample size Level of evidence Definition Incidence of wound
drainage
Results Duration of drainage Amount of drainage
Adelani 9 Retrospective
N = 2221 TKAs
3 N/A N/A 0.2% 17 patients had non-infectious wound complications (including persistent wound
drainage) and 12 patients had deep infection. Patients with complications had lower Knee Society function scores and a higher incidence of mild or greater pain.
Dennis 10 Opinion N/A >7 days after TJA N/A N/A Persistent wound drainage (not associated with erythema or purulence) can be
managed with wound care and immobilization. If wound drainage persists beyond 5 to 7 days, spontaneous cessation of drainage is unlikely and surgical debridement is indicated.
Hansen 11 Prospective
N = 5627 THAs
4 >3-4 days after TJA Drainage that has soaked
through the postoperative dressings
2.0% NPWT was started after 3-4 days of wound drainage in 109 patients and applied for
2 days. 76% did not need additional surgery, 10% needed superficial debridement, 11% needed deep debridement, and 3% required component removal. Predictors for additional surgery were INR >2, previous hip surgery and NPWT >48 hours.
Jaberi 3 Retrospective
N = 11,785 TKAs / THAs
3 >2 days after TJA Drainage that has soaked
through the postoperative dressings
2.9% 300 patients with wound drainage >48 hours were treated with local wound
care and oral antibiotics. Wound drainage stopped between 2-4 days in 72%. The remaining patients underwent single debridement (76%) or additional treatment (repeat debridement, resection arthroplasty or long-term antibiotics). Timing of surgery and malnutrition predicted failure of the first debridement.
Lonner 12 Opinion N/A Several days after TJA N/A N/A Wound drainage beyond several days after surgery may increase the risk of
infection. Drainage will usually stop after 24-48 hours of immobilization. If not, open debridement should be performed, including obtaining cultures, irrigation and meticulous wound closure. Exercises may be resumed once the wound is stable.
Maathuis 13 Retrospective
N = 558 TKAs / THAs
3 >5 days after TJA N/A 16.5% Comparison of an algorithmic approach to an ad hoc approach. In the algorithmic
approach, registration of persistent wound drainage was two-fold (21% vs 11%), but the number of open debridements was lower (17% vs 30%) and the salvage rate higher (94% vs 85%)
Patel 4 Retrospective
N = 2437 TKAs / THAs
2 >5 days after TJA ≥2x2cm area of gauze covering
the wound is wet or when fluid is noted to be originating from the surgical wound
20.1% Persistent wound drainage results in longer hospital stay. Each day of wound
drainage after day 5 increased the risk of wound infection by 42% following THA (p<.001) and by 29% following TKA (not significant after correction for BMI).
Saleh 7 Prospective
N = 2305 TKAs / THAs
3 Wound drainage N/A N/A 33 patients developed a superficial wound infection. Hematoma formation and
days of wound drainage were significant predictors of superficial wound infection. 58% developed a prosthetic joint infection, patients with >5 days of wound drainage had 12.7 times more risk of developing a prosthetic joint infection.
Surin 5 Retrospective
N = 803 THAs
3 N/A N/A 12.6% 115 patients had superficial wound drainage and cultures were positive in 70
wounds. 34 patients developed prosthetic joint infection. Patients with superficial wound drainage had a 3.2 times higher risk of developing a prosthetic joint infection. The risk was further influenced by the character of the exudate and the use of prophylactic antibiotics.
Vince 1 Review / opinion N/A Limited amount of
time N/A N/A Persistent wound drainage should be treated by wound care and immobilization. If drainage does not stop after 3 to 7 days, open debridement should be performed.
Aggressive surgery may prevent sepsis. Drainage that starts in the late postoperative phase is a great concern as it usually results from a prosthetic joint infection.
Weiss 8 Retrospective
N = 597 TKAs
4 ≥4 consecutive days
beyond day 5 after TJA
≥2x2cm area of gauze covering the wound is wet or when fluid is noted to be originating from the surgical wound
1.3% 8 patients with persistent wound drainage. Open debridement was performed at
an average of 12.5 days after index surgery. 25% of patients had positive tissue cultures. All patients were successfully treated with adjuvant antibiotics.
