Adolescent Urology

Medical issues in adolescence offer special challenges. Adolescents are not children, but they can present with childhood problems. Additionally, although are not adults, they can develop conditions more often encountered in the older population. Therefore, management algorithms need to be tailored to consider not only the diagnosis but also the age of the patient, as the latter may be the most important factor.

These special-considerations clearly apply to urological conditions. In this article, the commonly encountered and sometimes controversial urological problems in adolescents are discussed.

Undescended testicles

Cryptorchidism is one on the most common congenital abnormalities in male infants. In utero, the testes develop intra-abdominally and spontaneously descend through the inguinal canal into the scrotum. Up to 3% of full-term boys and 30% of premature males, however, may have undescended testicles at birth [1]. There is a relatively high rate of spontaneous testicular descent in the first 3 to 6 months of life, such that the overall incidence of cryptorchidism is approximately 1% at 1 year of age. Because this number stays constant through adulthood, it is believed that if a testicle has not descended by 1 year of age, then it is unlikely to do so.

It has been known that the delayed consequences of cryptorchidism include an increased risk infertility and malignant degeneration. Over the past several years, many long-term studies have been published suggesting that the potential for infertility is greater with bilateral undescended testes when compared unilateral cryptorchidism. Paternity rates are similar in men with a history of unilateral cryptorchidism and normal controls, whereas men with bilateral cryptorchidism had significant decreased rates (75% versus 53%, respectively) [2,3]. Furthermore, the age of surgical correction may not be a factor in the development of infertility [4].

A history of cryptorchidism increases the relative risk of developing a testicular neoplasm by a factor of 40. When they develop, tumors usually occur in the third or fourth decade of life. Approximately 25% of these tumors arise in the normally descended testis. Seminoma is the most common subtype and, there has been no conclusive evidence that early orchidopexy is protective.

Ideally, cryptorchidism should be treated by 1 year of age. After this time, it is unlikely that the testicle will descend spontaneously. Additionally, there is good evidence that irreversible histologic damage may occur to the cryptorchid testicle by 3 years of age. Regardless, a significant number of children still present in late childhood and adolescence with undescended testes. This may occur for one of several reasons. The most common scenario is that children are not referred for definitive treatment, because either the parents or physician observe the child for years, hoping that the testicle will descend spontaneously. Secondly, a testicle may be present in the scrotum early in childhood but subsequently ascends into a cryptorchid position. This specific cause for testicular ascent is unclear, but it may be related to the vertical growth of a child who has a testicle fixed in place because of a patent process vaginalis [5]. Lastly, a small number of boys with retractile testes early in childhood will present in later childhood with true cryptorchidism.

The management of a prepubertal child with a palpable undescended testicle is straightforward. Surgical orchidopexy is the standard of care. Much has been written on the use of hormonal therapy, usually injections of human chorionic gonadotropin (hCG) as a means of medical management of cryptorchidism. The success rates of hCG are low in comparison to orchidopexy, however [1]. The greatest utility of hCG therapy may be to differentiate between retractile testes and true undescended testes. This situation is encountered commonly in an overweight child whose testis is floating in the peri-pubic fat pad. A course of hCG therapy (500 to 1000 IU intramuscularly twice weekly for 5 weeks) may lead to descent of the testes into the scrotum, thus obviating the need for surgery. Human chorionic gonadotropin therapy is not indicated in boys with true undescended testes. Hormonal therapy has no role after puberty, simply because the child produces endogenous androgens to affect testicular descent.

Undescended testes in children with nonpalpable testes represent a more complex situation. Several clinical possibilities exist. First, a testicle may not be present. Second, a testis may exist, but it may be small and nonviable. Third, there may be a viable testis located in the abdomen. In differentiating among these three possibilities, imaging studies have a limited role. Many patients undergo ultrasonography, but this is of little benefit. Detection of a testis on ultrasonography mandates a surgical exploration for orchidopexy. Failure to visualize a testis on ultrasound, however, does not mean that a testis is not present. In this instance, the testis may be intra-abdominal. Thus, a negative ultrasound does not obviate surgical exploration. MRI of the abdomen is a promising technique that may allow noninvasive determination of whether a testis is present and also determine the location of the organ [6]. The standard of care for a nonpalpable testis, however, remains surgical exploration.

