Objectives: Surgical incision infections, along with urinary tract infections, are among the most common infective complications after kidney transplant. The aim of this retrospective study is to evaluate the incidence and predisposing factors of surgical incision infection development in renal transplant recipients.

Materials and Methods: Between 1 January 2012 and 31 December 2015, there were 238 consecutive kidney transplant procedures performed in our unit. Of these, 146 patients received deceased donor kidney allografts and 92 had transplants from living related donors. Deceased donor data, data about surgical procedures, and recipient data were collected.

Results: This study demonstrated a surgical incision infection rate of 7.56%. Predisposing factors were found to be kidneys from deceased donors, antithymocyte globulin as antirejection therapy, body mass index > 30 kg/m2, cold ischemia time > 16.3 hours, delayed graft function, postoperative serum glucose > 280 mg/dL, second kidney transplant, and BK virus infection.

Conclusions: Surgical incision infection is a common postoperative infection after kidney transplant. The findings of this study elucidated the potential role of specific risk factors in surgical incision infection development (increased cold ischemia time, delayed graft function, antithymocyte globulin administration). Further evaluation of these findings in a prospective study is needed to avoid potential bias.

Key words : Immunosuppression, Renal transplantation, Wound infection

Introduction

It has already been established that renal transplant recipients are susceptible to infections. Surgical incision infections (SIIs), along with urinary tract infections, are among the most common infective complications after kidney transplant.^1,2 Meticulous analyses of early and recent reports have shown postoperative wound infection rates in renal trans­plant recipients to vary from 2% to 40%, with most studies demonstrating a rate from 4% to 16%.^3-10

Despite this low rate of wound infection in renal transplant recipients, infectious wound complica­tions, when combined with immunosuppression, can be devastating and pose a vexing medical, surgical, and economic problem. Medically, wound infections may put the survival of the patient or the renal allograft at risk, thus lengthening hospital stay and increasing cost, which could be a great financial burden to the patient or the social security services. The rationale behind the effect of immunosup­pression on wound infection and healing could be attributed to less inflammatory responses to microorganisms and to the lengthening of the healing process induced by steroids.^11,12

Beyond immunosuppression, renal transplant recipients may run a greater risk for developing SIIs, due to preexisting medical conditions such as diabetes mellitus (DM) and end-stage renal disease. The incision made in renal transplant recipients is assumed to be contaminated because the urinary bladder is opened to perform the ureterocystostomy anastomosis, and urine spillage after bladder opening could increase the risk of wound infections in patients undergoing kidney transplant.¹³ The urinary bladder in patients with renal failure has been shown to contain microorganisms, a scenario usually seen in anuric or severely compromised patients.¹⁴

Despite renal transplant being classified as a clean-contaminated procedure,6 due to the peculiarities of immunosuppressed patients, the use of prophylactic antibiotics has gained widespread acceptance, and perioperative intravenous antibiotics are commonly used.

The aim of this case-control study was to evaluate the incidence and predisposing factors of SII development in renal transplant recipients during the first 100 days after transplant treated at the largest transplant unit in Greece. The incidence of infection was further stratified for recipient age, sex, presence of DM, acute rejection episodes, anti­rejection therapy, and donor source.

Materials and Methods

Between 1 January 2012 and 31 December 2015, there were 238 consecutive kidney transplant procedures performed in our unit. Of these, 146 patients received deceased donor kidney allografts and 92 received transplants from living related donors. No patient was lost during the 100-day follow-up. Internal Review Board approval was obtained. All 146 deceased donor kidney allografts were kept in cold storage after retrieval. Data regarding type of deceased donors (that is, expanded criteria donor or standard criteria donor), data about surgical procedure (time of procedure and cold ischemia time [CIT]), and recipient data (age, body mass index, occurrence of delayed graft function [DGF], DM, and occurrence of SII) were collected.

Living donor kidney procurement
All kidneys retrieved from living donors were through open nephrectomy. Immediately after retrieval, kidneys were flushed with 1000 mL of Belzer UW solution (Bridge to Life, Columbia, SC, USA).

Kidney transplant procedure
Kidney transplant (regardless of the source, that is, living or deceased donors) at our unit is routinely performed retroperitoneally in the right or the left iliac fossa through a “hockey stick” incision. Vascular anastomoses are performed end-to-side to external iliac vessels, and the ureteroneocystostomy is completed by using the extravesical Lich-Gregoire technique. Double J catheter is routinely placed during transplant. At the time of surgery, a Foley catheter is inserted into the bladder and removed within 7 days. A suction drain is placed around the kidney graft, deep in the wound. Musculofascial layer approximation is performed in a continuous fashion with PDS II Sutures (polydioxanone, Ethicon, Somerville, NJ, USA). Subcutaneous tissue is ap­proximated by 3-0 Vicryl (polyglactin 910, Ethicon) in a continuous or interrupted fashion. Skin closure is usually performed with clips.