BMI: body mass index; INR: international normalized ratio; N/A: not applicable or not described; NPWT: negative pressure wound therapy; THA: total hip arthroplasty; TJA: total joint arthroplasty; TKA: total knee arthroplasty.
Chapter 2
Wound drainage is usually a non-infectious disturbance in wound healing of short duration that occurs during the first days after TJA,2 but it may be an
early symptom of a (developing) PJI. Research published between 1973 and 1983 described PWD as one of the main risk factors for developing a PJI,5,15-19
even though several researchers could not observe a correlation between PWD
and PJI.20-23 Contemporary research underscored the adverse effects of wound
complications, such as an increased risk of PJI, readmission, prolonged hospital stay, re-operations, and higher health care costs.1-4,6-8,12,24
Regarding the consequences of PWD after total knee arthroplasty (TKA), Galat et al. found a 6% increased cumulative risk of PJI in patients who required
early surgical treatment for any early wound healing complication after TKA.2
Moreover, these patients had 5.3% risk of major additional surgical intervention (resection arthroplasty, muscle flaps or amputation) in the first two years following TKA.2 A different study by Galat et al. showed an increased risk of
10.5% for PJI and 12.3% risk for major re-operation within two years after TKA in patients who required surgical intervention for post-operative hematoma.25
Regarding the consequences of PWD after both total hip arthroplasty (THA) and TKA, Parvizi et al. demonstrated that patients who developed a PJI were more likely to have experienced PWD and hematoma than patients without PJI (16.8 and 12.6 times more likely respectively).26 Similar results were reported
by Saleh et al.7
Although most studies on wound-related complications after TJA have focused on the risk of developing PJI, wound-related complications also predispose patients to worse functional outcome.1-4,7-9,12,24,27-32 Mortazavi et
al. found substantially worse patient satisfaction and lower Harris Hip Scores
in patients requiring additional surgery for hematoma after THA.31 Adelani
et al. observed similar worse functional outcome for patients with wound complications after TKA.9 Moreover, published data suggest that patients with
PWD after TKA have an increased risk of residual pain and poor functional outcome, similar to patients who develop an infectious complication after TKA.9
Patient expectation after wound complications following TJA should therefore be tempered, even if wound complications do not result in PJI.
Review on persistent wound drainage
2
Theoretical and practical considerations
Wound drainage after TJA can be physiological in the first days after index surgery. However, it is unknown when wound drainage should be perceived as persistent or abnormal. Many other issues related to wound complications remain unanswered as well, such as the following: to what extent will wound drainage impair wound healing and/or offer a retrograde gateway for entry
of pathogens into the joint space?8 Where does wound drainage originate? If
it originates from deeper layers of the joint, does it represent an early deep infection or merely normal drainage from defects in the soft tissues? If it originates from outside the joint, does it represent normal wound drainage or a draining hematoma or abscess?1 All these issues are important for the
decision-making process but remain difficult to clarify.
Definition of PWD
Literature lacks a proven definition of PWD in terms of both duration and amount of drainage. Previous studies used a definition of duration of wound drainage varying from two to nine days after index surgery (Table 1).3,8 In 2013,
the first International Consensus Meeting (ICM) on PJI defined PWD as >2x2cm of drainage in the wound dressing beyond 72 hours after index surgery.27,33 This
consensus stated that limiting the definition of PWD to 72 hours postoperative allows for early intervention that may prevent the adverse consequences of PWD. However, the definition of PWD should be further specified and evaluated.
Clinical and serological signs of a developing infection
Clinical signs of wound infection (superficial or deep) include systemic and local signs. Systemic signs involve fever, chills, and tachycardia. Local signs include induration, painful skin erythema (especially around the sutures), warmth,
purulent drainage, and presence of a sinus tract.34 However, some of these
clinical signs are frequently observed in the first days after uncomplicated TJA surgery as an early physiological response to surgical trauma.
