Subcutaneous node-induced bladder contracture is a relatively common complication of advanced renal subcutaneous node. According to statistics from 837 cases of renal subcutaneous node at Zhongshan Hospital affiliated with Shanghai First Medical College, there were 81 cases of subcutaneous node-induced bladder contracture, accounting for 9.67%. Bladder contracture is primarily caused by severe fibrosis resulting from subcutaneous node lesions invading the bladder muscle layer and is a major cause of contralateral hydronephrosis. The diagnostic criteria for bladder contracture have not yet been standardized. In summary, the capacity standards for bladder contracture include three categories: 100 milliliters, 80 milliliters, and below 50 milliliters.

bubble_chart Clinical Manifestations

After contracture, the bladder's capacity significantly decreases, leading to marked urinary frequency. At the same time, intravesical pressure increases, the bladder neck widens, the prostatic urethra dilates, and the urethral sphincter fails to prevent urine leakage, resulting in incontinence. Clinically, inflammatory spasms caused by bladder subcutaneous nodules often present with dysuria, pyuria, and hematuria in addition to urinary frequency, and symptoms improve with anti-subcutaneous nodule treatment. In contrast, bladder contracture symptoms primarily include urinary frequency and incontinence, usually without dysuria, pyuria, or hematuria, and do not improve with anti-subcutaneous nodule therapy.

bubble_chart Diagnosis

The diagnosis of bladder contracture due to subcutaneous node primarily relies on clinical symptoms, urinalysis, and cystography, and should be differentiated from inflammatory spasms caused by bladder subcutaneous node. In terms of clinical symptoms, inflammatory spasms caused by bladder subcutaneous node often present with dysuria, pyuria, and hematuria in addition to urinary frequency, and improve with anti-subcutaneous node treatment. In contrast, bladder contracture typically manifests as urinary frequency and incontinence without dysuria, pyuria, or hematuria, and symptoms do not improve with anti-subcutaneous node treatment. Sometimes, symptoms may worsen due to further fibrosis of the bladder. In urinalysis, inflammatory spasms caused by bladder subcutaneous node show pyuria and hematuria that correlate with the degree of urinary frequency, whereas bladder contracture presents with significant urinary frequency but few inflammatory cells in the urine. On cystography, inflammatory spasms from bladder subcutaneous node are painless during contrast injection, with the bladder appearing normal or folded and exhibiting bladder neck spasms. In contrast, bladder contracture patients experience only a sense of fullness during contrast injection, with the bladder appearing small, round, and irregularly edged without folding. In severe cases, the bladder neck may be open, and the posterior urethra dilated. If necessary, saddle anesthesia can be used for differentiation: inflammatory spasms due to bladder subcutaneous node may show increased bladder capacity under saddle anesthesia, whereas bladder contracture does not.

The treatment of bladder contracture often requires surgery. If there is no urethral stricture and the patient's condition permits, sigmoid colon bladder augmentation should be performed, which has shown good long-term follow-up results. If urethral stricture is present, urinary diversion surgery should be chosen. For patients with severe conditions who cannot tolerate major surgery, permanent nephrostomy or ureterostomy may be considered.