There is no difference in the management of prepubertal boys with cryptorchidism from infants with the same condition. Postpubertal boys have different clinical and physiologic issues to consider. A postpubertal cryptorchid testis will have varying degrees of abnormal histology. Although hormonal function probably is maintained, spermatogenesis will be impaired markedly [7]. Furthermore, whether late orchidopexy will be protective against malignant degeneration is unknown. A postpubertal cryptorchid testis is often much smaller than the descended testis, as the latter has been able to develop and grow normally during pubertal hormonal simulation. Therefore, in a postpubertal male with cryptorchidism, the safest course of action may be to consider orchiectomy if a normal contralateral testicle is present. The role of testicular biopsy in the decision-making has not been clarified.


The term varicocele refers to dilated varicose veins draining the testicle. Although relatively uncommon in early childhood, varicoceles may be found in 15% of teenagers [1]. This number is similar to the incidence of varicoceles in adults. Varicoceles represent a soft fleshy mass superior and distinct from the testis that usually disappears when the patient is recumbent. They are detected most often during routine examinations. Large varicoceles have been described as having the appearance and consistency of a bag of worms.

The etiology of varicoceles is unclear. Varicoceles nearly always develop on the left side. The reason for this may be related to the anatomical and embryological differences between the two sides. The right spermatic vein drains directly into the inferior vena cava, and the left spermatic vein drains directly into the left renal vein, which has a slightly higher pressure than the vena cava. Additionally, there is partial compression of the left renal vein as it passes between the aorta and superior mesenteric artery. The right spermatic vein drains tangentially into the vena cava, unlike the acute 90 drainage of the left spermatic vein into the renal vein. Some authors feel that this predisposes the left spermatic vein to turbulent flow. The sudden development of a large varicocele, especially in a younger child, may be a sign of spermatic vein obstruction caused by the presence of a retroperitoneal mass.

The clinical and physiologic sequelae of varicoceles vary. Varicoceles can cause scrotal discomfort. This pain typically is described as a dull ache. Often, this discomfort is aggravated by activity or episodes of increased intra-abdominal pressure. Presumably, the inciting cause is the engorgement and distention of the veins within the scrotum related to increased intra-abdominal pressure.

Another problem associated with varicoceles is subfertility. Indeed, varicoceles represent the most common surgically- correctable cause of infertility. The reasons for this subfertility are unclear. Proposed theories include scrotal hyperthermia with secondary testicular injury, reflux of injurious metabolites, testicular hypoxia, and primary bilateral testicular dysfunction.

It is important to remember that although the presence of a varicocele increases the risk of having male-factor infertility, most men with varicoceles have normal fertility.

The dilemma associated with the management of adolescents with varicoceles relates to the evaluation and endpoints of therapy. Most teenagers with varicoceles are diagnosed as part of a routine school or sports physical examination. It is relatively uncommon for teenagers to present with associated pain or discomfort. Most teenagers are not concerned about fertility, which is the other potential physiologic consequence of varicoceles. The best way to assess for fertility potential would be to perform semen analyses. This rarely is performed in adolescents, however. A more practical and but less precise method is to evaluate testicular volume. If both testicles are equal in size, then a clinician assumes that the varicocele has not affected testicular health and that obs\ervation is appropriate. If, however, on serial evaluation, there is evidence that the left testicle is not developing, it would suggest that the varicocele may be affecting testicular health and that treatment is required. Testicular volume is assessed most easily with the use of a hand-held orchidometer. Routine ultrasonographic measurements are not necessary. A size difference of greater than 2 cc on serial examinations is considered significant. Studies have shown that when surgery is performed because of documented and progressive testicular volume loss, there often is catch-up growth of the involved testicle.