Fever or pyrexia (generally defined as temperature >38.5ºC / >101ºF) is physiological in the first three to five days after index surgery.35-45 In this
postoperative phase, additional tests for an underlying infectious cause of fever is unwarranted as it results in patient discomfort, has minor clinical yield, and is accompanied by considerable health care costs.35,36,39-46 However, temperatures
Chapter 2
>39ºC, particularly if present for multiple days and/or later than three to five days after surgery, require further diagnostic tests.46
Described blood serology parameters in the diagnosis of PJI are C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and white blood cell count (WBC). After uncomplicated TJA surgery the CRP level increases rapidly and reaches maximum level (up to 200-400 mg/L) within two to three days, followed by a quick decrease and normalization to preoperative level in two to eight weeks after uncomplicated TJA, even in patients with rheumatoid arthritis.47-61
An infectious complication in patients with PWD should be suspected if CRP levels increase later than 72 hours after TJA, or remain elevated beyond seven days after TJA.52,57-59,61,62
The WBC and ESR are less appropriate for the diagnosis of PJI in case of PWD, since the WBC increases only slightly after surgery and returns to normal within seven days after index surgery, while the ESR increases only gradually, with peak level between day five and 14 and normalization in 19 days up to nine months after index surgery.47,54,55,59-61,63
An algorithmic approach to the decision-making process
In clinical practice, assessment of the origin (intra- or extra-articular) and type of wound drainage (physiologic or infectious secretion) is often difficult. Weiss and Krackow concluded that wound drainage can offer a pathway where pathogens can enter the wound and joint, acting as a retrograde pathway for
infection.8 This implies that PWD should be perceived as potential imminent
PJI, hence justifying a low threshold for early surgical intervention.1,64 However,
advocating early surgical intervention may result in unnecessary operations, while delaying early surgical intervention may result in development of PJI. An evidence-based algorithmic approach on PWD may ease the decision-making process in the diagnosis and timing of treatment. In literature, some authors merely provided general statements on the evaluation of wound complications.1,2,27 Only few studies specifically addressed PWD3-8,13 and only
one of these studies described an algorithmic approach.13 In this study, the
algorithmic approach was compared with an ad hoc approach in which the surgeon decided upon own discretion. Even though the reported percentage of PWD was two times higher in the algorithmic cohort (21% vs 11%), the number of surgical interventions was lower (17% vs 30%) and the salvage percentage
Review on persistent wound drainage
2
lead to increased awareness of PWD and an improved decision-making process with a lower frequency of surgical interventions and better outcome.
Timing of treatment
The optimal timing of starting non-surgical or surgical treatment in patients with PWD remains to be established. Patel et al. stated that each day of PWD beyond day five after TJA surgery increased the risk of wound infection with 42% after THA and 29% after TKA.4 Saleh et al. found a 12.7 times higher risk
of developing PJI when the wound drained for more than five days after THA/ TKA compared with patients with shorter duration of wound drainage. Based on these findings, they advised on performing open debridement in case of
hematoma or PWD for more than seven days postoperative.7
More recently, Jaberi et al. (defining wound drainage as persistent when drainage soaked postoperative dressings for more than two days) showed that draining wounds after THA and TKA healed uncomplicated within two to four days of non-surgical treatment (wound care and antimicrobial treatment) in
72% of patients.3 The remaining 28% underwent open debridement. This was
successful in 76% of patients, while the remaining 24% underwent subsequent treatment including repeated debridement, resection arthroplasty, or suppressive antimicrobial treatment. These authors recommended early surgery within seven days after index surgery even though their successful DAIRs were performed at a mean of 14 days (range 4-32 days) after index
surgery.3 Based on these studies, the ICM formulated the statement that
surgical treatment should be performed if wound drainage persists for longer than five to seven days after index surgery.27
Non-surgical treatment strategies
Non-surgical treatment strategies are usually performed prior to surgical intervention.27 Since PWD is associated with an increased risk of PJI, observation
only is highly discouraged.3,4,7,8 Acceptable non-surgical treatment is adequate
wound care by using absorbent dressings and pressure bandages (hand-made spica for the hip), supplemented by several days of joint immobilization and interruption of physical therapy.3,65 Bed rest and braces may impair early
rehabilitation, but this outweighs the potential risk of prolonging the duration
