Ureteral Stricture

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A ureteral stricture is characterized by a narrowing of the ureteral lumen, causing functional obstruction. The most common form of ureteral stricture is ureteropelvic junction (UPJ) obstruction, which is characterized by a congenital or acquired narrowing at the level of the UPJ (see Ureteropelvic Junction Obstruction). The objective of this article is to discuss the incidence, etiology, diagnosis, therapy, and management outcomes of ureteral strictures.

Ureteral strictures may be classified as follows:

Extrinsic malignant strictures include those caused by primary or metastatic cancer. Primary pelvic malignancies, particularly cancers of the cervix, prostate, bladder, and colon, frequently cause extrinsic compression of the distal ureter. Retroperitoneal lymphadenopathy, caused by a wide range of malignancies, particularly lymphoma, testicular carcinoma, breast cancer, or prostate cancer, may cause proximal to midureteral obstruction.

Extrinsic benign compression due to idiopathic retroperitoneal fibrosis may also cause unilateral or bilateral ureteral obstruction, leading to azotemia.

Transitional cell carcinoma (TCC) may cause malignant intrinsic obstruction.

Malignant ureteral obstruction is differentiated from benign ureteral obstruction by (1) the presence of an extrinsic mass on a CT scan or sonogram and (2) the appearance of the ureter on contrast-study images.

Ureteral TCC may manifest as ureteral obstruction. Ureteral TCCs typically have an irregular mucosal pattern and are associated with dilatation of the ureter below the lesion (goblet sign). Benign strictures are usually smooth, without distal dilatation. In some cases, biopsy may be required to differentiate benign from malignant strictures. Biopsy samples can usually be collected ureteroscopically or with a fluoroscopically directed ureteral brush. Ureteral tumors can also be diagnosed during transureteral resection of the tumor with specialized ureteral resectoscopes.

Benign intrinsic strictures, which are the focus of this article, may be congenital (eg, congenital obstructing megaureter), iatrogenic, or noniatrogenic (eg, those that follow passage of calculi or chronic inflammatory ureteral involvement [eg, tuberculosis and schistosomiasis]).

The widespread use of upper tract endoscopy has led to an increased frequency of iatrogenic ureteral stricture. Early ureteroscopy studies reported ureteral stricture rates of 3%-11% in patients undergoing ureteroscopy for calculus management. More recent studies using smaller fiberoptic endoscopes; laser lithotripsy; and smaller, less traumatic instruments report a ureteral stricture rate of less than 1%.

In a review of 24 patients with highly impacted ureteral stones that were impacted for an average of 11 months, 24% of the patients developed postoperative ureteral strictures; therefore, impaction is a major risk factor. Ureteral perforation during these procedures has also been identified as a risk factor for stricture disease. [1, 2]

Factors associated with ureteral stricture development during ureteroscopy include the following:

Large scope size

Prolonged case duration

Stone impaction

Size

Proximal location

Perforation

Use of intracorporeal lithotripsy

Ureteral strictures may complicate urinary diversions. The frequency of ureterointestinal anastomotic strictures during urinary diversion is 3%-5%. Ureteral injuries may result from any pelvic or retroperitoneal surgery, particularly abdominal hysterectomy and sigmoid colectomy. Gynecologic surgery is responsible for up to 75% of iatrogenic ureteral injuries.

Vakili et al performed a prospective analysis of 479 patients undergoing hysterectomy for benign disease. [3] Iatrogenic ureteral injury occurred in 8 patients (1.7%), comparable with previous ranges reported in the literature (0.02%-2.5%). Risk factors for urinary tract injury during hysterectomy include malignancy, pelvic radiation, endometriosis, prior surgery, and surgery for prolapse, although at least half of all ureteral injuries have no identifiable risk factors. Ureteral injuries or injury repairs may also result in strictures, although strictures of these etiologies are less common than strictures caused during endoscopy or anastomosis.

Iatrogenic benign strictures may result from various causes, including the following:

Ureteroscopy

Open or laparoscopic injury

Radiation therapy

Urinary diversions

Renal transplantation

Ureteral strictures are typically due to ischemia, resulting in fibrosis. Wolf and colleagues define a stricture as ischemic when it follows open surgery or radiation therapy, whereas the stricture is considered nonischemic if it is caused by spontaneous stone passage or a congenital abnormality. [4] Less commonly, the etiology is mechanical, such as from a poorly placed permanent suture or surgical clip.

Pathologic analysis of the strictures reveals disordered collagen deposition, fibrosis, and varying levels of inflammation, depending on factors such as etiology and interval since the causative insult.

The resulting ureteral obstruction may vary widely from mild, causing only asymptomatic proximal ureteral dilation and hydronephrosis, to severe, causing complete obstruction and subsequent loss of renal function.

Some patients with ureteral strictures are asymptomatic; others are symptomatic only during periods of diuresis or develop severe renal colic. The degree of symptoms correlates poorly with the degree of obstruction; at times, severe obstruction is asymptomatic or silent. Renal failure and azotemia may be due to bilateral strictures, such as in cases of bilateral ureteroenteric strictures, external compression due to retroperitoneal malignancy, or retroperitoneal fibrosis; recovery depends on the duration of ureteral obstruction.