There are two main therapeutic options: surgical ligation of the veins or embolization of the veins by interventional radiologists. The latter has the potential advantage of avoiding an incision and general anesthesia, and a faster recovery. Success rates, however, are not as high with embolization as with surgical ligation [8]. Furthermore, unlike adults who simply may require local anesthesia for embolization, adolescents often require general surgery, precluding this potential advantage. In the United States, transvenous embolization of varicoceles is not performed commonly in adolescents.

Open surgical repair of varicoceles can be performed in several different ways. The main principle is to divide as many veins as possible. Although the varicocele is most evident in the scrotum, a trans-scrotal approach is ill advised because of the large number of veins present at that level and also the potential for injury to the testicular artery. Most pediatric urologists advocate approaching the varicocele through the groin or through a retroperitoneal approach. Recently, laparoscopic approaches also have been described [9]. Regardless of the technique, success rates with surgical repair are greater than 90% [8]. The main complications include recurrence of the varicocele and secondary development of hydrocele.

The acute scrotum

The term acute scrotum refers to severe pain within the scrotum that may mandate immediate surgical exploration for testicular salvage. Any physician caring for a boy with a painful scrotum must consider the possibility of testicular torsion. This refers to spontaneous twisting of the testicle with subsequent vascular compromise. The specific reason why a testicle may twist is unknown. There is a well-described anatomical abnormality known as the bell clapper deformity, however, which permits such a twist to occur. In the normal situation, the testicle and epididymis are fixed within the scrotum posteriorly. When a bell clapper deformity is present, there are no points of fixation circumferentially, allowing the testicle to twist within the scrotum. In this situation, the testicle hangs within the scrotum by means of its vascular pedicle analogous to the pendulum of a bell.

When complete testicular torsion occurs, there is a limited amount of time available when the testicle is still viable and salvageable. Studies have shown that after 6 hours of twist, about 90% of testicles will be necrotic. After 24 hours, this rate approaches 100%. Thus, in any boy with testicular pain, timely diagnosis and treatment are of utmost importance.

Most boys with testicular pain do not have testicular torsion. Indeed, true testicular torsion is a relatively uncommon occurrence. A more common cause of scrotal pain is torsion of the appendix testis. The appendix testes are small tissues attached to the testicle and epididymis, which represent embryological remnants with no known function. These appendages can twist spontaneously, leading to inflammation and necrosis, which cause significant pain and discomfort. The torsion of these appendages has no long-term significance.

Another cause of scrotal discomfort is epididymitis. True epididymitis is rare in the otherwise healthy prepubertal population. Teenagers who may be sexually active may develop it as a sexually transmitted disease. Some boys may develop epididymitis as a result of voiding dysfunction. In general, bacterial epididymitis usually occurs in boys with anatomical or functional abnormalities of the urinary system. When it occurs in an otherwise healthy male, it mandates a complete evaluation of the urinary tract.

The most important aspect of the evaluation of a boy with testicular pain is the history and physical examination. Typically boys with testicular torsion will relate sudden onset of severe testicular pain. Often there is associated abdominal or inguinal discomfort and nausea and vomiting. These boys may have difficulty ambulating. Because of the sensitive nature of the organ involved, there often is a delay before teenager tells an adult about the problem. This delay in presentation represents the most common reason why boys with testicular torsion often present with necrotic nonsalvageable testicles.

The physical examination will vary depending on when the child presents. If a boy presents soon after onset of pain when the testicle is still viable, the classic findings will include a high riding testicle whose longitudinal length is located in the horizontal plane (horizontal lie). The testicle will be diffusely tender. There may also be abdominal and inguinal tenderness. Early in the process, the scrotal wall will be normal with no thickening or swelling and only minimal redness. Usually, a cremasteric reflex is not present. Indeed, the presence of a cremasteric reflex may be less suggestive of testicular torsion. If the boy presents late, the physical findings are related to testicular necrosis. There may be diffuse scrotal wall thickening, erythema, and edema. There often is so much swelling that the testicle is not palpable; early signs such as the horizontal lie are not appreciable.

Some boys will have intermittent testicular torsion. These boys will present with occasional episodes of sudden and severe testicular pain that will resolve spontaneously. By the time these children are seen by medical personnel, the testicle has untwisted. Physical findings and radiographic studies will be normal. If the history is suggestive of this entity, elective testicular fixation is advisable for these boys.