of PWD and increasing the risk of PJI.1,12 Good results were reported on the
Chapter 2
(NPWT).11,67-69 However, a Cochrane meta-analysis could not find definitive
evidence for the effectiveness of NPWT.69
The ICM advised on early analysis and correction of anticoagulation,
anemia, glucose regulation in diabetic patients, and malnutrition.27 One
study retrospectively evaluated 11,785 THAs/TKAs and found malnutrition to predispose for failure of surgical debridement and an increased risk of PJI in patients with PWD. Therefore, they recommended consultation of a nutritional
physician in case of wound drainage persisting longer than 48 hours.3 With
regard to anticoagulation, Parvizi et al. showed that patients with a mean International Normalized Ratio higher than 1.5 had an increased risk of developing wound complications and PJI after THA/TKA. Hence, they stressed the importance of cautious anticoagulant treatment in order to prevent
formation of a hematoma and subsequent wound drainage.26
Although antimicrobial treatment during PWD has been described,3 current
consensus discourages antimicrobial treatment due to a lack of evidence on decreasing the risk of PJI.11,12 Furthermore, it may confound culture results thus
impairing the diagnosis of an early PJI. And finally, concerns about the increase of antimicrobial resistance cannot be ignored.34
Surgical treatment strategies
Most publications advocate early surgical treatment in case wound drainage persists despite a period of adequate non-surgical treatment.1,3,10,27 Surgical
treatment typically consists of open deep debridement and thorough irrigation, using six to nine liters of saline administered by low-pressure pulsatile jet
lavage.70 Optionally, diluted povidone-iodine or chlorhexidine gluconate can
be used to irrigate the joint cavity.71-73 However, it should be recognized that
these recommendations on irrigation are derived from literature on primary TJA and trauma surgery, mostly from animal and basic science studies.
Whenever possible, modular components should be exchanged as it offers a better potential for thorough debridement and irrigation deep to these modular components. Moreover, modular component exchange is advised because the polyethylene component (acetabular liner or tibial inlay) may be
colonized by pathogens.8 The soft tissue should be meticulously closed in a
multilayer fashion.12,27 NPWT is a plausible alternative when wound closure is
Review on persistent wound drainage
2
Administration of prophylactic antimicrobial treatment is advised prior to incision.34,74 Various deep tissue samples for bacterial cultures are obtained,
preferably five samples to increase pathogen detection. Each tissue sample is obtained using a clean instrument to avoid contamination. Tissue swabs are not
advised.34 Tissue samples should be cultured up to 14 days and antimicrobial
treatment is continued until culture results are definitive.34 In case of positive
culture results, targeted antimicrobial treatment should be continued in consultation with an infectious diseases specialist, usually six to twelve weeks. Jaberi et al. found positive deep periprosthetic tissue cultures in 34% (28 of 83 cases) after surgical treatment for PWD after THA/TKA. Cultures were more often positive in the failure group (17 of 20, 85%) compared with the success
group (11 of 63, 17%).3 Weiss and Krackow, reporting PWD in eight of 597
primary TKAs, showed that 25% (two of eight cases) had positive cultures after
surgical debridement at a mean of 12.5 days after surgery (range 8-18 days).8
However, issues can be raised on the statistical power of this study cohort.
Summary
The reported incidence of PWD after TJA varies between 0.2% and 21%, with higher incidences after revision TJA. This wide range in incidence is mainly caused by the variation in definitions of PWD. The ICM formulated a definition that defines PWD as >2x2cm for longer than 72 hours, but this definition should be further specified and validated.
Clinical signs of infection and blood serology can be helpful in diagnosing PJI in case of PWD, although some clinical signs can be a normal physiological response in the first days after TJA. An increase in CRP later than 72 hours after index surgery or persistent elevated levels of CRP beyond seven days can indicate development of an infectious complication.
Non-surgical treatment of PWD generally involves absorbent dressings, pressure bandages and temporary joint immobilization. Present consensus discourages the use of antimicrobial treatment. Nutritional consultation and correction of anticoagulation and metabolic imbalances should be considered. Surgical treatment should be performed when wound drainage persists for more than five to seven days after index procedure despite adequate non-surgical treatment. Nonetheless, establishing this time frame needs validation in
Chapter 2
future research. Surgical treatment should include thorough open debridement and irrigation, obtaining tissue samples (cultured up to 14 days) and exchange of modular components. Empirical broad-spectrum antimicrobial treatment is administered in consultation with an infectious diseases specialist.
