bubble_chart Overview

The obstruction of the urinary system leads to the dilation of the renal pelvis and calyces, where urine is retained, collectively referred to as hydronephrosis. Due to the increased pressure caused by the abdominal mass of urine within the kidney, the renal pelvis and calyces expand, and the kidney parenchyma atrophies. If the retained urine becomes infected, it is called infected hydronephrosis; when the kidney tissue necrotizes and loses function due to infection, and the renal pelvis fills with pus, it is called pyonephrosis or suppurative kidney. The primary disease cause of hydronephrosis is obstruction at the ureteropelvic junction.

bubble_chart Etiology

The causes of hydronephrosis are divided into congenital and acquired types, as well as hydronephrosis caused by extraurinary and lower urinary tract diseases.

(1) Congenital obstructive causes include: ① Segmental dysfunction: Due to the absence, hypoplasia, or anatomical disorder of the muscles at the ureteropelvic junction or upper ureter, normal peristalsis in this segment is affected, leading to dynamic obstruction. If this condition occurs at the ureterovesical junction, it results in congenital megaureter, causing renal and ureteral dilation and hydronephrosis. ② Intrinsic ureteral stenosis: Most commonly occurs at the ureteropelvic junction, with the narrowed segment typically 1–2 mm but sometimes extending 1–3 cm, causing incomplete obstruction and secondary tortuosity. Electron microscopy reveals excessive collagen fibers around and within the muscle cells in the obstructed segment, eventually damaging the muscle cells and forming an inelastic narrowed segment dominated by collagen fibers, which impedes urine flow and leads to hydronephrosis. ③ Ureteral tortuosity, adhesions, bands, or membranous structures: These may be congenital or acquired, often occurring at the ureteropelvic junction or lumbar ureter, with nearly two-thirds of cases seen in children and infants. ④ Compression by aberrant vessels: About one-third of cases involve aberrant renal hilar vessels located anterior to the ureteropelvic junction. Other causes include horseshoe kidney and impaired renal rotation during embryonic development. ⑤ High insertion of the ureter: This may be congenital or caused by asymptomatic renal pelvis dilation due to peripelvic fibrosis or vesicoureteral reflux, leading to upward migration of the ureteropelvic junction without detectable stenosis during surgery. ⑥ Congenital ureteral ectopia, cysts, duplex ureter, etc.

(2) Acquired obstruction: ① Post-inflammatory or ischemic scarring leading to localized fixation. ② Vesicoureteral reflux causing ureteral tortuosity, combined with perirureteral fibrosis, eventually resulting in obstruction at the ureteropelvic junction or ureter. ③ Tumors or polyps in the renal pelvis or ureter, which may be primary or metastatic. ④ Ectopic kidney (floating kidney). ⑤ Stones, trauma, and post-traumatic scar stenosis.

(3) Obstruction caused by extrinsic diseases: Extrinsic lesions causing obstruction include arterial or venous pathologies; female reproductive system disorders; pelvic tumors or inflammation; gastrointestinal diseases; retroperitoneal lesions (including retroperitoneal fibrosis, abscesses, hemorrhage, tumors, etc.).

(4) Obstruction caused by lower urinary tract diseases: Conditions such as prostatic hyperplasia, bladder neck contracture, urethral stricture, tumors, stones, or even phimosis can also impede upper urinary tract drainage, leading to hydronephrosis.

bubble_chart Pathological Changes

Regardless of the reason that obstructs the normal flow of urine, a membranous barrier gradually forms at the ureteropelvic junction, resembling a sluice gate. The renal pelvis expands into a cyst and gradually enlarges; the renal parenchyma also progressively stretches and thins, accompanied by congestion. The renal calyces gradually dilate along with the expansion of the renal pelvis and parenchyma, while the renal pyramids and renal columns are compressed and thinned, eventually almost disappearing. The glomeruli can still maintain their urinary excretion function, but due to the necrosis of the renal tubules and the loss of concentrating ability, the urine becomes dilute. Various pathological changes can occur during the course of the disease.