Immunosuppression protocol
Immunosuppression regimens, at the time of kidney transplant, were available for all participants. We typically use induction treatment with basiliximab or daclizumab in all patients who undergo kidney transplant. This is why we excluded basiliximab or daclizumab as potential risk factors for SII development. Recipients of kidneys from extended criteria donors or any case with a CIT significantly longer than the mean time of our center (more than 16 h), or in the occasion of established DGF, receive induction therapy with antithymocyte globulin (ATG). During the treatment with ATG, calcineurin inhibitors are discontinued and are reinstituted 1 to 2 days before its cessation. All patients receive corticosteroid treatment at the time of kidney transplant. Patients are given 500 to 1000 mg of methylprednisolone during surgery, followed by 20 to 40 mg/day orally (depending on the immunologic risk), and a gradual steroid taper in the absence of rejection. Maintenance immunosuppression consists of calcineurin inhibitors, cyclosporine or tacrolimus, with mycophenolate acid (MPA) formulations and methylprednisolone. Patients with high immunologic risk are preferentially treated with tacrolimus and an MPA formulation at full dose, whereas those with a history of cancer are treated with an inhibitor of the mammalian target of rapamycin, aiming at a goal of 6 to 8 ng/mL, if combined with MPA, and 4 to 6 ng/mL, if combined with a calcineurin inhibitor.¹⁵

Prophylaxis protocol for infection
Patients who undergo kidney transplant are treated with ticarcillin-clavulanate intravenously for 3 days during the peritransplant period (with 1 dose preoperatively). Treatment is then discontinued if there are no signs of inflammation, with decreasing white blood cell count and C-reactive protein levels, and no other complications such as hematoma, lymphocele, or urinary leakage. In addition, patients are treated with ganciclovir intravenously for 1 week, followed by oral valganciclovir for 3 to 6 months, depending on the risk for cytomegalovirus infection. Similarly, patients are treated with a prophylactic regimen of sulfamethoxazole-trimethoprim orally for 3 to 6 months, again depending on the individualized immunosuppression burden and the associated risk of opportunistic infections. A proton-pump inhibitor is given to all patients for the first posttransplant month, and then it is discontinued unless there is an active gastric ulcer or gastritis.

For living donor transplants, asymptomatic bacteriuria are treated according to the sensitivity results of culture until 2 consecutive urine cultures turn negative before proceeding to nephrectomy and kidney transplant. For deceased donor procedures, no donor or preservation fluid cultures are performed routinely, unless there are data about a urine or systematic infection of the donor. In this case, allograft and preservation fluid culture tests are performed, with the recipient receiving appropriate prophylaxis according to the sensitivity results.

Acute rejection and its treatment
A diagnosis of acute rejection was suggested by an increase in serum creatinine of 25% or more, from the baseline level and confirmed by ultrasonography-guided percutaneous biopsy. All biopsy-proven acute rejection episodes were treated on the basis of the histologic type, by either intravenous methylprednisolone (3-5 pulses, 500-1000 mg each) with subsequent tapering, or a course of ATG, with or without plasmapheresis. The Modification of Diet in Renal Disease formula was employed to estimate the glomerular filtration rate of the graft. Delayed graft function was defined as the need for dialysis during the first week after kidney transplant.

BK virus infection diagnosis and surveillance
Viruria was detected by polymerase chain reaction for BK virus DNA and cytology for BK virus inclusion-bearing epithelial cells. Viremia was detected by polymerase chain reaction for BK virus DNA in the plasma. Kidney biopsy was performed to diagnose BK virus nephropathy. The principal treatment for BK virus nephropathy was the reduction in immunosuppressants and leflunomide administration. Surveillance was performed by BK virus polymerase chain reaction.

Follow-up algorithm
Patients were continuously monitored for the occurrence of SII in the immediate posttransplant period. While patients were hospitalized, daily physical examinations, including surgical wound checks, were carried out, as well as twice weekly urine cultures. After discharge from the hospital, patients were routinely examined in the transplant clinic. Patients were also instructed on recognizing signs and symptoms of infection. Any temperature of 37.8°C or higher was investigated by protocol, which included chest radiography, physical exam­ination, urine and blood cultures as indicated, and wound culture if drainage was present. Ultraso­nographic examination was performed to diagnose fluid collection around the kidney, which was aspirated and cultured if present.

