Contributors of Campbell-Walsh-Wein, 12th edition
Duncan T. Wilcox, Kyle O. Rove, Aaron D. Martin, Christopher C. Roth, John P. Gearhart, Heather N. Di Carlo, Francisco Tibor Dénes, Roberto Iglesias Lopes, Aseem Ravindra Shukla, Arun K. Srinivasan, Carlos R. Estrada, Stuart B. Bauer, Paul F. Austin, Abhishek Seth, Martin A. Koyle, Armando J. Lorenzo, John C. Thomas, Douglass B. Clayton, and Mark C. Adams
Lower urinary tract and bowel dysfunction in children
Epidemiology and pathophysiology
Functional disorders of the lower urinary tract (LUT) encompass abnormalities in bladder filling and include a broad spectrum of clinical entities. Anomalies of bowel and urinary tract frequently coexist, whether functional, anatomic, and/or neuropathic. Constipation may adversely affect bladder function, leading to low functional capacity, incontinence, urinary tract infection (UTI), and triggering or exacerbating vesicoureteral reflux (VUR). LUT dysfunction accounts for up to 40% of pediatric urology clinic visits. Daytime incontinence varies with both age and gender in school-age children and seems to be more common in girls. The most common urinary symptoms include holding maneuvers and urgency. Enuresis stems from a maturational delay in the ultimate development of bladder control, with three organ systems implicated in its pathogenesis: the bladder, kidney, and brain. Approximately 15% of children will have some degree of nighttime wetting at 5 years of age, with a spontaneous resolution rate of approximately 15% per year, so 15 years of age only 1% to 2% of teenagers will still wet the bed.
Clinical presentation
LUT conditions resulting in urinary stasis are associated with UTI. There is a known association between LUT and VUR, and VUR may be secondary to bladder dysfunction. Clinicians should also be cognizant of association with neuropsychiatric disorders such as attention-deficit/hyperactivity disorder (ADHD) in children with daytime wetting, as these comorbidities may interfere with treatment success. Relationship between abnormal bowel and bladder activity is termed bowel-bladder dysfunction (BBD), and, if present, clear identification and management of any concomitant bowel dysfunction is paramount for successful treatment of voiding symptoms.
Diagnosis and testing
Evaluation of incontinence, voiding dysfunction, or known LUT pathology begins with thorough history and physical exam. History includes evaluation of urinary symptoms and infections (UTI), diet, bowel function, and developmental milestones, including toilet training. Clinicians should also be cognizant of association with neuropsychiatric conditions such as ADHD in children with daytime wetting because this is likely to interfere with treatment success. Examination should include inspection of the back spine for signs of occult spinal dysraphism or tethered cord such as lipoma, mass, or hair tuft. Constipation/bowel function should be assessed; the Bristol stool scale is often a useful guide ( Fig. 6.1 ). The Rome IV criteria are recommended for diagnosis of functional constipation in children ( Table 6.1 ). If constipation and fecal impaction are obvious on history and physical examination, management based on clinical grounds without imaging studies is recommended. A 7-day bowel and bladder diary and 48-hour frequency volume charts are invaluable in diagnosing simple and complex LUT voiding dysfunction
| Must include 1 month of at least two of the following in infants up to 4 years of age: |
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| In toilet-trained children, the following additional criteria may be used: |
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Noninvasive testing may include urinalysis +/- culture if irritative voiding symptoms (dysuria, urgency, or frequency) are present. Ultrasonography should include prevoid and postvoid bladder volumes, bladder wall thickness, rectal diameter, and presence of debris. Uroflowmetry provides information regarding flow characteristics during urination, including shape or pattern. Addition of electromyography (EMG) allows for appreciation of coordination between pelvic floor musculature, sphincteric relaxation, and bladder emptying, which can help diagnosis synergistic or dyssynergic voiding patterns.
LUT dysfunction secondary to neurologic deficit or severe obstructive uropathy should be assessed with formal urodynamic studies establish bladder pressures. Urodynamic findings that increase concern for upper urinary tract injury include: (1) impaired compliance (>20 mL per cm H 2 O is normal); (2) detrusor sphincter dyssynergia (DSD) coupled with poor emptying, inability to void, and/or elevated voiding pressures; (3) sustained, elevated detrusor pressure (Pdet) during filling; (4) elevated detrusor leak point pressure (DLPP) (>40 cm H 2 O); and (5) elevated voiding pressures in the setting of poor flow. Routine invasive urodynamics in pediatric patients with LUT symptoms in the absence of neuropathy rarely change management and should be limited.
Treatment
Conservative measures are exhausted before initiating pharmacotherapy, physical therapy, biofeedback, neuromodulation, and/or surgical intervention. The ultimate goal of any structured behavior modification program is to return the child to normal micturition habits. If evidence of bowel dysfunction is present, a regimen that includes high fiber (daily fiber intake is age in years +15–20 = total grams to be ingested) and increased fluid intake is initiated, as well as timed voiding every 2 hours. If increased fiber is not feasible or successful, polyethylene glycol can be titrated such that children are eventually having daily Bristol type 4 stools.