(1) Reflux of renal pelvis urine: After hydronephrosis occurs, a portion of the urine can still be drained from the ureter, but another portion will reflux into three pathways: ① the perirenal space; ② the veins around the renal pelvis; ③ the lymphatic vessels around the renal pelvis. Under normal circumstances, the lymphatic capacity of the kidney increases with the increase in urine flow, such as during osmotic diuresis or ureteral obstruction. Acute obstruction of the renal lymphatic vessels can lead to natriuresis and diuresis, causing little change in renal function. However, when the lymphatic vessels of both kidneys are ligated along with ureteral obstruction, necrotic changes in the kidneys can occur within a few days. At the onset of ureteral obstruction, only reflux in the renal tubules and renal sinus occurs. As the pressure continues to rise, a portion of the urine enters the lymphatic and venous systems at the site equivalent to the renal pelvis outlet and begins to extravasate. In chronic hydronephrosis, most of the urine enters the renal venous system, which increases the burden on the kidneys.

After urine reflux, three changes will occur: ① The increased pressure in the renal pelvis accelerates urine reflux; reflux, in turn, can reduce the pressure in the renal pelvis, allowing the kidney to continue secreting urine. ② Through reflux, metabolic products can flow back into the circulatory system and be excreted by the normal kidney. ③ Through this pathway, infections can also enter the renal parenchyma, causing inflammation, or enter the circulation, leading to bacteremia.

(2) Renal balance and compensation: After hydronephrosis occurs, just as with the loss of renal function due to other causes, the remaining tissue can undergo hypertrophic changes and compensate for part of the function. However, this effect weakens with age, and generally after the age of 35, this compensatory function is almost lost.

The concept of renal balance was proposed by Hinman in 1919, referring to the situation where, due to trauma or disease, part or one kidney loses function, and after the removal of that kidney, the contralateral kidney can adjust the overall renal function. After hydronephrosis, due to the increased pressure in the proximal urinary tract causing renal tissue damage, a significantly enhanced repair capacity is generated. If infection occurs or the obstruction is not completely relieved, it will affect the repair and hyperplastic compensatory capacity. Eventually, due to the damage to the renal parenchyma caused by hydronephrosis, degenerative changes further develop into atrophy. However, because the contralateral kidney itself has the ability to regulate balance, the overall renal function will still appear normal until irreversible changes occur in both sides, leading to damage in overall renal function. If the obstruction is relieved and the hydronephrosis subsides, according to the principle of disuse atrophy (Hinman, 1922), the originally hypertrophied and compensatory renal tissue or another transplanted kidney will atrophy. It has now been proven that during the growth and development of animals, renal growth is completed under the stimulation of growth hormones, while compensatory growth occurs under the stimulation of an unidentified humoral factor. If an immature kidney is transplanted into a normal animal, the immature kidney can continue to develop; but if a kidney that has already undergone compensatory hyperplasia is transplanted into an animal with only a single hyperplastic compensatory kidney, both hyperplastic kidneys due to compensation will atrophy until they return to normal size. In experimental animals and patients with hydronephrosis, if the obstruction is relieved, even though the contralateral kidney has already undergone compensatory hyperplasia and hypertrophy, the hydronephrotic kidney can still recover its function.

(3) Impact of Obstruction on Renal Function The impact of obstruction on renal function depends on the degree of obstruction, whether it is unilateral or bilateral, and whether it is acute or chronic. ① **Acute Complete Obstruction**: Within the first 90 minutes of acute complete obstruction, renal blood flow increases, primarily due to the dilation of preglomerular stirred pulse vessels. However, from 90 minutes to 5 hours, preglomerular vasoconstriction occurs, leading to reduced renal blood flow. If the obstruction persists, ureteral pressure rises. After 5 hours, preglomerular vasoconstriction can cause a bilateral reduction in renal blood flow and a decrease in ureteral pressure. These post-obstruction changes in renal blood flow are believed to be mediated by vasoactive prostaglandins, which induce sustained vasoconstriction. In cases of acute complete ureteral obstruction, the glomerular filtration rate (GFR) decreases, and tubular function is impaired. In partial obstruction, tubular transit time is reduced in the initial hours, but reabsorption remains relatively efficient, resulting in decreased urine output, increased osmolality, and reduced urinary sodium concentration. ② **Chronic Complete Unilateral Obstruction**: Renal function impairment begins with renal vasoconstriction and tubular atrophy by the second week. By the sixth week, ureteral pressure gradually declines to 1.99 kPa (15 mmHg), and renal blood flow decreases to 20% of that in the contralateral kidney. ③ **Chronic Partial Obstruction**: The pattern of renal function impairment resembles that of complete obstruction. Even grade I obstruction can cause significant damage. ④ **Physiological Differences Between Unilateral and Bilateral Obstruction**: In experimental animals, differences between the two can be observed within 24 hours. In unilateral obstruction, a greater proportion of nephrons remain unperfused and unfilled, whereas in bilateral obstruction, most nephrons remain perfused, though total renal blood flow and glomerular perfusion are similarly reduced. The mechanisms of renal function impairment differ between unilateral and bilateral obstruction. In unilateral obstruction, vasoconstriction of the preglomerular stirred pulse vessels reduces blood flow and glomerular perfusion. In bilateral obstruction, pressure in the proximal tubules and resistance in the efferent stirred pulse vessels increase. Upon relief of obstruction, natriuresis and diuresis occur immediately in bilateral obstruction but not in unilateral obstruction. ⑤ **Metabolic Changes in the Kidney**: These changes primarily manifest as reduced oxygen utilization and increased carbon dioxide production, gradually leading to a low-oxygen metabolic state. The kidney loses its ability to utilize fatty acids, α-ketoglutarate, and to produce glucose. The lactate-to-pyruvate ratio increases during metabolism, indicating a shift toward anaerobic metabolism in hydronephrotic kidneys. With persistent obstruction, renal metabolic function progressively deteriorates, and irreversible changes become evident after 6 weeks.

