1. Discomfort after stent placement
The most common complication of both acute and chronic stent placement is the discomfort associated with the stent. To better understand this issue, Joshi and his colleagues designed the Ureteral Stent Symptom Questionnaire (USSQ) to quantify post-stenting discomfort in patients with urolithiasis and benign obstruction. The questionnaire covered six major health problems associated with stenting, including urinary tract symptoms, somatic pain, general health, work performance, sexual health and some other problems.
This study is the first to assess the range of post-stenting discomfort problems, providing a standardized scale. The study showed that over 80% of patients with benign lesions with stent placement had irritative voiding symptoms, pain, and discomfort. This discomfort was not limited to urinary tract symptoms, but also included the entire torso, which greatly affected daily function.
In a later study, the USSQ evaluated the relationship between the position of the distal stent ring in the bladder and post placement discomfort and found that those patients whose distal stent ring crossed the bladder midline showed more problems on the USSQ after 7 and 28 days of placement.
A subsequent randomized trial examining the location of the distal stent ring showed that a stent that was too long in the bladder caused severe urinary difficulty, urinary urgency, and a greater impact on quality of life. Pain is exacerbated during voiding and can radiate to the ipsilateral torso, which may be secondary to ureteral pressure reflux and stent movement.
Previous studies have shown that stents can move about 2 cm during daily activities, causing physical irritation of the ureter, resulting in inflammation of the urethral epithelium of the bladder and kidney where the stent ring is located, and thus may cause additional pain and discomfort. Future studies should focus on the design of the stent and the choice of biomaterials, which may reduce irritation in cases where stent movement is unavoidable.
2. Loss of ureteral peristalsis
It is now widely believed that stents can affect ureteral peristalsis by inducing excessive peristalsis in the ureter over a period of time. For a short period of time after stent placement, the ureter will peristaltically move excessively to clear the stent (due to partial obstruction), and eventually the peristalsis disappears. Whether this state of peristaltic disappearance itself is associated with pain and discomfort is unclear, but some studies have suggested that the urinary voiding process slows down as a result, which may also account for the mild ipsilateral pelvic effusion that occurs after tube placement.
Interestingly, patients’ pain and urinary symptoms are significantly reduced with selective alpha-blockers such as tamsulosin, which inhibits ureteral constriction and reduces peak ureteral systolic pressure. Similarly, alfuzosin significantly improves urinary tract symptoms and somatic pain, especially in urination and ipsilateral somatic pain.
Whether this reduction in symptoms is due to loss of peristalsis due to inhibition of ureteral contraction by alpha-blockers or due to recovery of peristalsis following the easing of a sustained state of ureteral smooth muscle contraction caused by stent placement is unclear.
If the latter is correct, then maintenance of ureteral peristalsis after stenting is beneficial, while reducing pelvic effusion due to previous loss of peristalsis. Future studies are needed to better understand whether loss of ureteral peristalsis is a beneficial outcome of stent placement and whether maintenance of peristalsis improves the overall function of the stent.
3. Stent displacement
Stent displacement, especially end displacement and detachment, is not uncommon. A variety of factors are involved in this process, including stent length, material, and diameter. It has been shown that silicone stents with a diameter of 4.8 Fr are more prone to distal displacement than polyurethane stents with a diameter of 6 Fr.
Patient-related factors are stent implantation time and kidney motion with respiration, but these factors still need to be studied in more depth. Although the appropriate length of the stent is determined by the patient’s height, studies have shown that a more applicable distance between the ureter and the renal pelvis and bladder junctions reduces the frequency of distal displacement.
Distal stent displacement can offset the benefits of stenting and exacerbate stent-related symptoms. However, this can be easily adjusted by cystoscopy. What is challenging is the uncommon proximal stent shift, the incidence of which has been reported to be 1-4.2%. Management of proximal stent displacement requires retrograde stent removal via ureteroscopy.