Boys with a torsed appendix testis have a different history and examination. The pain typically is more gradual in onset and is usually not quite as severe as that associated with true testicular torsion. Most of the time, these boys present a day or so after onset of pain. The severity of the pain is typically not as great as compared with those with testicular torsion. Systemic signs such as nausea and vomiting or associated abdominal pain are often not present. Boys with appendix testis torsion also tend to be slightly younger than boys with testicular torsion. The physical examination in these boys can be quite varied. The classic blue dot sign is pathognomonic for appendix testis torsion, but is also relatively uncommon. This sign refers to visualization of the ischemic or necrotic appendix testis through the scrotal wall on the superior aspect of the testicle. The most common finding in patients with appendix testis torsion is diffuse scrotal wall thickening, erythema, and tenderness. The cremasteric reflex may be present. Duplex ultrasonography in these boys shows marked reactive hyperemia of the epididymis that often leads to the mistaken diagnosis of epididymitis.

Boys with epididymitis usually have pain and swelling that gradually worsen over time. They may have associated urethral discharge and abnormal urine sediment. The patient also may be febrile. The diagnosis of epididymitis always should be confirmed with a duplex ultrasound study demonstrating increased blood flow to the involved testis and epididymis. A common clinical mistake is to assume that the firm, twisted spermatic cord palpable posterior to the testis seen in early torsion is an inflamed epididymis.

The fundamental question that needs to be answered in boys with testicular pain is determining whether testicular torsion is present. If testicular torsion is present, emergent surgical exploration is necessary. If a boy does not have testicular torsion, then medical management with observation, analgesics, or antibiotics is required.

Because there is a direct relationship between duration of pain and salvageability of the testicle in boys with testicular torsion, the duration of time from the onset testicular pain determines the management. For example, if a boy presents within 6 hours of onset of pain, the time associated with performing ultrasonography may contribute to increased ischemic time and, ultimately, testicular necrosis. This patient may be best served with prompt surgical exploration without any diagnostic studies. If a boy presents with 12 hours of pain, however, the likelihood of testicular salvage in the face of prolonged testicular torsion is very low. In this instance, imaging studies may be helpful. The study of choice is a color flow Doppler ultrasound, which demonstrates the presence or lack of blood flow within the testicle. The reliability and accuracy of the study depends on the experience of the ultrasonographer. Falsely normal Doppler ultrasound studies (ie, testicle has Doppler signals, but is actually ischemic) have been reported [10]. Therefore, if there is strong clinical suspicion, surgical exploration should be pursued.

Scrotal masses

Scrotal masses are encountered commonly by primary care providers when educating the patient on the importance of self-examination and also as part of routine physical examinations for sports programs. Scrotal examination should be approached by carefully palpating and identifying the intrascrotal contents. The examiner should palpate the testicle and the epididymis, located behind and superior to the testicle. Furthermore, the spermatic cord, consisting of the testicular vessels and vas deferens, should be assessed.

When evaluating scrotal masses, one need\s to classify them based on whether they are extratesticular or intratesticular, solid or cystic, and painless or painful. Masses truly arising from the testicle are more likely to represent malignancies, whereas extratesticular masses are more likely to be benign. Although a carefully performed physical examination may be diagnostic, confirmation using scrotal ultrasonography is recommended, not only to confirm location of the mass but also to differentiate between solid and cystic lesions.

Solid masses are much more likely to represent neoplastic conditions, especially when painless. Transillumination using a hand- held light source may differentiate between solid and cystic structures. Although testicular cancer is more common in men in the third and fourth decades of life, adult testicular cancers may develop in any boy after the onset of puberty. The types of tumors that may develop in adolescents and teenagers are similar to those encountered in adult males and require the same diagnostic and therapeutic algorithms. Solid extratesticular masses are less common but also must be considered possible neoplastic conditions. Extratesticular tumors that may be found in teenage boys include para-testicular rhabdomyosarcoma or ademomatoid tumors of the epididymis.

