One of the most important aspects of prevention of surgical site infection (SSI) is identification of the risk factors, which helps surgeon and patient decision-making and might allow management aimed at reducing risk.1–4 Although the literature on risk factors for infection in orthopedics in general is plentiful, infection after fracture fixation has received considerably less focus. Unfortunately, the fracture infection literature all too often has conflicting results, perhaps because of differences in methodology, injury, and sophistication in accounting for potential confounders from study to study. We are currently working to create an all-encompassing predictive risk score for infection after fracture fixation, but most of the work thus far has been fracture-specific and might not apply from one fracture to another.5
We herein present much of the literature regarding infection risks after fracture fixation and contrast and extrapolate work done in other subspecialties of orthopedics, including arthroplasty and spine surgery, to provide a concise and useful evidence-based review of the risk factors for infection after fracture fixation surgery.
FACTORS STONGLY ASSOCIATED WITH POSTOPERATIVE INFECTION
Diabetes, hyperglycemia, end-stage renal disease (ESRD) requiring hemodialysis, human immunodeficiency virus (HIV), acquired immunodeficiency syndrome, hepatitis C, and alcohol abuse are risk factors for infection with no studies to suggest otherwise.
Diabetes and Hyperglycemia
Patients with diabetes mellitus are, in general, more frequently affected by infectious diseases.6 The pathophysiology of the susceptibility of diabetics to infections involves the hyperglycemic environment and the negative affect it has on the body’s immune system because of impaired neutrophil function, deficiencies in the complement system and cytokine production, and immunoglobulin dysfunction.6 Considering this increased susceptibility along with the frequently coexisting risk factors of peripheral neuropathy and vascular insufficiency, it is not surprising that diabetes has been found to be an independent risk factor for postoperative infection after orthopedic surgery, including fracture fixation.
Many studies in the arthroplasty and spine literature have found diabetes to be an independent risk factor for postoperative infection.7–10 This finding was also shown to be true regarding orthopedic trauma surgery.11 Bachoura et al,11 in 2011, found that diabetes was one of the 6 factors that independently predicted SSI after surgery to treat orthopedic trauma. The odds ratio (OR) for diabetes in that study was 2.1. Fracture-specific studies of ankle fractures have also found diabetes to be an independent predictor of infection. In 2015, Basques et al12 found that insulin-dependent diabetes was the strongest independent predictor for postoperative infectious complication, with an OR of 3.51. Similarly, Ovaska et al13 assessed 131 ankle infections and compared them with an equal number of controls using univariate analysis. The authors found diabetes to have the greatest OR (2.2). Recognizing the impact of diabetes and hyperglycemia on infection risk, Richards et al14 examined hyperglycemia in patients without diabetes and found it to be an independent risk factor for SSI occurring after operative intervention for isolated orthopedic injuries.
ESRD and Hemodialysis
Similar to studies of infection risk associated with diabetes, studies of postoperative infection risk associated with chronic kidney disease requiring hemodialysis have been conducted in cases of total joint arthroplasty. In 2002, Sunday et al15 retrospectively reviewed the results of total joint arthroplasty performed in 14 patients with ESRD undergoing hemodialysis and found that all 14 experienced a complication including SSI, which led the authors to question whether arthroplasty should be performed at all in this population. In 2014, Miric et al16 found that patients with chronic kidney disease were at significantly higher risk for superficial SSI (P=0.04) in addition to 90-day readmission (P=0.003) and mortality (P≤0.001). After adjusting for confounding variables, those patients had 1.9 times the chance of developing SSI. Erkocak et al17 found that 20% of the patients receiving hemodialysis who underwent total joint arthroplasty developed SSI. Cavanaugh et al18 similarly found that patients with chronic kidney disease and/or ESRD had a greater risk of SSI and wound complications than those without and that the risks were even greater in patients undergoing dialysis.