Biofeedback uses electronic or mechanical instruments to relay perceptual evidence to assist a child in controlling bladder function. Pharmacologic intervention for LUT dysfunction encompasses anticholinergic agents and α-adrenergic receptor antagonists (i.e., α-blockers) to enhance bladder filling and emptying, respectively. Oxybutynin was among the first generation of modern antimuscarinic medications available for treating incontinence in children. The main side effects include constipation, dry mouth, blurred vision, reduced sweating, flushing, and altered behavior and cognition. Electrical nerve stimulation, also known as neuromodulation, has been used to treat refractory nonneurogenic LUTD in children. In neuromodulation, electrical stimuli are exerted in a noninvasive manner to alter the existent neural transmission pattern and modulate detrusor activity.
Initial approach in children with nonmonosymptomatic nocturnal enuresis is as detailed above for LUT dysfunction. Conventional therapies for nocturnal enuresis include behavior modification, the enuresis moisture alarm, and pharmacologic therapy (e.g., desmopressin, anticholinergics, imipramine).
As with bladder management, bowel management algorithms favor conservative measures ( Fig. 6.2 ). Surgical management of defecation disorders includes antegrade enemas, delivered through a catheterizable channel (Malone antegrade continence enema [MACE]) or a cecostomy tube. Retrograde (transanal) washouts with a balloon catheter in the rectum represent a viable and less invasive alternative. Patient selection is critical, and candidates should have failed maximal conventional measures before proceeding to invasive options.
Prognosis
Addressing concomitant bowel dysfunction and ruling out underlying medical disease (such as posterior urethral valves, spinal dysraphism, diabetes mellitus) is key to symptomatic improvement.
Pediatric bladder anomalies
Prenatal bladder anomalies may be detected as early as the 10th week of gestation. Bladder agenesis is very rare and compatible with life only if the ureters drain ectopically, resulting in hypoplasia due to inadequate filling or storing of urine during development. An enlarged bladder, or “megacystis” with oligohydramnios raises concern for LUT obstruction; however, megacystis resolving before delivery may have no postnatal sequela. Postnatally, megacystis in association with abdominal distention, vomiting, and failure to pass meconium raises suspicion for the megacystis microcolon intestinal hypoperistalsis syndrome.
Bladder diverticula are usually discovered postnatally and may be associated with infection, hematuria, incontinence, or obstruction. Children with generalized connective tissue diseases, such as Ehlers-Danlos, Williams, or Menkes syndrome, are at risk for development of multiple and/or very large posterolateral bladder wall diverticula. Paraureteral diverticula may be acquired/secondary to infravesical obstruction.
Urachal anomalies ( Fig. 6.3 ) may present in the immediate postnatal period with umbilical drainage. Urachal anomalies must be distinguished from omphalitis, which typically presents as a superficial cellulitis and a patent omphalomesenteric duct remnant, which can present with feculent umbilical drainage. Management of an infected urachal cyst or sinus with abscess includes initial drainage and antibiotics followed by complete excision of the patent urachus with a bladder cuff.
Nephrogenic adenoma is a rare benign inflammatory bladder tumor associated with a reaction to infection or trauma. Treatment involves resection although up to 80% may recur.
Hemorrhagic cystitis in children is often related to chemotherapy with cyclophosphamide or ifosfamide as well as BK virus, cytomegalovirus, and adenovirus in immunocompromised children. Mesna is given with cyclophosphamide therapy to help prevent hemorrhagic cystitis
Posterior urethral valves
Epidemiology and pathophysiology
PUV are the most common cause of LUT obstruction (LUTO) in boys with an incidence of 1.6–2.1 per 10,000 births. Most valves appear as leaflets arising from the verumontanum that fuse anteriorly ( Fig. 6.4 ). PUV during fetal development results in detrusor hypertrophy with high storage and voiding pressures. PUV may lead to dilation of the posterior urethra, bladder neck hypertrophy, bladder wall thickening, vesicoureteral reflux, upper tract dilation, and—in one third of affected patients—end-stage renal disease.
Clinical presentation
Neonatal presentation.
Many infants are detected due to prenatal hydronephrosis, oligohydramnios, and/or a thick-walled bladder. Initial postnatal course is dictated by the severity of comorbidities such as pulmonary hypoplasia and renal failure.
Delayed presentation.
Despite widespread prenatal sonography, two thirds of children with PUV present after birth; therefore, a high degree of suspicion is warranted in boys presenting with LUT symptoms such as recurrent infections, overflow incontinence, gross hematuria and/or renal dysfunction.
Diagnosis and testing
Prenatal diagnosis.
Thickened dilated bladder, upper tract dilation, and oligohydramnios have a high sensitivity for PUV on prenatal ultrasonography; a dilated posterior urethra results in the “keyhole sign”. Severity of obstruction is indicated by amniotic fluid volume, renal dysplasia, and fetal urinary makers.
Postnatal diagnosis.
Much like the antenatal period, classic ultrasound findings include distended bladder with thickened wall and dilated posterior urethra. Voiding cystourethrogram (VCUG) remains the definitive study to confirm PUV. The bladder often appears thickened and trabeculated with multiple diverticuli, and high-grade VUR is seen in approximately 50% of boys ( Fig. 6.5 ). Postnatal biochemical evaluation of renal function includes electrolytes and creatinine.
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