(4) Functional Recovery After Relief of Hydronephrotic Obstruction In humans, if the ureter is completely obstructed for a period and then relieved, the recovery of kidney function takes longer than observed in experimental animals. Some authors reported a case where certain kidney functions were only confirmed to have recovered 69 days after the relief of complete ureteral obstruction. In patients with bilateral chronic obstructive hydronephrosis, the urine acidification process—including ammonia excretion, acid titration, and bicarbonate absorption—shows abnormalities. In human studies, after partial urinary tract obstruction, all measurements of kidney function indicate impairment unless the urine is diluted. After the obstruction is relieved, some functions can be restored.

The diuretic process that occurs after the relief of bilateral ureteral obstruction or solitary kidney obstruction is due to the higher osmotic negative pressure and elevated glomerular filtration rate caused by retained fluids and electrolytes. After diuresis, water and electrolyte replacement therapy must be increased and prolonged to prevent the delayed recovery of normal water and electrolyte balance due to the negative balance caused by diuresis. After the obstruction is relieved, kidney function begins to recover, with the speed of recovery depending on the severity of kidney injury, the presence of infection, and the extent of damage to the contralateral kidney.

(5) Other Changes Caused by Hydronephrosis Acute unilateral ureteral obstruction can cause hypertension, primarily due to increased renin secretion, whereas chronic unilateral hydronephrosis rarely leads to hypertension caused by elevated renin secretion. When unilateral hydronephrosis without renal artery stenosis induces increased renin secretion, surgical repair can completely resolve the hypertension and restore normal conditions. Bilateral hydronephrosis is rarely associated with hypertension caused by increased renin secretion. The relationship between hypertension and chronic hydronephrosis is mainly due to water and sodium retention leading to volume expansion.

Upper urinary tract obstruction can cause ascites, but spontaneous intraperitoneal urine leakage (urinoma) is rare. In experimental bilateral ureteral ligation in rats, urinary ascites can occur. After acute ureteral obstruction, urine leakage may occur at the renal fornix, and this type of leakage can even occur in infants with posterior urethral valve obstruction. Huashan Hospital in Shanghai reported a case of upper ureteral stone with acute obstruction, confirmed by high-dose intravenous drip pyelography, showing similar fornix urine leakage.

In experimental urinary ascites, the ratio of urea to creatinine in the ascitic fluid should be measured. In normal individuals, the urine-to-plasma creatinine ratio ranges from 30:1 to 100:1. When urine crosses the peritoneum to form urinary ascites, the creatinine ratio to plasma can be as low as 2:1, whereas in non-urinary ascites, the ratio is 1:1.

Patients with hydronephrosis often develop secondary polycythemia. Primary polycythemia is accompanied by splenomegaly, leukocytosis, and thrombocytosis, whereas various kidney diseases often cause polycythemia, which is characterized by pure erythrocytosis with normal arterial oxygen saturation. After the removal of a hydronephrotic kidney, the red cell mass decreases. Even after the relief of obstructive hydronephrosis, erythropoietin levels remain high in the blood, and the mechanism behind this is still unclear.

bubble_chart Clinical Manifestations

(1) Asymptomatic Hydronephrosis This refers to hydronephrosis in a quiescent state, which may persist for many years without manifesting symptoms and is only discovered when secondary infection occurs or symptoms of compression on adjacent organs arise.