HIV, Acquired Immunodeficiency Syndrome, and Hepatitis C
HIV has long been associated with increased infection risk secondary to immunosuppression, especially as the disease advances.19 Hoekman et al20 showed that the relative frequency of postoperative infection was significantly higher in patients who were seropositive for HIV and had associated clinical symptoms than in patients who were seronegative (P=0.01). This finding was supported by Jellis et al21 who reported a 33% infection rate after treatment of closed fractures with internal fixation and a staggering 72% infection rate for open fractures. In 1994, Paiement et al22 showed that even asymptomatic patients with HIV were at significantly higher risk for postoperative infection after orthopedic trauma surgery (P=0.035), with a risk >3 times as high as seronegative patients with closed fractures and a risk >4 times as high as seronegative patients with open fractures. Guild et al23 found an infection rate of 23% in HIV-positive patients after fracture fixation compared with 3.9% in HIV-negative patients. The authors found that a CD4 count <300 was associated with development of postoperative infection. It is important to note that the introduction of triple antiretroviral therapy has greatly altered the prognosis of HIV-positive patients. Currently, the risk after arthroplasty is considered the same or only slightly higher than that of the general population when patients are receiving triple antiretroviral therapy.24 Further research is needed to determine whether this is also true after fracture surgery.
Considerably fewer data implicate hepatitis C in postoperative SSI. However, in a large propensity-matched analysis conducted in 2017, hepatitis C was found to increase the risk of postoperative complication after major orthopedic surgery, with the most common complication being infection.25 Hepatitis C and HIV commonly occur together, compounding the risk.26 In addition, liver cirrhosis, a long-term sequela of hepatitis C infection, has been shown to increase the risk of postoperative infectious complications associated with arthroplasty and fracture fixation.27,28
Alcohol abuse is an accepted causative factor for traumatic injuries. It has also been shown that alcohol exposure negatively influences cellular immunity by altering the cytokine response.29 This, in addition to the malnutrition and liver disease that commonly accompany alcohol abuse, leads to increased infection rates in both general and orthopedic surgery.
In 1997, Rantala et al30 reported that alcohol abuse was an independently significant risk factor for SSI (P<0.0001). This was similarly shown by Eliasen et al31 in 2013. The authors found that the relative risk of general infections and wound complications in patients with preoperative alcohol consumption were 1.7 and 1.2, respectively, compared with patients who did not drink alcohol. Specific to fracture fixation, Parkkinen et al32 found that alcohol abuse was an independent risk factor for infection after plate fixation of proximal tibial fracture (OR, 6.7). In a study of deep SSI occurring after ankle fracture surgery, Ovaska et al13 found alcohol abuse to be independently associated with infection (OR, 3.8). The OR for infection in diabetics in that study was 2.2.
It is worth noting that none of these studies directly investigated the degree to which the physiological effects that alcohol has on the immune system drives the increased susceptibility to SSI versus the effects of the concomitant malnutrition and/or liver disease. Both malnutrition and liver disease frequently coexist with alcohol abuse as a result of decreased nutritional intake along with maldigestion and malabsorption caused by the direct toxicity of alcohol on the digestive system.33 With malnutrition and liver disease both having been shown to increase the risk of infection after fracture fixation,28,34 it can be assumed that it is the combination of these factors that renders alcohol abuse such a strong predictor of postoperative infection.