Surgical incisional infection diagnosis
Surgical incisional infections were diagnosed in accordance with the published guidelines of the US Centers for Disease Control and Prevention for Surgical Site Infection,¹⁶ which were slightly modified to include SII that developed up to 3 months after surgery.^6,17,18 Surgical incisional infection was defined as an infection occurring within 30 days of surgery that involved skin or subcutaneous or deep soft tissues at the surgical wound site, with at least one of the following: purulent discharge from the incision, organisms isolated from an aseptically obtained culture of fluid or tissue, or one or more features of infection (pain or tenderness, swelling, redness, heat, or fever) with a diagnosis of infection by the surgeon or physician. Surgical incisional infections were classified as superficial (skin and subcutaneous tissue), deep (muscle and fascia), and organ specific with or without systematic disease manifestations (sepsis).8 Ultrasonographic examination was routinely used to aid in proper differential diagnosis. Surgical inci­sional infection was treated according to causative organism and the depth of its spread.

Sample collection for microbiologic analyses
Microbiologic analysis was performed when clinical signs of SSI, such as redness, edema, elevated local temperature, and fluid collection within the wound, were observed. Specimens were collected by superficial swab or collection of purulent fluid and sent to the Department of Medical Microbiology of Laikon General Hospital. The specimens were cultured aerobically and under anaerobic conditions at 37°C for 24 to 48 hours using standard microbiologic media: Columbia agar with 5% sheep blood, MacConkey agar, D-coccosel agar, Schaedler agar with 5% sheep blood, Schaedler broth, and Sabouraud agar. Identification and susceptibility tests were performed using Kirby-Bauer disk diffusion technique.

Statistical analyses
Results were statistically analyzed using the Fisher exact test and Cox regression analysis. All statistical analyses were performed with the Statistical Package for the Social Sciences, version 17.0 (SPSS Inc., Chicago, IL, USA).

Results

As we have already mentioned, the total number of kidney transplant procedures during the referred period was 238. Of these, 146 allografts originated from deceased donors and 92 originated from living donors (Table 1). Eighteen recipients (7.56%) developed SII of any severity. All infections were diagnosed in the early period after transplant, between the 4th and 16th postoperative day (mainly during week 2). Of these patients, 7 (38.9%) developed organ-specific SII, which could have contributed to graft loss in 4 of these cases during the follow-up period, 5 (27.8%) developed deep SII, and 6 (33.3%) were diagnosed with superficial SII. Patients with organ-specific SII were administered intravenous antibiotics in addition to excision of infected debris and vacuum therapy. Antibiotics were administered according to the results of microbiologic identifications (Table 2). The most common bacterial species isolated was Escherichia coli (50%), 4 cases were affected with more than 1 microorganism, and 3 cases were caused by resistant strains (1 extended-spectrum beta-lactamase, 1 Klebsiella pneumoniae carbapenemase, and 1 multidrug resistant Pseudomonas species). No fungal infection was noted. Four of the organ-specific patients displayed early postoperative hemorrhage, and 3 of these patients underwent a second-look operation without any specific findings in 2 of the 3 patients. In 1 patient, hemostasis could not be achieved due to anastomotic rupture, and graftectomy was performed (the patient also had signs of ongoing general infection). Patients with deep SII also received intravenous antibiotics with excision of infected debris and vacuum therapy. During follow-up, no incisional hernia or mortality was observed. Patients with superficial SII were treated with intravenous antibiotics administered in 1 of 18 patients (5.55%) or oral and daily wound dressing and irrigation. The decision of appropriate antibiotic administration depended on the specific pathogen identified in infected wounds and additional clinical signs of infection (ie, elevated temperature and rise in white blood cell count or C-reactive protein levels). Surgical debridement was administered in 3 patients. In 11 patients, wounds were allowed to heal per secundam. In the remaining 7 patients with incisional dehiscence, reoperation was needed. Treatment ceased in all patients after successful healing of the wound. All cases were cured during follow-up. All cases were on MPA + CNI + steroids (83% were on tacrolimus). Fourteen patients (77.8%) were maintained with an immuno­suppressant regimen consisting of MPA + CNI + steroids, with a mean level of cyclosporine of 505 ng/mL and a mean tacrolimus level of 6.7 ng/mL. Common laboratory examinations in these patients showed a significantly increased C-reactive protein value in all patients (Table 3).