Cystic lesions of the scrotum are much more common than solid lesions. A cystic mass within the epididymis is usually a spermatocele, which is a cystic dilation of the epididymal tubule. Spermatoceles require intervention only if the progressive enlargement causes pain. A cyst within the spermatic cord most likely represents a hydrocele of the cord. A cystic mass that surrounds the entire testicle such that the testicle itself is hard to feel represents a hydrocele. Small asymptomatic hydroceles may be observed, but larger ones that fluctuate in size or cause pain or discomfort should be corrected surgically.

Testicular microlithiasis

Testicular microlithiasis is an ultrasonographic finding of unclear significance. Boys with testicular microlithiasis usually have this detected at the time of scrotal ultrasonography performed for either scrotal pain or a scrotal mass. The microlithiasis itself is actually not palpable clinically and does not cause any symptoms. On ultrasound, small punctate, echogenic areas of calcification may be found throughout the testicle. The degree of calcification can vary from having only a few lesions to innumerable ones leading to a snowstorm appearance. There have been reports suggesting an association of testicular cancer in men with testicular microlithiasis [11]. It is unknown whether testicular microlithiasis is a preneoplastic condition, is simply associated with an increased risk of cancer development, or is of no significance at all. Although many case reports document the simultaneous existence of testicular microlithiasis and testicular cancer, there has been no study that shows that testicular microlithiasis is a risk for developing testicular cancer. It is possible that the same underlying abnormality that predisposes to germ cell tumors also may predispose to microlithiasis and that the microlithiasis itself may not be an independent risk factor. Regardless, the implications for and management of teenagers diagnosed as having testicular microlithiasis are unclear. The best course of action may be to address the uncertainties of the condition with the families and to emphasize the importance of monthly self-examination, which is something that all postpubertal males should perform anyway [12].

Urinary tract infections

Urinary tract infections (UTIs) are a relatively common problem in children. Indeed, 5% of febrile children will have a UTI as the source of the fever. Although there is a greater likelihood of structural or congenital abnormalities in children with UTIs, most children will still be anatomically normal. An initial evaluation to help differentiate between lower tract infection (cystitis) and upper tract infection (pyelonephritis) is useful. In general, cystitis is characterized more by symptoms such as urgency, frequency, incontinence, suprapubic pain, and dysuria. High-grade fever is less common. Pyelonephritis is a more systemic illness characterized by fever, malaise, and flank pain. Differentiation based on signs and symptoms is not perfectly accurate; however, it remains useful clinically, at least in older children. A UTI can be diagnosed only in the presence of a positive urine culture. The presence of dysuria, microscopic hematuria, urgency or frequency in the absence of a positive culture is not an infection. Ultimately, the main reason to prevent UTIs is that recurrent upper tract infections may lead to renal parenchymal scarring. Such scarring subsequently increases the risk of hypertension and even renal failure.

Although renal scarring may be the greatest consequence of UTIs in children, the development of renal injury after a single infection is uncommon in older children [13]. Progressive renal injury usually is the result of repeated, inappropriately-treated infections, especially in the face of underlying congenital dysplasia.

Older children do not necessarily need any formal evaluation after an initial episode of lower UTI. A careful history in these children often will identify underlying dysfunctional bladder or bowel habits that most often lead to the infection. Parents often are surprised to note that the bacteria leading to infection are nearly always enteric in origin. The prevention of UTIs must include normalizing voiding habits and ensuring proper hygiene.

Recurrent lower UTIs and even a single upper UTI require a radiographic evaluation. At a minimum, this includes imaging of the kidneys, preferably with a renal ultrasound. Renal ultrasonography is easy to perform, noninvasive, and obviates any concern for contrast reactions. Intravenous pyelography has no role in the routine evaluation of children with recurrent UTIs.

Dimercaptosuccinic (DMSA) scanning is very accurate at defining renal parenchymal involvement or injury. It has little role in the routine evaluation of children with infections, however. Some have argued that invasive studies such as cystography should be performed only in patients who have evidence of renal parenchymal involvement with a positive DMSA scan. A normal DMSA study may suggest that an infection may be clinically insignificant, as renal injury is unlikely from that specific infection.