FACTORS WITH VARIABLE RISK OF POSTOPERATIVE INFECTION
Smoking is another commonly studied potential risk factor for infection that has conflicting results in the literature and seems to be dependent on the specific fracture and body region that is involved. Several studies have shown that smoking is not an independent risk factor for infection, including the study by Schemitsch et al35 who used the Study to Prospectively Evaluate Reamed Intramedullary Nails in Tibial Fractures (SPRINT) data and found that smoking was not associated with adverse events, including infection, after intramedullary tibial nailing in 1226 patients. Metsemackers et al36 also found this to be true in their study of 480 tibial nail cases. Richards et al14 assessed all fractures requiring acute fixation and also found that smoking was not associated with infection. Although several studies in the arthroplasty literature have linked smoking to postoperative infection,7,10 no studies that examined orthopedic trauma patients in general found that result. Fracture-specific studies of bicondylar tibial plateaus, ankle fractures, and elbow fractures found increased risk of infection in smokers.13,37,38 However, those injuries have in common a tenuous soft-tissue envelope with wounds that are prone to high tension because of the location and associated marked swelling. These factors, when combined with the microcirculatory impact of smoking, can lead to tissue ischemia and subsequent wound breakdown and infection. It can also be said that smoking is linked to so many other patient variables, including age, socioeconomic status, and other medical comorbidities, that when more variables are examined, the more likely it is that smoking will not be shown to be an independent risk factor.
Similar to the literature on smoking, the literature on obesity and risk of infection after fracture fixation is mixed. A lack of association has been shown with arthroplasty10 and with specific fractures, including those about the elbow, calcaneus, pilons, and plateaus.38,39 Paryavi et al,39 with their risk score for infection, showed that body mass index >30 was actually protective from infection for calcaneus, pilon, and tibial plateau fractures. Perhaps this suggests that fractures with a generally more tenuous soft-tissue envelope, the same fractures that might be put at risk by smoking, benefit from more robust soft tissues. This is in conflict, however, with the 2017 study by Olsen et al,40 which showed that obesity was strongly associated with infection after ankle fracture fixation. The study by Olsen and colleagues did not show an association between smoking and infection. In addition, the 2016 study of proximal tibial fractures by Parkkinen et al32 showed that obesity did increase the risk of infection. Obesity has been shown to be a risk factor for infection consistently associated with pelvic and acetabular surgery.41,42 With pelvic and acetabular surgery, the location of the surgical wounds are in areas that are perhaps more susceptible to the affects of obesity, including the gluteal region where increasing pressure while recovering in bed can lead to skin breakdown and along intertriginous skin folds where friction and moisture can lead to maceration and proliferation of bacteria.43 Suzuki et al41 examined 326 consecutive patients who underwent acetabular fracture surgery with multivariate analysis showing that obesity was an independent risk factor for SSI. Sagi et al,42 in 2013, also showed that obesity was an independent risk factor for infection with an OR of 8, which increased to an OR of 12 when combined with a leukocytosis.
The use of immunomodulators has been considered to be a risk factor for infection in orthopedic surgery based on previous studies largely assessing arthroplasty or spine surgery in patients with rheumatoid arthritis who were taking biological and non–biological disease-modifying antirheumatic drugs, tumor necrosis factor alpha inhibitors, and corticosteroids.44–47 For example, Sherrer et al47 performed a large retrospective registry study evaluating all elective orthopedic surgeries in 2472 patients with inflammatory rheumatic diseases and found that patients taking these medications had a significantly higher risk of infection (P=0.036). In a similar retrospective study of 1768 patients with rheumatoid arthritis undergoing any orthopedic surgery, it was found that tumor necrosis factor alpha inhibitors were not a risk factor for SSI, suggesting that the association between these medications and infection might not be as strong as previously thought.48 It is important to note that these previous studies included patient populations that are different from the usual orthopedic trauma patient population undergoing fracture fixation. Limited data are available on the risk of immunomodulators and SSI after fracture fixation.