The mean age ± standard deviation of this group of patients with SII was 53.83 ± 9.99 years (range, 35-75 y), whereas the mean age of patients without SII was 58.25 ± 11.2 years (range, 15-74 y) (P = not significant). Most SIIs were noted in male patients (5:1 ratio), whereas the “healthy’’ population had an almost equal sex distribution (1.5:1 ratio) (odds ratio [OR] = 3.3; P < .05). In the SII group, most allografts were retrieved from deceased donors (89%), whereas in patients without SII, the proportion was significantly lower at 60% (P < .05; OR = 4.64). In the SII group, most donors were standard criteria donors (17:1 ratio), but the ratio in the group without SII was even higher, reaching 21:1 (OR = 1.23; P = not significant). The mean body mass index in the SII group was 26.3 kg/m² and 25.7 kg/m² in the non-SII group (P = not significant). By setting a cut-off value of body mass index at 30 kg/m², the OR between the 2 groups reached 1.8 (P < .05). Of interest, in the group with SII, only 1 patient (5.5%) with DM was noted, whereas the incidence of DM in the group without SII reached 10%. However, the group with SII demonstrated higher postoperative levels of blood glucose (mean value of 295 mg/dL) compared with those without SII (268 mg/dL; P < .05; OR for blood glucose > 280 = 3.36). Another interesting finding was the high prevalence of urine BK virus infection in patients with SII (2 cases, 11% group-specific frequency, 40% disease-specific frequency; OR = 9.04; P < .01). No case of cytomegalovirus infection was noted. Delayed graft function was observed in 10 of 18 patients (56%), and primary nonfunction was not observed in any patient with SII, whereas those without SII showed DGF reaching 31% (P < .05; OR = 2.98) and primary nonfunction occurred in 1 patient (0.45%). Mean CIT for all kidneys implanted in the SII group was 17.9 hours, which was significantly higher than that in those in the non-SII group (15.1 h, P < .01). By setting a cut-off value of 16.3 hours, which is the mean CIT in our recipients as previously described,15 patients with CIT > 16.3 hours had an OR of 12.5 in developing SII. The mean operative time in the SII group was 188 minutes, with 155 minutes in the non-SII group (P < .05). Regarding administration of ATG for acute rejection episodes, we noted a significant difference between the 2 groups, with more than 20% of patients with SII receiving ATG and only 2.27% of patients without SII receiving ATG (P < .01; OR = 12.28). Three patients in the SII group had already undergone a kidney transplant (17%), whereas the relevant frequency in the non-SII group was < 2% (P < .01; OR = 10.8). Finally, during follow-up, 4 patients (22%) in the SII group lost their grafts, with relevant loss of graft frequency in the non-SII population being < 4% (P < .01). Table 4 summarizes the comparisons between SII and non-SII groups.

Discussion

There is no consensus regarding the criteria used in defining SII after kidney transplant or even the ideal duration of follow-up. Here, we found that SII represents an early posttransplant infection, mainly developing during week 2 after kidney transplant. A second peak of frequency was noted around 60 days after transplant, with an eventual decrease around 30 days postoperatively. That was the reason we set a follow-up of 100 days to describe the SII phenomenon. Previous studies have revealed a median time from transplant to SII of 20 days (range, 2-76 d), which could occasionally appear later, particularly in cases of deep incisional infections or fungal SII.^18-20

Most relevant literature results have identified high BMI, DM, acute cellular rejection, reoperation, DGF, sirolimus use, grafts from deceased donors, female recipient, prolonged CIT, and urinary fistula as potential risk factors associated with post­transplant SII in kidney transplant recipients.^8,20-23 Our data analyses revealed several interesting results. First, we found that patients with SII had higher mean BMI and that a BMI > 30 kg/m² could be a risk factor for SII development. Obesity was also correlated with DGF in our series,24 which is also a potential risk factor for SII. Despite the common belief that DM is a predisposing factor for SII and delayed wound healing, in our study, DM was not a risk factor for SII development. However, we did find that increased serum glucose levels (> 280 mg/dL) early after transplant were correlated with increased frequency of SII.

Similar to previous studies, we confirmed that reoperation and previous transplant are correlated with increased incidence of SII. Reoperation is reportedly a major risk factor for SIIs, most likely because of the contamination due to repeated handling of the surgical site.²⁵ On the contrary, our results did not confirm that female sex and sirolimus use could lead to increased frequency of SII,²⁶ since in our series none of the patients in the SII group received sirolimus and men far outnumbered women.