The need for voiding cystourcthrography (VCUG) is controversial. Not all children with recurrent infections need to have a VCUG. VCUG should be performed only if one is concerned that vesicoureteral reflux may be present. Thus an adolescent with lower tract UTIs and not pyelonephritis does not need a VCUG. On the other hand, a child with recurrent pyelonephritis requires a VCUG. It is rather arbitrary whether to perform nuclear cystography or fluoroscopic cystography, because the radiation doses to the gonads are similar using either technique. Standard VCUG has the advantage that associated anatomic abnormalities such as bladder diverticulae, urethral abnormalities, and constipation can be assessed. Nuclear cystography has the advantage of being slightly more sensitive at the detection of reflux.

Boys with UTIs always require a formal evaluation, because infections are so uncommon in males. This evaluation entails kidney ultrasound and usually a VCUG. Infections in anatomically normal boys usually are related to dysfunctional bladder/bowel habits or being uncircumcised. The latter factor becomes less important beyond a year of age.

Vesicoureteral reflux in the adolescent population

The management of vesicoureteral reflux in young children is well- established. The mainstay of therapy is daily prophylactic antibiotics, treatment of any underlying dysfunctional bladder and bowel habits, and observation. Over the course of time, most children will have resolution of reflux. Surgical intervention is reserved for those with persistent infections despite prophylaxis, evidence of progressive renal injury, or persistence of reflux after a period of observation.

Decision-making is more difficult in older children whose reflux is less likely to resolve. The clinical management always has been to ensure eradication of reflux before the onset of puberty because of concern over the potential impact of febrile infections during pregnancy. There is very little information available on the risks posed by persistent reflux in women who are pregnant, however. There are significant data, however, showing that pre-existing renal scarring or reflux nephropathy may complicate pregnancy, especially if there is associated hypertension or renal insufficiency [14]. There is no information on the significance of persisting reflux into normal kidneys in pregnant women.

The traditional management for prepubertal girls with persistent reflux is standard open surgical correction. Surgical correction can be performed readily with minimal morbidity and with a 99% chance for cure. Surgical correction is designed to prevent recurrent upper tract infection. Children may continue to have lower tract infection despite successful eradication of reflux.

Two other management options for persistence of reflux are available and should be considered. One may consider simply discontinuing prophylactic antibiotics. Because renal injury usually only occurs in children younger than 4 to 5 years old, parenchymal damage is very unlikely in older children with pyelonephritis. A clinician may consider discontinuing prophylactic antibiotics and offering surgical correction reserved to those who continue to have infections. There are few reports of this approach, but in selected situations, observation may be appropriate. In one study, only 12% of children who had antibiotics discontinued developed recurrent infection [15]. Appropriate candidates for observational management incl\ude older children with low-grade reflux, no evidence of renal injury, and no definable bladder or bowel dysfunction.

Another option is the use of injection therapy. Cystoscopic injection of material into the submucosal space adjacent to the ureteral orifice has been used for nearly 20 years. The injected material creates a functional valve mechanism, correcting reflux with relatively high success rates [16-18]. This minimally invasive approach has been used extensively in Europe, but widespread use in the United States has been limited by the lack of a US Food and Drug Administration (FDA)-approved injectable substance.

Deflux (Q-Med, Uppsala, Sweden), a dextranomer/hyaluronic acid copolymer is a newer substance that has received FDA approval. This material is nonallergenic, stable, and does not migrate to distant organs. It is easy to inject. Short-term success rates of greater than 85% have been demonstrated. Success rates are higher in children with lower grades of reflux. The long-term efficacy of this method is unknown. The role of Deflux in the management of vesicoureteral reflux remains to be defined, and its greatest role may be in older children with low-grade reflux that persists after a period of observation.