FACTORS WITH LIMITED RISK OF POSTOPERATIVE INFECTION
Age and Sex
Limited data suggest that increasing age and male sex are risk factors for infection. However, most studies show no association between these variables and infection after fracture fixation. In 2016, Parkkinen et al32 found that age older than 50 years was associated with increased risk of infection after plate fixation of proximal tibial fractures. This was a retrospective review of 655 proximal tibial fractures with 34 deep infections. The OR of age older than 50 years was 3.1. Rasouli et al,8 in 2014, found male sex to be an independent risk factor for postoperative infection after total joint arthroplasty, but in the fracture literature, only Richards et al,14 in 2012, found a statistically significant relationship between male sex and infection after acute fixation (P=0.02). Morris et al,37 in 2013, retrospectively reviewed 302 tibial plateau fractures with 43 deep infections and did not find age and sex to be independently associated with infection. Similarly, in a review of 597 pelvic and acetabular fractures with 17 infections, Sagi et al42 failed to show an association between age or sex and the development of deep postoperative wound infection. In examining 174 open fractures, Bowen et al49 found no association between age or sex and postoperative infection, and in a more general review of all fractures undergoing fixation, Bachoura et al11 found similar results. The study by Bachoura and colleagues included 1611 patients. Of these, 75 infections occurred. It is possible that with the small sample sizes and low event rates observed in these studies, the power was such that it was not possible to detect age and sex as independent predictors. It should be noted that these studies were all retrospective in nature with relatively small sample sizes.
Presently, no studies in the literature support the premise that a ballistic injury is an independent risk factor for infection after fracture fixation. The literature regarding ballistic injuries is relatively sparse, and controversy exists regarding antibiotic administration and the need for operative irrigation and débridement of such injuries. Howland and Ritchey,50 based on their retrospective series, do not recommend routine use of antibiotics. Marcus et al51 reported similar rates of infection occurring after ballistic injuries regardless of whether patients received antibiotics. Dickey et al52 showed no significant difference in infection between patients who did and did not receive antibiotics (P>0.1); however, the patients were all treated nonoperatively. It is important to note that the vast majority of the patients in these studies sustained low-velocity gunshot wounds. High-velocity gunshot wounds result in notably more soft-tissue injury compared with low-velocity gunshot wounds and, as such, likely increase infection rates to the same extent as open fractures, although, again, high-quality data on this are limited. In a systematic review of gunshot-induced fractures of the extremities, Sathiyakumar et al53 stated that evidence for superficial débridement of low-velocity gunshot wounds is weak, as is evidence for extensive débridement of high-velocity wounds and evidence for antibiotic administration for either low-velocity or high-velocity wounds, leading the authors to conclude that more high-quality research is needed before making any recommendations for the treatment of ballistic fractures.
FRACTURE CHARACTERISTICS THAT INCREASE INFECTION RISK
It is well known in orthopedic trauma that certain fractures have greater risk of postoperative infection than do others. Generally, fractures in regions with more tenuous soft-tissue envelopes, such as the tibial plateau, pilon, and calcaneus, are associated with greater infection rates than fractures of the hip or femur. Historically, infection rates after calcaneus fracture open reduction and internal fixation have been among the highest in orthopedics, with reported rates ranging from 5% to 25%.54–60 Pilon fractures were once considered to be at even greater risk before the 2-stage approach popularized by Sirkin et al61 and Patterson et al,62 with rates of infection and wound problems >30%. Currently, the rates of infection range from 1% to 16%.62–64 This is similar to ankle fractures for which the reported rates range from 1% to 8%.65,66 Plateau fractures are associated with infection rates ranging from 3% to 22%.37,67–70 In contrast to these fractures with higher rates of infection, a femoral fracture is associated with an ~1% infection rate.71–73 Fractures of the upper extremity tend to be associated with lower infection rates than fractures of the lower extremity. Series on both-bone forearm fractures report rates of infection from 0.9% to 5.5%,74–78 whereas humeral fractures are associated with reported rates ranging from <1% to 4% in more recent studies.79,80 Pelvic and acetabular fractures are associated with infection rates of ~3% to 6%.41,42,81,82 All of the rates of infection are affected by other injury characteristics, with increased rates occurring in the setting of open injuries and compartment syndrome.