Technical surgical challenges and intraoperative complications also increased the risk of SII. Transfusion itself played an immunosuppressive role and, in the case of SII, is an indirect marker of an intraoperative complication. Other studies of solid-organ transplant have identified an association between multiple transfusions during transplant and a higher risk of SII.^27,28 In our series, 2 of the SII patients received multiple transfusions during the early postoperative period because of hemorrhage. Moreover, technical challenges and intraoperative complications could lead to an increased operative time and/or CIT. Previous studies have demon­strated that CIT of more than 30 hours and operative time of longer than 200 minutes could increase the risk of SII.8 Our data showed that the SII group showed an increased operative time compared with the non-SII group. Moreover, 4 patients with SII had a CIT > 30 hours. By setting an indicative cut-off value of CIT at 16.3 hours (mean value in our recipients), increased CIT was shown to be a strong risk factor for SII development.

Calcineurin inhibitors are still the main cause of immunosuppression in maintenance regimens administered to kidney recipients. Tacrolimus is the agent of choice and is increasingly used, with 70% of patients receiving tacrolimus at discharge compared with 20% who receive cyclosporine.²⁹ The use of mycophenolate mofetil, the most frequently pre­scribed antiproliferative agent, is also increasing, with approximately 80% of patients taking this drug at discharge.²⁹ In the SII group in our unit, most patients (15/18; 83.3%) were on tacrolimus, whereas only 16.7% were on cyclosporine (OR = 2.9).

This study found that the incidence of SII was higher among patients who received kidneys from deceased donors than among those who received kidneys from living donors. Ho and associates10 also identified a lower incidence of SII in kidney transplant recipients from living donors, and Silva and associates³⁰ reported a higher incidence of bloodstream infection in recipients of kidneys from deceased donors. That association could be explained by the long CIT for deceased donations, the better control of previous infectious in living donor recipient, and the need for more potent immunosuppression in recipients of kidneys from deceased donors.4 In the same frame, it was shown that recipients receiving allografts from extended criteria donors pose a higher risk of SII compared with recipients of standard criteria allografts,⁸ despite the satisfactory allograft survival rates compared with living donor and standard criteria allografts.³¹ We confirmed this finding despite the OR being only marginally above 1 (1.28).

In the present study, we demonstrated that SII after kidney transplant has a significant effect on graft survival since 4 of our patients with SII lost their graft during the 100-day follow-up. Of interest, no deaths from any cause were noted during this same period. Recent studies have reported that SII reduces graft survival within the first 30 days, as well as within the first 5 years, after kidney transplant.^4,18

In addition, the risk of SSI is higher among patients receiving ATG for induction therapy or for acute rejection episodes.^32,33 In our series, ATG was used only in cases of acute rejection episodes, since basiliximab was used as induction agent. Our results indicate that ATG could be a potential risk factor for SII. This finding should be interpreted with caution and confirmed with relevant prospective studies since it could be a confounding factor and the real correlation being established between acute rejection episodes and SII.

The main agents isolated in our series were E. coli and coagulase-negative staphylococci, results that confirm previous findings in the field, where the spectrum mainly included Staphylococcus aureus, coagulase-negative staphylococci, Enterococcus species, Enterobacteriaceae (Klebsiella pneumoniae, E. coli), and Pseudomonas aeruginosa.^4,23 Surgical incision infections caused by Staphylococcus species suggest that endogenous skin flora are the infecting inoculum.⁶ However, contamination cannot be excluded in some patients, as SII can be attributed to coagulase-negative staphylococci. The relevant role of gram-negative bacilli could be related to contamination from urine during the bladder anastomosis or to improved antibiotic prophylaxis activity against staphylococcal species.³⁴

Finally, we found that BK virus urinary infection could be a risk factor for SII development, beyond being an established factor for early graft loss.^35,36 Two of our patients with SII had an ongoing BK virus infection at the time of SII diagnosis. The total number of patients with BK virus infection in our renal transplant recipients, among more than 2000 kidney transplant procedures,³⁷ was 5. We present this finding with great caution, since larger series are needed to confirm such a correlation. In addition, no cytomeg­alovirus infection was found in the SII group.

Conclusions

Surgical incision infection is a common postoperative complication after kidney transplant. This case control study evaluated the incidence and the potential risk factors for SII occurrence over a 100-day follow-up. The findings of this study are either novel (role of BK virus infection) or confirmatory of the potential role of specific risk factors in SII development (increased CIT, DGF, ATG adminis­tration). However, further evaluation of these findings in a prospective study is needed to avoid potential bias.

Study limitations
The present study had limitations, mainly due to its retrospective nature. However, we were able to compare a group of patients with SII with a group of renal allograft recipients with similar characteristics, offering reliable comparisons. Thus, we believe that this case-control study offers emerging data about the incidence and risk factors of SII in renal transplant recipients.

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