When the distal stent ends below the pelvic rim, stent removal with a lithotomy basket or Fogarty catheter has a success rate of >90%. Special cases of proximal displacement include stent proximal displacement above the pelvic rim, above the stenotic segment or the site of recent surgical repair. In these cases, the percutaneous approach has a higher success rate.
4. Urinary tract infection
Bacterial colonization of ureteral stents is a significant problem, with reported colonization rates of 42-90%. Although bacteria are able to interact and adhere to the bare stent surface, this direct interaction does not appear to be the primary mechanism of bacterial adhesion and colonization. Recent studies have shown that urinary conditioned membranes can alter the physical properties of the surface of the scaffold. Bacteria express a protein called adhesin, which recognizes and adheres to proteins forming the major component of urinary biofilms.
A long-standing hypothesis that the presence of this membrane increases bacterial adhesion was tested by Elwood et al. in 2013, who found no difference in adhesion and colonization of Escherichia coli and Staphylococcus compared to scaffolds containing conditioned membranes versus those that did not. Their findings refute the hypothesis that urinary conditioned membranes increase bacterial adhesion and colonization and also suggest that preventing the deposition of these membranes does not inhibit bacterial adhesion and colonization, as the bacteria appear to act only on the bare scaffold surface.
Interestingly, despite a 90% incidence of stent bacterial colonization, only a small percentage of patients with positive stent bacterial cultures develop symptomatic urinary tract infections. The incidence of urinary tract infections increased when stents were placed for longer than 90 days. In a 250-patient consecutive survey, urine cultures before and after placement, and bacterial cultures at the tip of the distal stent showed that time of stent placement, systemic disease, including diabetic nephropathy and chronic renal failure without dialysis (blood creatinine of 200-500 μmol/l) were significantly associated with bacteriuria and bacterial stent colonization.
Considering the increased risk of urinary tract infections, the authors recommend a shorter duration of stent placement and prophylactic antimicrobial therapy for high-risk patients. However, in this regard, it is important to consider that those patients with systemic disease are at a much higher risk of carrying antibiotic-resistant strains due to their prior antimicrobial therapy. Therefore, efficient antibiotic prophylaxis regimens must be patient-specific and must carefully consider the patient’s medication history and prior antibiotic use.
Currently, urine culture is the most commonly used method to detect bacterial colonization and infection status of stents after placement. However, a negative urine culture does not mean that the stent is free of bacterial colonization, as the sensitivity of urine culture for detecting bacterial colonization in stents is only 21-40%, but increases with the duration of placement. In fact, the rate of positive urine cultures (despite positive stent cultures) is relatively low during short-term placement. This suggests that the bacteria colonizing the stent have not yet infected the urine, but that they have infected the stent during stent placement.
In addition, the species of bacteria in the urine is usually different from the species found on the stent. The species of bacteria on the stent varied with the segment in which the stent was tested. These findings reveal the fact that, similar to the biofilm found on Foley catheters, the membranes found on ureteral stents often consist of multiple Gram-positive and Gram-negative bacteria, rendering antibiotic therapy against a single urine culture ineffective.
5. Stent cortical formation
Similar to bacterial colonization, the occurrence of stent crust formation increases with time of placement. In stent-inserted urolithiasis patients, the incidence of crusts was 9.2% for stent removal within 6 weeks, 47.5% for removal within 6-12 weeks, and up to 76.3% for removal after 12 weeks.
Although the number of crusts appeared to be greater in the proximal and distal convoluted portions, the portion of the ureteral lumen was usually clearer or the last to form crusts. This may be due to the “clearing” effect of ureteral peristalsis, while the coiled portion of the stent is in constant contact with urine in the kidney and bladder.
The process of crust formation is very complex, and despite the application of multiple materials with different physical properties, none of them can prevent the deposition of crystals and eventually lead to crust formation. Of all the materials available, silica gel is the least likely to form guano and hydroxyapatite crusts.
