Introduction
Kidney stones are a common and frequently occurring disease of the urinary system. The incidence is 10.34% in men and 6.62% in women [
1]. Percutaneous nephrolithotomy (PCNL) is the main treatment method for kidney stones [
2,
3]. PCNL has been used as an important minimally invasive method for the treatment of kidney stones because of its small trauma and rapid recovery [
2,
3]. Indwelling double J-tube after PCNL can provide advantages such as urinary tract obstruction, drainage of urine, and protection of renal function [
4,
5]. But after PCNL operation, the ureteral stent can cause the patient’s waist and abdomen discomfort, bladder irritation, hematuria, stent tube displacement, and other adverse events, especially urinary tract infection is one of the more common complications [
4,
5]. There are some data suggesting an association between indwelling ureteral stents and urinary tract infections, including a recent prospectively performed study reporting an 11% incidence of UTIs in stented patients [
4,
5]. In clinic, antibiotics are mainly used to treat acute pyelonephritis (AP) associated with ureteral stent after PCNL. However, clinical observations have shown that this infection is not effectively treated with ordinary second-generation cephalosporins and quinolone antibacterials such as levofloxacin, which indicates that the pathogenic bacteria of this kind of infection are drug resistance and difficult to treat. Accordingly, this study retrospectively analyzed the clinical data of 415 patients with indwelling ureteral stent after PCNL treatment in our hospital from December 2016 to May 2019 to explore the risk factors, bacterial strains, and drug susceptibility of AP associated with ureteral stent after PCNL, and provide a reference for clinical intervention.
Discussion
Ureteral stent is the most commonly used medical implant for urological surgery. It is widely used in clinical practice because it can relieve urinary tract obstruction, drain urine, and protect renal function [
14,
15]. After PCNL operation, ureteral stent is usually retained for 4–6 weeks, but some patients need to keep ureteral stent for a long time because of the complex condition. During the indwelling of ureteral stent after PCNL, AP associated with ureteral stent after PCNL is a more common complication, and some severe cases can induce retrograde urogenic sepsis endangering the life of patients [
16‐
18]. Previous studies have suggested that the incidence of bacteriuria and urinary tract infection related to ureteral stent is 11–45% [
4,
5]. In this study, we found that the incidence of AP associated with ureteral stent after PCNL was approximately 13.01%. The results are similar to previous reports, suggesting that the incidence of AP associated with ureteral stent after PCNL is higher, and urologists need to pay more attention.
Studies suggest that infections are a more common complication after PCNL. Long operation time, intraoperative bleeding, excessive intrapelvic pressure, and urinary tract obstruction are all risk factors for postoperative infection of PCNL [
19‐
21]. In this study, we found that diabetes mellitus, postoperative stone residue, urinary leucocytes ≥ 100/HP, positive urine culture results, ureteral stent retention time ≥ 8 weeks, and high S.T.O.N.E. score (especially the large stone size, severe obstruction, and multiple kidney calices involved) are independent risk factors for AP associated with ureteral stent after PCNL. The possible reasons for the findings are the following: (1) the immune defense of diabetes patients is reduced, and the blood glucose of some patients is not well controlled for a long time, and the whole body glucose metabolism is disordered, which is conducive to the invasion, production, and reproduction of bacteria. In addition, it is difficult to remove the residual bacteria in diabetic patients before PCNL operation. The ureteral stent is more conducive to the continuous colonization and reproduction of bacteria [
22,
23]; (2) as a foreign body, the ureteral stent is accompanied by the friction damage of the ureteral stent to the ureteral mucosa when the human body moves, which destroys the defense mechanism of the urinary tract epithelial system. In addition, the long-term retention of the ureteral stent (≥ 8 weeks) can form stone crystals on the surface of the ureteral stent, which is conducive to the adsorption, growth, and reproduction of bacteria [
4,
5]; (3) PCNL was positive for urine culture before surgery, and turned negative after active anti-infective treatment. However, for some complex stones with high S.T.O.N.E. scores (especially the large stone size, severe obstruction, and multiple kidney calices involved), residual stones are present after surgery, and bacterial colonies are often present in the residual stones. These bacterial colonies, under the natural protective barrier provided by the bacterial biofilm, prevent the killing of bacteria by antibacterial drugs and eventually lead to bacterial reproduction and infection recurrence [
4,
5,
21].
It is suggested that
Escherichia coli,
Enterococcus,
Klebsiella pneumoniae,
Proteus mirabilis, and
Pseudomonas aeruginosa are the common pathogens of urinary tract infection induced by urinary stones [
24,
25]. In this study, we found that among the pathogens causing AP associated with ureteral stent after PCNL, Gram-negative bacteria were mainly
Escherichia coli,
Klebsiella pneumoniae, and
Pseudomonas aeruginosa, and Gram-positive bacteria are mainly
Enterococcus faecalis and
Staphylococcus epidermidis. In recent years, the unreasonable use or abuse of antibiotics in China, the drug resistance of pathogenic bacteria is becoming more and more serious, especially in patients with kidney stones and urinary tract infection. In China, the resistance rate of
E. coli to quinolones (levofloxacin) and gentamycin was close to 50%, and the resistance rate to cephalosporins increased gradually, among which 79.2% and 66.5% to the first and second-generation cephalosporins respectively [
26‐
28]. In this study, we also found that the pathogens of AP associated with ureteral stent after PCNL had strong resistance to quinolones (levofloxacin) and the first and second-generation cephalosporins (the resistance rate was more than 50%). These results suggest that quinolones (levofloxacin) and the first and second-generation cephalosporins are no longer suitable for the treatment of AP associated with ureteral stent after PCNL. In this study, we analyzed the pathogenic bacteria of AP associated with ureteral stent after PCNL. We found that the pathogenic bacteria were sensitive to β-lactam combined enzyme inhibitors (piperacillin/tazobactam) and aminoglycoside antibiotics (amikacin), and the resistance rate was less than 15%. Therefore, for mild to moderate infections, β-lactam combined with enzyme inhibitors (piperacillin/tazobactam) and aminoglycoside antibiotics (amikacin) are highly sensitive to pathogens and can be used as the first choice of drugs, but aminoglycoside antibiotics (amikacin) should be used carefully due to renal toxicity and ototoxicity. In addition, we also found that the pathogenic bacteria were sensitive to carbapenems (meropenem, imipenem), glycyl tetracyclines (tigecycline), azolidone antibiotics (linezolid), glycopeptide antibiotics (teicoplanin, vancomycin), and other drugs, and the resistance rate was less than 10%. Therefore, for severe infections, we recommend the use of this class of restricted antibiotics for anti-infective treatment in the absence of susceptibility to the pathogen.
In conclusion, diabetes mellitus, postoperative stone residue, leukocyte count ≥ 100/HP, positive urine culture result, ureteral stent retention time ≥ 8 weeks, and high S.T.O.N.E. score (especially the large stone size, severe obstruction, and multiple kidney calices involved) were independent risk factors of AP associated with ureteral stent retention after PCNL. Escherichia coli, Enterococcus faecalis, Staphylococcus epidermidis, Klebsiella pneumoniae, and Pseudomonas aeruginosa are the main pathogens of AP associated with double J-tube after PCNL. The pathogenic bacteria were sensitive to amikacin, β-lactam combined with enzyme inhibitor compound, carbapenems, and other drugs.
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