(2) Symptomatic Hydronephrosis ① Pain: Lumbar pain is a significant symptom. In chronic obstruction, symptoms are often mild, presenting only as dull lumbar pain. Most acute obstructions can cause noticeable lumbago or typical renal colicky pain. Some patients, however, may not experience pain even with acute bilateral obstruction or complete obstruction. Dietl's crisis: This refers to intermittent hydronephrosis caused by obstruction at the ureteropelvic junction, alternating between oliguria and polyuria. After consuming large amounts of water, renal colicky pain, nausea, and vomiting may occur. In children, hydronephrosis often presents as an abdominal mass, sudden severe pain or colicky pain in the upper abdomen, followed by copious urination; when the pain subsides, the mass shrinks or even disappears. ② Renal Enlargement and Abdominal Mass: Chronic obstruction can lead to kidney enlargement or an abdominal mass, though other symptoms may not necessarily be present. Long-term obstruction may result in a palpable cystic mass in the abdomen. ③ Polyuria and Anuria: Chronic obstruction-induced renal impairment may manifest as polyuria, while complete bilateral obstruction, a solitary kidney, or complete obstruction in a single functional kidney can lead to anuria. Partial obstruction may result in urine output exceeding normal levels, presenting as significant polyuria. With intermittent obstruction of the renal pelvis by kidney stones, intermittent polyuria may occur. During polyuria, the abdominal mass may disappear or abdominal distension and fullness pain may ease. ④ Hematuria: Upper urinary tract obstruction rarely causes hematuria, but if the obstruction is due to stones or tumors, hematuria may accompany renal colicky pain. In cases of partial obstruction, intermittent obstruction may occur, with increased urine output and possible hematuria following colicky pain. Secondary infection may also be accompanied by hematuria or pyuria. ⑤ Gastrointestinal Symptoms (nausea, vomiting, decreased appetite, etc.): These occur in two scenarios: one is reflex gastrointestinal symptoms during acute upper urinary tract obstruction; the other is gastrointestinal symptoms caused by uremia due to renal impairment in the late stage [third stage] of chronic obstruction. ⑥ Secondary Refractory Urinary Tract Infection: Once an obstructed urinary tract develops a secondary infection, it is often difficult to cure and prone to recurrence. During episodes, symptoms such as fear of cold, fever, and lumbago may occur and extend to the lower urinary tract, causing bladder irritation.

(3) Signs The most prominent sign is renal fullness and tenderness upon percussion in the renal area, or even a palpable mass, following upper urinary tract obstruction-induced hydronephrosis. In cases of intermittent obstruction due to incomplete blockage, an intermittently palpable abdominal mass may occur. Generally, hydronephrotic masses are not firm, non-tender, smooth, and nodule-free; when complicated by infection, pain, tenderness, and systemic infection symptoms and signs may appear.

bubble_chart Diagnosis

(1) Medical History Due to the fact that its clinical manifestations are related to the site of obstruction, duration, speed of onset, presence of secondary infections, and the nature of the primary lesion, the following should be noted during diagnosis: ① In the early or latent chronic stages of obstruction, there may be no symptoms; ② The patient's sensitivity is closely related to the detection of symptoms. For patients with abdominal masses, chronic lumbar and back soreness, refractory urinary tract infections, or unexplained low-grade fever, the possibility of upper urinary tract obstruction should be considered, and further examinations should be conducted. Special attention should be paid to children with intermittent abdominal masses and polyuria.

(2) Signs Further examinations can be conducted based on signs such as kidney area tenderness, masses, or abdominal lumps to determine whether upper urinary tract obstruction exists.