It is important to note that the extent to which a material forms a crust depends largely on the test equipment used. Often some companies’ claims of materials’ resistance to crust formation characteristics are based on simple in vitro experiments only and do not describe what happens to these materials in patients. While simple in vitro experiments can demonstrate that those materials and/or coatings may resist crust formation, the actual elaboration of their function in clinical applications can only be based on relevant in vivo animal models or clinical trials.
Although the exact mechanism of stent crust formation remains unclear, most believe that crust formation is secondary to the formation of a stent urine biofilm. Biofilm formation begins when urinary proteins are electrostatically adsorbed onto the surface of the stent biomaterial. Interestingly, because the crust does not form instantaneously, most stents detach the hydrophilic shell from the surface within a short time after implantation, and this shell prevents biofilm formation. Thus, constant changes in the physical properties of the stent surface are beneficial in preventing biofilm deposition and subsequent crust formation.
One study showed that the crustal composition of the stent was identical to the composition of the concurrent stones. It is obvious that they are both infiltrated in the same urine and the same composition is supersaturated to form stones. Whether the crystals act and adhere directly to the stent material, and whether they are more tightly adherent through interaction with the biofilm component, is not known.
Two studies analyzed the composition of biofilms on the surface of scaffolds with and without crust formation. Overall, over 300 proteins were found to be present on the scaffold surface. Ig κ, IgH G1, α1 antitrypsin, histone H2b and H3a were highly associated with scaffold shell formation, while uromodulin and histone H2a were less associated.
The authors hypothesized that these positively charged proteins may attract negatively charged crystals and form a skin shell. Another study suggested a different mechanism. He detected that scaffold biofilms contain calcium-binding proteins, such as urinary regulator and S-100 protein. These proteins allow calcium-containing crystals to adhere to the surface of the scaffold. This study also identified the presence of blood proteins such as plasma albumin, globulin and fibronectin. These proteins in the stent biofilm can interact with hydroxyapatite via electrostatic forces, suggesting another mechanism for stent cortical formation.
Even when stents are placed for a moderate period of time (less than 8 weeks), crust formation is still common. Severe crust formation increases the difficulty of stent removal, potentially requiring multiple procedures. To guide the management of stent crusts, Acosta-Miranda et al. established the Forgotten, crust-forming and calcified (FECal) stent grading system based on their clinical experience with these problems. Stents are graded according to the area of crust formation, and each grade has a corresponding therapeutic measure.
In the system, grade 1 crust formation affects only the distal stent convoluted portion, grade 2 is associated with crust formation in the proximal convoluted portion, grade 3 includes crust formation in both grade 2 and the ureteral portion of the stent, grade 4 shows crust formation in both the distal and proximal convoluted portions, and grade 5 shows crust formation in the entire stent.
This grading system reflects the increasing difficulty of stent removal with increasing grading. grade 5 stent crusts are associated with a duration of placement greater than 2 years, which usually occurs in patients who forget to remove the stent. grades 4 and 5 crusts often require multiple extraction procedures (1.94-2.7).
The authors also noted that removal of stones from the distal portion of the stent prior to treatment of the proximal portion could increase the success rate of extraction. Some authors recommend preoperative nephrograms to confirm the function of the renal unit, because in patients with poor renal function, management of severe stent crusts may require ureterectomy and open bladder lithotripsy.
Prolonged stent placement makes the occurrence of grade 4 and 5 conditions in the FECal grading system inevitable, which typically occurs in patients who forget the time of extraction. To reduce the occurrence of grade 4 and 5 stents, some research groups have recommended the use of electronic stent registries (ESRs) to enter stent information, including time of placement and expected time of removal, into the patient’s electronic medical record (EMR).
The ESR system should alert the physician prior to the expected time of removal, and the physician should also be alerted when a stent change is not recorded in the EMR or when the removal record is deleted. This system has significantly reduced the incidence of forgotten stent removals, from 12.5% to 1.5% after one year, which provides strong support for the use of this system in urology.