Urinary incontinence

Urinary incontinence can be a devastating problem for an adolescent. The history is the most important part of the evaluation. To understand the pathophysiology of the incontinence, questions with regard to the nature of the wetting and the child’s general voiding habits should be asked. Specific questions include whether the child voids before going to school or during the school day (determine presence of infrequent voiding habits), whether the child feels like he needs to void more often than his friends, and whether he always has to look for a restroom in new environments (suggesting an overactive bladder). Additionally, specific details regarding the degree and timing of incontinence, the presence of urgency or frequency, and the coexistence of any dysfunctional bowel habits should be pursued. By asking very pointed questions with regard to the nature, timing, and situations associated with leakage, the underlying etiology often can be deduced. Invasive studies rarely are required. Specifically, VCUGs are not helpful, because vesicoureteral reflux never causes incontinence.

Incontinence in adolescents is usually dysfunctional in nature. It is rare for incontinence in this age group to be related to anatomic abnormalities. Progressively worsening incontinence or an inability to void may be a sign of an underlying spinal cord abnormality such as occult spinal dysraphism. Although rare, these spinal cord abnormalities need to be considered in any child who does not respond to therapy or if there are associated neurological symptoms or signs.

Urinary incontinence can be classified into one of several subtypes. Incontinence most often occurs because of bladder instability, infrequent voiding patterns, sphincter dysfunction, or vaginal reflux. A separate subcategory is the entity known as giggle incontinence. In general, patients with bladder instability will present with severe urgency and frequency. Vincent’s curtsy, whereby a girl will squat on her heel compressing her perineum and urethra shut, is a classic sign of bladder instability in young children; it is quite uncommon in older children and adolescents. Older children may relate significant urgency and frequency, often leading to the mistaken notion that the child has a bladder with a small capacity. Usually, these children have anatomically normal bladder capacities, but have low functional capacity because of the underlying bladder instability. The etiology of this unstable bladder may be related to associated bowel dysfunction and fecal retention. Often, episodes of cystitis and subsequent bladder inflammation may precipitate the development of an unstable bladder. These children may be treated with anticholinergics with gratifying results. Equally important is the treatment of any associated fecal retention. Indeed, studies have shown that treatment of bowel dysfunction alone may lead to significant improvement in incontinence [19].

On the opposite end of the spectrum are children with infrequent voiding habits. These children often are mislabeled as being lazy. They have developed the habit of only voiding once or twice during the course of the day. As result of this, they can have episodes of urgency with leakage of small amounts of urine. Occasionally, children with a history of infrequent voiding will develop UTIs and may develop an unstable bladder as described previously. Management of infrequent voiding patterns usually requires education and bladder retraining. A timed voiding program in conjunction with a bowel regimen is often successful. Severe cases of infrequent bladder emptying that may lead to bladder decompensation and hydronephrosis (the so-called non-neurogenic neurogenic bladder) require aggressive treatment with intermittent catheterization to prevent renal injury.

Some children can have urinary incontinence and infections because of incomplete emptying. This usually is detected only by noting an elevated postvoid residual on a screening renal ultrasound. Incomplete emptying may be caused by incomplete sphincter relaxation or inappropriate sphincter contraction during voiding. Sphincter dysfunction can be very hard to objectively assess, but treatment usually involves behavioral modification in the form of double and frequent voiding programs. Biofeedback techniques also may be used to try to teach the child sphincter relaxation. These methods are quite labor-intensive, however, and long-term efficacy is not known.

Reflux of urine into the vagina during voiding may occur in girls, especially those who are overweight, whose labia do not separate when seated on the toilet. The labia then act as a barrier, forcing a small amount of urine back into the introitus and vagina. This urine then can trickle into the underpants upon arising. The key to diagnosing this form of leakage is that the child notices the wetting after voiding. These children usually do not have any associated urgency, frequency, or any definable dysfunctional voiding habits. Treatment involves having the child manually separate the labia when seated to ensure that the introitus is unobstructed during voiding.