Proposed algorithm
Based on this literature review, the authors developed an algorithm to facilitate the decision-making process of PWD after TJA (Figure 1). Although we aimed to differentiate between PWD in THA and TKA in this algorithm, we did not find enough scientific evidence to make this distinction. In addition to the algorithm, we also propose a classification of PWD that divides wound drainage into four categories based on the amount of drainage (Table 2). As this classification is merged into the algorithm, the amount of drainage is combined with the duration of drainage (Figure 1), in which larger amounts of wound drainage are tolerated for a shorter period. Hopefully, this algorithm offers the orthopaedic surgeon a practical clinical guideline by finding the right balance between overtreatment and undertreatment, weighing risks and benefits. Currently, a multicenter randomized controlled trial on the optimal treatment of PWD after TJA is being conducted to examine the validity and applicability of such a classification and algorithm in daily clinical practice.75
Table 2. Proposed classification of persistent wound drainage after total joint arthroplasty
Category Description
1 (Limited) A stripe of blood in the wound dressing in the line of the wound or less than 2x2cm
in size a
2 (Moderate) More than 2x2cm drainage in absorbent gauze or dressing but without the need for
changing the wound dressing (i.e. dressing is not soaked)
3 (Excessive) One dressing change per day due to soaked absorbent gauze or dressing
4 (Massive) Two or more daily dressing changes due to soaked absorbent gauzes or dressings
a According to the 2013 international consensus meeting on periprosthetic joint infection.28,33
Conclusion
This review summarizes the available literature addressing several issues in the field of PWD after TJA. There are limited scientific data on PWD and absence of an
Review on persistent wound drainage
2
evidence-based guideline regarding diagnosis and treatment, partially caused by the lack of a universally accepted definition. We developed a classification of PWD and an algorithmic approach for the management of PWD after TJA to offer the orthopaedic surgeon a practical guideline for daily clinical practice.
2 4 POD 5 POD 7 POD 10 Persistent drainage cally suspected? cally suspected? Increasing lab (ESR/CRP/Leuco) OR Cat. 3?
(immobilizer knee, bedrest), pressure bandage knee or hip spica, nu onal
n
If possible + tel. consult POD 9
Baseline lab (ESR/CRP/Leuco), 24
(immobilizer knee, bedrest) and pressure bandage
knee or hip spica
Surgical and t
24
(immobilizer knee, bedrest) and pressure bandage
knee or hip spica
Persistent drainage 1 Persistent drainage (Cat. 1 4) 1 1 1 Persistent drainage ge 2 3+4 Cat. 4
Cat. 2 and 3 Cat. 1
Yes No No No Yes Yes
Figure 1. Proposed algorithm for diagnosis and treatment of persistent wound drainage after total joint arthroplasty
Chapter 2
References
1. Vince K, Chivas D, Droll KP. Wound complications after total knee arthroplasty. J Arthroplasty 2007; 22(4 Suppl 1): 39-44.
2. Galat DD, McGovern SC, Larson DR, Harrington JR, Hanssen AD, Clarke HD. Surgical treatment of early wound complications following primary total knee arthroplasty. J Bone Joint Surg Am 2009; 91(1): 48-54.
3. Jaberi FM, Parvizi J, Haytmanek CT, Joshi A, Purtill J. Procrastination of wound drainage and malnutrition affect the outcome of joint arthroplasty. Clin Orthop Relat Res 2008; 466(6): 1368-71. 4. Patel VP, Walsh M, Sehgal B, Preston C, DeWal H, Di Cesare PE. Factors associated with prolonged
wound drainage after primary total hip and knee arthroplasty. J Bone Joint Surg Am 2007; 89(1): 33-8.
5. Surin VV, Sundholm K, Bäckman L. Infection after total hip replacement: with special reference to a discharge from the wound. J Bone Joint Surg Br 1983; 65(4): 412-8.
6. Butt U, Ahmad R, Aspros D, Bannister GC. Factors affecting wound ooze in total knee replacement. Ann R Coll Surg Engl 2011; 93(1): 54-6.