Obtain a detailed patient history and pay particular attention to symptoms during periods of diuresis (eg, after ingestion of caffeinated or alcoholic drinks). Take note of any history of prior malignancy, surgery, or radiation therapy. Important physical examination findings include abdominal pain, fullness or tenderness, and costovertebral angle tenderness.

Ureteral strictures are often found during routine follow-up imaging after ureteroscopy or intestinal urinary diversion. In this setting, asymptomatic hydroureteronephrosis proximal to the site of obstruction may occur. Most patients with significant strictures after ureteroscopy are symptomatic. They present with flank pain, flank fullness, or abdominal fullness.

In a review of 131 patients who underwent ureteroscopy and follow-up radiographic imaging, Karod et al found no asymptomatic patients with residual obstruction. [5] Thirteen of 21 patients with persistent flank pain had residual obstruction, one from a ureteral stricture.

Less frequently, persistent urinary tract infection or pyelonephritis is associated with unilateral ureteral obstruction. Patients with preexisting renal insufficiency or an abnormal contralateral kidney may present with an increased serum creatinine level or azotemia. Also, patients with strictures in solitary or functionally solitary kidneys (eg, renal transplant patients) may present with renal failure.

Indications for intervention in patients with ureteral strictures include pain, infection, or obstruction, which may threaten a patient’s renal function. Less common indications may include stone formation proximal to an obstruction or hematuria.

The ureter is a muscular tube lined by transitional epithelium that courses from the renal pelvis to the bladder in the retroperitoneum.

The length of the ureter is 20-30 cm, depending on the individual’s height. The lumen size is 4-10 mm in circumference, depending on its location. The narrowest areas include the UPJ, the overpass by the ureter where it crosses over the bifurcation of the iliac arteries, and the ureterovesical junction (UVJ).

In both men and women, the ureter courses posterior to the gonadal vessels and anterior to the iliopsoas muscles, crosses the common iliac artery and vein, and enters inferiorly into the pelvis. In men, the vas deferens loops anterior to the ureter, prior to the ureter entering the bladder. In women, the ureter courses posterior to the uterine arteries (hence, the “water under the bridge” analogy) and close to the uterine cervix prior to reaching the intramural bladder.

The ureteral blood supply is provided from multiple sources. Superiorly, branches from the renal and gonadal arteries may contribute. As the ureter courses through the retroperitoneum, the aorta contributes numerous small branches. In the pelvis, the iliac, vesical, uterine, and hemorrhoidal arteries also contribute to the ureteral blood supply.

The major contraindication to ureteral stricture surgery (endoscopic or open) is an active and untreated urinary tract infection. A relative contraindication is uncorrected bleeding diathesis.

When ureteral stricture surgery (endoscopic or open) is contemplated, many patient factors should be considered.

If the patient has a terminal malignancy, is extremely elderly, or has a high surgical risk and tolerates internal stenting well, long-term stenting may be most appropriate. Chung et al analyzed 101 patients with extrinsic ureteral obstruction managed with indwelling ureteral stents. [6] Within 1 year, the stents failed in 41% of the patients. Thirty percent of patients needed percutaneous nephrostomy tube placement at a mean of 40 days. Predictors of stent failure included cancer, a baseline creatinine level of greater than 1.3 mg/dL, and poststent systemic treatment.

If the affected kidney has less than 25% renal function, balloon dilation and endoureterotomy are more likely to fail. [4] Therefore, the patient is at significant risk for eventually requiring open surgery or nephrectomy. Few data exist on the outcomes of open surgery based on preoperative renal function. Renal function may significantly improve in some patients with poor function due to obstruction after the obstruction is corrected. If the renal function is less than 10%, recovery is unlikely and initial nephrectomy may be most appropriate.

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Benjamin Newell Breyer, MD, MS Assistant Professor, Trauma and Reconstruction, Department of Urology, University of California, San Francisco, School of Medicine

Benjamin Newell Breyer, MD, MS is a member of the following medical societies: Alpha Omega Alpha, American College of Surgeons, American Urological Association, Endourological Society

Disclosure: Nothing to disclose.

Christopher J Kane, MD, FACS Professor of Surgery, Chief of Urology, University of California, San Diego, School of Medicine

Christopher J Kane, MD, FACS is a member of the following medical societies: American College of Surgeons, American Urological Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Bradley Fields Schwartz, DO, FACS Professor of Urology, Director, Center for Laparoscopy and Endourology, Department of Surgery, Southern Illinois University School of Medicine

Bradley Fields Schwartz, DO, FACS is a member of the following medical societies: American College of Surgeons, American Urological Association, Association of Military Osteopathic Physicians and Surgeons, Endourological Society, Society of Laparoendoscopic Surgeons, Society of University Urologists

Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: Cook Medical; Olympus.

Daniel B Rukstalis, MD Professor of Urology, Wake Forest Baptist Health System, Wake Forest University School of Medicine

Daniel B Rukstalis, MD is a member of the following medical societies: American Association for the Advancement of Science, American Urological Association

Disclosure: Nothing to disclose.

Ureteral Stricture

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