(3) Laboratory Tests ① Routine Urinalysis: In early Grade I hydronephrosis patients, routine urinalysis may be normal. When the renal calyx expands, hematuria and proteinuria may appear. Significant proteinuria and casts are uncommon in upper urinary tract obstructive diseases. ② Renal Function Tests: For patients with unilateral upper urinary tract obstruction and hydronephrosis, renal function tests generally show no abnormalities due to compensation by the contralateral kidney. If the phenol red test and indigo carmine excretion test indicate impairment, it suggests bilateral kidney damage. In severe bilateral hydronephrosis, slow urine flow through the renal tubules leads to significant urea reabsorption, while creatinine is generally not reabsorbed, resulting in a urea-to-creatinine ratio exceeding the normal 10:1. When renal parenchymal damage severely affects kidney function, both blood creatinine and endogenous creatinine clearance rates will rise. ③ Anemia: Occurs when bilateral hydronephrosis leads to reduced kidney function.

(4) X-ray Examinations ① Plain Radiography of the Urinary Tract: Shows an enlarged kidney shadow. If calcifications are present in the urinary tract, it suggests obstruction caused by kidney or ureteral stones. ② Intravenous Pyelography (IVP): Unless kidney function is severely impaired, IVP usually provides detailed information, including the site and cause of obstruction; the degree of dilation of the renal pelvis, calyces, and ureter; and an estimate of kidney function based on the thickness of the renal cortex and the density of contrast imaging. High-dose IVP combined with video recording and cinefluoroscopy can dynamically observe the peristaltic function of the kidneys and ureters to distinguish between mechanical and dynamic obstruction, as well as compare peristaltic function on both sides. ③ Retrograde Pyelography: For patients with poor kidney function or inadequate IVP results, retrograde pyelography can be performed to determine the site, cause, and degree of obstruction. However, caution is required to avoid introducing bacteria into the hydronephrotic kidney during retrograde catheterization, which could lead to pyonephrosis, or exacerbating obstruction due to catheter or contrast agent-induced mucosal edema, converting partial obstruction into complete obstruction. ④ Percutaneous Nephrostomy and Ureterography: For cases where IVP results are unsatisfactory, retrograde pyelography fails, or retrograde pyelography is contraindicated, percutaneous puncture of the hydronephrotic kidney under B-ultrasound guidance can be performed for antegrade pyelography to assess the site and degree of obstruction, as well as the condition of the proximal ureter and renal pelvis. Urine collected during the procedure can be used for cytological examination and culture, and a catheter can be left in place for drainage. ⑤ Angiography: For patients suspected of having obstruction related to vascular malformations, renal angiography, abdominal aortography, inferior vena cava angiography, or renal vein angiography can be performed as needed to clarify the relationship between obstruction and vascular abnormalities. Angiography can also provide information on renal blood supply and cortical thickness. ⑥ Cystourethrography: For patients with bilateral hydronephrosis and ureteral dilation, this examination can reveal conditions such as vesicoureteral reflux or neurogenic bladder.

(5) Ultrasonography Can assess the degree of hydronephrosis and ureteral dilation, the extent of renal parenchymal atrophy, preliminarily identify the site and cause of obstruction, and guide percutaneous puncture for pyelography.

(6) Radionuclide Examination ① Radionuclide Renogram: In obstructive renography, the vascular phase and secretory phase are somewhat suppressed, which is related to the severity and duration of the obstruction, mainly manifested as a delayed decline in the excretion phase. The renogram helps estimate the differences in bilateral renal function and the degree of obstruction but cannot provide quantitative analysis. ② ¹³¹ I Scanning γ Imaging reveals poor radionuclide uptake: The slow transit of radionuclides through the renal cortex results in scintillation in the renal pelvis abdominal mass.

(7) CT can determine the location of obstruction, aid in the detection of the disease cause, and clearly display the degree of renal and ureteral dilation as well as the thickness of the renal cortex. It also allows for simultaneous comparison of the structure and function of both sides.

(8) Percutaneous nephroscopy and ureteroscopy enable direct observation of the obstruction site within the lumen. These procedures also allow for biopsy, dilation, incision, catheterization, and other treatments, as well as the creation of a nephrostomy.

(9) Cystoscopy allows direct visualization of both ureteral orifices and catheterization for separate urine collection. This facilitates renal function tests, quantitative urea analysis, colorimetric tests for phenolsulfonphthalein or indigo carmine, and estimation of renal pelvis capacity based on urine volume. Additionally, retrograde pyelography can be performed via catheterization.