7. Saleh K, Olson M, Resig S, Bershadsky B, Kuskowski M, Gioe T, et al. Predictors of wound infection in hip and knee joint replacement: results from a 20 year surveillance program. J Orthop Res 2002; 20(3): 506-15.
8. Weiss AP, Krackow KA. Persistent wound drainage after primary total knee arthroplasty. J Arthroplasty 1993; 8(3): 285-9.
9. Adelani MA, Johnson SR, Keeney JA, Nunley RM, Barrack RL. Clinical outcomes following re-admission for non-infectious wound complications after primary total knee replacement. Bone Joint J 2014; 96-B(5): 619-21.
10. Dennis DA. Wound complications in total knee arthroplasty. In: Sculco TP, ed. Knee arthroplasty, 1st
ed. New York, USA: Springer Vienna; 1997: p. 163-9.
11. Hansen E, Durinka JB, Costanzo JA, Austin MS, Deirmengian GK. Negative pressure wound therapy is associated with resolution of incisional drainage in most wounds after hip arthroplasty. Clin Orthop Relat Res 2013; 471(10): 3230-6.
12. Lonner JH, Lotke PA. Aseptic complications after total knee arthroplasty. J Am Acad Orthop Surg 1999; 7(5): 311-24.
13. Maathuis PGM, de Hartog B, Bulstra SK. Timing of open debridement for suspected infection of joint prosthesis: a report on 551 patients. Curr Orthop Pract 2009; 20(5): 541-5.
14. Howick J, Chalmers I, Glasziou P, Greenhalgh T, Heneghan C, Liberati A, et al. The Oxford 2011 levels of evidence. Oxford Center of Evidence-based Medicine.
15. McLaughlan J, Smylie HG, Logie JR, Smith G. A study of the wound environment during total hip arthroplasty. Postgrad Med J 1976; 52(611): 550-7.
16. Franco JA, Baer H, Enneking WF. Airborne contamination in orthopedic surgery: evaluation of laminar air flow system and aspiration suit. Clin Orthop Relat Res 1977; 122: 231-43.
17. Fitzgerald RH Jr, Nolan DR, Ilstrup DM, van Scoy RE, Washington JA 2nd, Coventry MB. Deep wound sepsis following total hip arthroplasty. J Bone Joint Surg Am 1977; 59(7): 847-55.
18. Schwan A, Bengtsson S, Hambraeus A, Laurell G. Airborne contamination and postoperative infection after total hip replacement. Acta Orthop Scand 1977; 48(1): 86-94.
19. Andrews HJ, Arden GP, Hart GM, Owen JW. Deep infection after total hip replacement. J Bone Joint Surg Br 1981; 63-B(1): 53-7.
20. Aglietti P, Salvati EA, Wilson PD Jr. A study of the effectiveness of a surgical unidirectional filtered air flow unit during total prosthetic replacements of the hip. Arch Orthop Trauma Surg 1973; 77(4): 257-68.
21. Aglietti P, Salvati EA, Wilson PD Jr, Kutner LJ. Effect of a surgical horizontal unidirectional filtered air flow unit on wound bacterial contamination and wound healing. Clin Orthop Relat Res 1974; 101: 99-104.
Review on persistent wound drainage
2
23. Freeman MA, Challis JH, Zelezonski J, Jarvis ID. Sepsis rates in hip replacement surgery with special reference to the use of ultra clean air. Arch Orthop Trauma Surg 1977; 90(1): 1-14.
24. Berbari EF, Hanssen AD, Duffy MC, Steckelberg JM, Ilstrup DM, Harmsen WS, et al. Risk factors for prosthetic joint infection: case-control study. Clin Infect Dis 1998; 27(5): 1247-54.
25. Galat DD, McGovern SC, Hanssen AD, Larson DR, Harrington JR, Clarke HD. Early return to surgery for evacuation of a postoperative hematoma after primary total knee arthroplasty. J Bone Joint Surg Am 2008; 90(11): 2331-6.
26. Parvizi J, Ghanem E, Joshi A, Sharkey PF, Hozack WJ, Rothman RH. Does “excessive” anticoagulation predispose to periprosthetic infection? J Arthroplasty 2007; 22(6 Suppl 2): 24-8.