Open fractures are associated with increased infection risk secondary to direct introduction of bacteria from the outside environment and the extensive soft-tissue injury that can accompany these fractures. In Gustilo and Anderson’s initial retrospective study,83 they observed a 5% infection rate overall for open fractures, which they reduced to a 2.5% rate with the addition of antibiotic therapy to their treatment algorithm. Despite this, type III fractures still had a 9% infection rate. Fernandes et al,84 in 2015, showed that open fractures, in general, resulted in higher infection rates than those observed with closed injuries, with an overall infection rate of 13%. The authors observed that the higher the Gustilo-Anderson grade was, the greater the infection risk was, with 80% of the infections occurring in type III fractures. Striking in this study was the 28% infection rate observed with open ankle fractures. Similarly, Muller et al,85 reported an open fracture infection rate of 21%. Morris et al37 found that open injury was an independent risk factor for deep SSI after fixation of bicondylar tibial plateau fractures. Roussignol et al86 and Yokoyama et al87 found increased rates of infection with open tibial fractures, with the rate of infection affected by the Gustilo-Anderson grade with type III open fractures having the highest rates. Although types I and II open fractures are associated with negligible increased risk of infection with appropriate irrigation, débridement, and antibiotic administration, type III open injuries have consistently been shown to be associated with increased rate of infection. It should be recognized, however, that the variability in infection risk after open fracture fixation is related to multiple factors in addition to the severity of the fracture and associated soft-tissue injury, including the degree of contamination, the patient’s vascular status, the adequacy of surgical débridement, and the administration of prophylactic antibiotics.88–92
Need for Flap Coverage
As noted above, the risk of infection occurring after fracture is increased with open injuries and further increased with increasing Gustilo-Anderson type. In 1984, Gustilo et al93 revised their open fracture classification, recognizing the increased risk of complications when a flap is required secondary to inadequate soft tissue. In that study, type IIIB fracture had a 52% infection rate whereas type IIIA fractures (fractures with adequate soft tissues not requiring a flap) had a 4% infection rate. Furthermore, D’Alleyrand et al94 found that a delay in flap coverage beyond 7 days independently increases the risk of complications, particularly infection.
Substantial evidence in the literature shows that compartment syndrome requiring fasciotomy is a significant risk factor for postoperative infection. In 2016, Blair et al95 showed that the risk for infection after operative management of tibial plateau fractures and tibial shaft fractures in patients with compartment syndrome was 20% compared with 4% in those who did not have compartment syndrome, with fasciotomy remaining a statistically significant risk factor for infection after binary regression analysis (P=0.001). Similarly, Morris et al37 found compartment syndrome requiring fasciotomies to be an independent risk factor for infection after open reduction and internal fixation of bicondylar tibial plateau fractures with an OR of 3.81. Parkkinen et al32 found the same result after plate fixation of proximal tibial fractures, with an OR of 4.5. Most recently, Dubina et al96 conducted a retrospective cohort study of 71 operative tibial plateau fractures with ipsilateral compartment syndrome treated with fasciotomy and compared them with a control group of 625 plateau fractures without compartment syndrome. The authors found compartment syndrome to be an independent risk factor for SSI, increasing the risk 3-fold (25% vs. 8%).
HOSPITAL INTERVENTIONS THAT INCREASE THE RISK OF INFECTION
It has been found across multiple fields of surgery that allogenic blood transfusion increases the risk of postoperative infection because of the immunosuppressive effects it has on the body.97 The increased risk of infection after transfusion has been studied extensively in orthopedic surgery, including in total joint arthroplasty, spine surgery, and trauma surgery, often with conflicting results. Koval et al98 studied the effect of transfusion in patients undergoing surgical fixation of hip fractures and found that the risk of infection nearly doubled, from 15% to 27%, in patients who received transfusion compared with those who did not.