(10) Renal pelvis pressure measurement involves percutaneous renal puncture and catheter insertion (≥F₁₈). Simultaneously, an F12–14 catheter is inserted into the bladder via the urethra and left open to drain bladder fluid. Normal saline or contrast medium is infused into the renal pelvis at a rate of 10 ml/min until the fluid fills the upper urinary tract and the inflow and outflow rates (both at 10 ml/min) equilibrate. The renal pelvis pressure (absolute pressure) is then recorded via a Y-connector connected to a manometer. Bladder pressure is measured simultaneously through the catheter, and the relative pressure is calculated by subtracting the intra-abdominal pressure (bladder pressure) from the absolute renal pelvis pressure. The normal range is 1.18–1.47 kPa (12–15 cm H₂O). A pressure >1.47 kPa (15 cm H₂O) indicates grade I obstruction; >2.16 kPa (22 cm H₂O) indicates grade II obstruction; and >3.92 kPa (40 cm H₂O) indicates severe obstruction.

If contrast medium is injected during pressure measurement, imaging or video recording can also be performed to identify the location and cause of the obstruction.

bubble_chart Treatment Measures

(1) Treatment Objectives On the basis of eliminating the {|###|}disease cause{|###|}, relieve obstruction, improve renal function, alleviate symptoms, eradicate infection, and restore the normal anatomical structure as much as possible.

(2) Treatment Considerations ① Age: Infants and young children should be treated as early as possible. Young adults may be observed appropriately, but surgery should be performed promptly if the condition progresses. For patients aged 50–60 or older, early surgical intervention should be considered to preserve intact renal function. ② Assessment of renal function and obstruction: a. At least 1/5 of normal renal tissue must be preserved to maintain the minimal life-sustaining function. Unless necessary, renal drainage should be avoided to prevent infection. b. For asymptomatic and infection-free hydronephrosis patients, follow-up examinations (ultrasound, CT, or intravenous pyelography) can be performed every 6–12 months. If there is no progression, surgery may be postponed. c. Obstruction at the ureteropelvic junction may lead to stone formation. Therefore, when removing stones, it is essential to investigate whether there is a {|###|}disease cause{|###|} contributing to stone formation. If stenosis is present, it should be corrected simultaneously. ③ Assessment of intrarenal versus extrarenal pelvis surgery: Intrarenal pelvis cases are more challenging to manage. ④ Timing of surgery for bilateral hydronephrosis: In cases of bilateral hydronephrosis without infection, the kidney with poorer function should be addressed first, allowing the contralateral kidney to continue compensatory hypertrophy under functional load. The kidney undergoing reconstructive surgery tends to recover better under certain stimulation. For cases with infection, the more severely affected side should be operated on first, followed by the contralateral side as soon as possible. If only the better-functioning kidney is infected, priority should be given to surgery to maximize renal function preservation and infection control, with the other side addressed after the condition stabilizes.

For unilateral hydronephrosis in a relatively well-functioning kidney where reconstructive surgery may still salvage renal function, surgery should be prioritized. If the contralateral kidney is already severely damaged and nonfunctional, the decision to perform nephrectomy should only be made after the surgical side’s renal function has recovered and the condition has stabilized.

(3) Treatment Methods:

1. Local management: For obstructive lesions that can be resolved locally, such as adhesion lysis, fibrous band resection, vascular repositioning and reanastomosis, or stone removal. If prolonged local compression has severely damaged ureteral development, the affected ureteral segment should be resected and reanastomosed.

2. For obstruction causing severe hydronephrosis, initial diversion and drainage (e.g., nephrostomy) may be necessary.

3. Reconstructive surgery: Key principles must be followed: ① Ensure the ureteropelvic anastomosis is at the lowest point of the renal pelvis. ② The ureteropelvic anastomosis should form a funnel-shaped structure to prevent {|###|}fistula disease{|###|}. ③ During repair, surrounding fibrous tissue, adhesions, and scar tissue should be excised, but blood supply must not be {|###|}injury{|###|}ed. ④ Excess renal pelvic wall should be excised to maintain appropriate pelvic tension. If hydronephrosis is extensive, the thinner renal cortex can be invaginated and fixed to reduce renal volume. ⑤ To minimize anastomotic {|###|}fistula disease{|###|} (urinary leakage), a double-J stent may be placed. To prevent perianastomotic scar fibrosis due to {|###|}fistula disease{|###|} (urine leakage) and hematoma stasis, a negative-pressure drainage tube can be placed externally for adequate drainage. ⑥ There are many reconstructive techniques, but current {|###|}disease cause{|###|} pathological perspectives favor resection of the diseased segment followed by reanastomosis.