27. Ghanem E, Heppert V, Spangehl M, Abraham J, Azzam K, Barnes L, et al. Wound management. J Orthop Res 2014; 32(Suppl 1): S108-19.
28. Ng VY, Lusteberger D, Hoang K, Urchek R, Beal M, Calhoun JH, et al. Preoperative risk stratification and risk reduction for total joint reconstruction: AAOS exhibit selection. J Bone Joint Surg Am 2013; 95(4): 1-15.
29. Fernandez-Fairen M, Torres A, Menzie A, Hernandez-Vaquero D, Fernandez-Carreira JM, Murcia-Mazon A, et al. Economical analysis on prophylaxis, diagnosis, and treatment of periprosthetic infections. Open Orthop J 2013; 7: 227-42.
30. Kurtz SM, Lau E, Schmier J, Ong KL, Zhao K, Parvizi J. Infection burden for hip and knee arthroplasty in the United States. J Arthroplasty 2008; 23(7): 984-91.
31. Mortazavi SMJ, Hansen P, Zmistowski B, Kane PW, Restrepo C, Parvizi J. Hematoma following primary total hip arthroplasty: a grave complication. J Arthroplasty 2013; 28(3): 498-503.
32. Zmistowski B, Karam JA, Durinka JB, Casper DS, Parvizi J. Periprosthetic joint infection increases the risk of one-year mortality. J Bone Joint Surg Am 2013; 95(24): 2177-84.
33. Parvizi J, Gehrke T, Chen AF. Proceedings of the international consensus on periprosthetic joint infection. Bone Joint J 2013; 95-B(11): 1450-2.
34. Zmistowski B, Della Valle C, Bauer TW, Malizos KN, Alavi A, Bedair H, et al. Diagnosis of periprosthetic joint infection. J Arthroplasty 2014; 29(2 Suppl): 77-83.
35. Shaw JA, Chung R. Febrile response after knee and hip arthroplasty. Clin Orthop Relat Res 1999; 367: 181-9.
36. Kennedy JG, Rodgers WB, Zurakowski D, Sullivan R, Griffin D, Beardsley W, et al. Pyrexia after total knee replacement: a cause for concern? Am J Orthop 1997; 26(8): 549-52.
37. Summersell PC, Turnbull A, Long G, Diwan A, Macdessi S, Cooke PJ, et al. Temperature trends in total hip arthroplasty: a retrospective study. J Arthroplasty 2003; 18(4): 426-9.
38. Athanassious C, Samad A, Avery A, Cohen J, Chalnick D. Evaluation of fever in the immediate postoperative period in patients who underwent total joint arthroplasty. J Arthroplasty 2011; 26(8): 1404-8.
39. Ghosh S, Charity RM, Haidar SG, Singh BK. Pyrexia following total knee replacement. Knee 2006; 13(4): 324-7.
40. Czaplicki AP, Borger JE, Politi JR, Chambers BT, Taylor BC. Evaluation of postoperative fever and leukocytosis in patients after total hip and knee arthroplasty. J Arthroplasty 2011; 26(8): 1387-9. 41. Ward DT, Hansen EN, Takemoto SK, Bozic KJ. Cost and effectiveness of postoperative fever
diagnostic evaluation in total joint arthroplasty patients. J Arthroplasty 2010; 25(6 Suppl): 43-8. 42. Guinn S, Castro FP Jr, Garcia R, Barrack RL. Fever following total knee arthroplasty. Am J Knee Surg
1999; 12(3): 161-4.
43. Tai TW, Chang CW, Lin CJ, Lai KA, Yang CY. Elevated temperature trends after total knee arthroplasty. Orthopedics 2009; 32(12): 886.
44. Bindelglass DF, Pellegrino J. The role of blood cultures in the acute evaluation of postoperative fever in arthroplasty patients. J Arthroplasty 2007; 22(5): 701-2.
45. Anderson JT, Osland JD. Blood cultures for evaluation of fever after total joint arthroplasty. Am J Orthop 2009; 38(8): 134-6.
46. Chen AF, Haddad FS, Lachiewicz P, Bolognesi M, Cortes LE, Franceschini M, et al. Prevention of late PJI. J Arthroplasty 2014; 92(2 Suppl): 119-28.