The data are not as strong regarding pelvic and acetabular surgery. Sagi et al42 assessed infection risk in patients undergoing pelvic and acetabular surgery and found transfusion to be a statistically significant risk factor for infection (P=0.056), although it was not found to be a strong predictor when determining positive predictive values or OR. This is similar to the study by Suzuki et al41 that found larger amounts of blood transfused to be a statistically significant factor for infection after acetabular fixation in the univariate analysis (P=0.001), although it was not found to be independently associated with infection in the multivariate analysis. These studies are less convincing of the impact of blood transfusion on infection risk than those in the arthroplasty literature, such as the study by Innwehofer et al99 that found transfusion to be an independent risk factor for infection after multivariate analysis. Because of the conflicting data and a limited number of studies establishing transfusion as an independent predictor of infection after fracture fixation, it is difficult to discern whether transfusion directly increases infection risk or whether it serves as a surrogate of other possible predictors of infection, such as length of surgery and injury severity.
Within pelvic and acetabular fracture surgery, evidence suggests that angioemobilization is an independent risk factor for infection. Sagi et al42 found preoperative angioemobilization to be an independent risk factor for deep postoperative infection with an OR of 11 and a positive predictive value of 67%. Furthermore, Manson et al100 performed a retrospective review of patients who underwent pelvic angiography before operative fixation of acetabular fracture. The authors found a 58% infection rate among patients who had undergone embolization compared with an infection rate of 14% in those who did not undergo embolization. This impact of embolization is contradicted by a recent single-center retrospective study by Firoozabadi et al101 who found a significantly higher rate of SSI after acetabular fixation in those who did not undergo embolization compared with those who did (P=0.04), although the rate of infection for those who went on to angiography without undergoing embolization was substantially higher (31%) than in the Manson and colleagues study.
METHICILLIN-RESISTANT STAPHYLOCOCCUS AUREUS (MRSA) COLONIZATION
Nasal colonization with MRSA, as detected with nasal swab cultures, has been shown to increase the risk of SSI in orthopedic surgery, although no studies presently in the literature studied solely orthopedic trauma patients. Studies by Kalmeijer et al102 and Hacek et al103 examined the effect of MRSA colonization on infection rates in patients undergoing hip and knee arthroplasty, and both studies showed an increased incidence of postoperative infection in those with positive MRSA nasal swabs. In 2009, Yano et al,104 who studied 2423 consecutive orthopedic surgeries including fracture fixation, found similar results. The results of all of these studies were summarized in the 2013 meta-analysis by Levy et al,105 who found that the OR of SSI in patients with positive MRSA nasal swabs was 5.92. This was similar to the results presented by Everhart et al10 who identified MRSA colonization as an independent risk factor for SSI after total joint arthroplasty, with an OR of 4.17. Although some evidence of reduction in SSI risk with decolonization strategies has been presented in the arthroplasty literature, no studies have examined this in a trauma population, thus presenting an opportunity for further research and potential risk reduction.
SUMMARY OF HIGH-IMPACT AND LOW-IMPACT RISK FACTORS
High-impact Risk Factors
- Acquired immunodeficiency syndrome
- Alcohol abuse
- Compartment syndrome
- Diabetes mellitus
- ESRD hemodialysis
- Fracture region (tibial plateau, tibial pilon, ankle, calcaneus)
- Hepatitis C
- MRSA colonization
- Need for flap coverage
- Open fracture
Low-impact Risk Factors
- Ballistic fracture
The ability to accurately identify risk factors for infection and stratify patients based on the risks is of great value because it allows clinicians to lower infection rates and reduce the burden on patients and the health care system in general.1 Although the literature as it pertains to orthopedic trauma surgery is often conflicting considering the wide variability in injury patterns, patient factors, and treatment strategies, it is important to critically assess each individual patient using the data that we have to identify, and perhaps modify, factors that might put the patient at higher risk for postoperative infection. The need continues for larger scale studies specific to postoperative infection in orthopedic trauma patients to clearly identify independent risk factors, thus enabling clinicians to optimize patient care through preventive measures and modified treatment protocols.
The authors thank Dori Kelly, MA, for professional manuscript editing.
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