A special form of urinary incontinence is the so-called giggle incontinence. This form of incontinence often is misinterpreted as being stress incontinence, a condition that is nonexistent in an otherwise healthy adolescent population. A careful history in such children will elicit the fact that urinary incontinence only occurs during episodes of laughter. Such children are often very athletic, and urinary incontinence rarely occurs during physical activity. This is a surprisingly common condition that is understood poorly. There is evidence that it may be an inheritable disorder [20,21]. The etiology of this condition may be related to the cataplexy- narcolepsy complex, and, thus, may be a central nervous system (CNS) disorder. Usually, the history is all that is required to make the diagnosis. These patients typically have totally normal voiding habits outside of incontinence that is related strictly to laughter. Invasive studies such as VCUG or urodynamics are unnecessary. Often behavioral modifications such as frequent voiding or voiding before events or situations that may lead to wetting are adequate. Anecdotally, anticholinergic medications or Kegel exercises have shown improvement, but these are usually unsuccessful. The most successful pharmacological therapy for giggle incontinence appears to be the use of CNS stimulants such as methylphenidate. These medications may be used on a daily basis or on an as-needed basis before situations where leakage may occur.


There are several urologic conditions in the adolescent male and female that require medical attention. The conditions discussed in this article represent some of the most common concerns in adolescents.


[1] Schneck F, Bellinger MF. Abnormalities of the testes and scrotum and their surgical management. In: Walsh P, editor. Campbell’s urology. Philadelphia: W.B. Saunders; 2002. p. 2353-94.

[2] Lee PA, O’Leary LA, Songer NJ, Coughlin MT, Bellinger MF, Laporte RE. Paternity after unilateral cryptorchidism: a controlled study. Pediatrics 1996;98:676-9.

[3] Lee PA, O’Leary LA, Songer NJ, Coughlin MT, Bellinger MF, Laporte RE. Paternity after bilateral cryptorchidism. A controlled study. Arch Pediatr Adolesc Med 1997;151(3):260-3.

[4] Lee PA, O’Leary LA, Songer NJ, Bellinger MF, Laporte RE. Paternity after cryptorchidism: lack of correlation with age at orchidopexy. Br J Urol 1995;75(6):704-7.

[5] Rabinowitz R, Hulbert WCJ. Late presentation of cryptorchidism: the etiology of testicular reascent. J Urol 1997;157(5):1892-4.

[6] Yeung CK, Tam YH, Chan YL, Lee KM, Metreweli C. A new management algorithm for impalpable undescended testis with gadolinium enhanced magnetic resonance angiography. J Urol 1999; 162(3 Pt 2):998-1002.

[7] Rogers E, Teahan S, Gallagher H, Butler MR, Grainger R, McDermott TE, et al. The role of orchiectomy in the management of postpubertal cryptorchidism. J Urol 1998;159(3):851-4.

[8] Kass EJ, Reitelman C. Adolescent varicocele. Urol Clin North Am 1995;22(1):151-9.

[9] Ugazzi M, Chiriboga A, Proano L. Laparoscopic treatment for varicocele. J Laparoendosc Surg 1996;6(Suppl 1):S9-13.

[10] Steinhardt GF, Boyarsky S, Mackey R. Testicular torsion: pitfalls of color Doppler sonography. J Urol 1993;150:461-2.

[11] Berger A, Brabrand K. Testicular microlithiasis-a possibly premalignant condition. Report of five cases and a review of the literature. Acta Radiol 1998;39(5):583-6.

[12] Furness III PD, Husmann DA, Brock III JW, Steinhardt GF, Bukowski TP, Freedman AL. Multi-institutional study oftesticular microlithiasis in childhood: a benign or premalignant condition? J Urol 1998;160:1151 -4 [discussion 1178].

[13] Smellie JM, Ransley PG, Normand IC, Prescod N, Edwards D. Development of new renal scars: a collaborative study. BMJ 1985;290(6486): 1957-60.

[14] Jungers P. Reflux nephropathy and pregnancy. Baillieres Clin Obstet Gynaecol 1994;8(2): 425-42.

[15] Cooper CS, Chung BI, Kirsch AJ, Canning DA, Snyder III HM. The outcome of stopping prophylactic antibiotics in older children with vesicoureteral reflux. J Urol 2000;163(1):269-72 [discussion 272-3].

[16] Caione P, Capozza N. Endoscopic treatment of urinary incontinence in pediatric patients: 2-year experience with dextranomer/hyaluronic acid copolymer. J Urol 2002;168:1868-71.

[17] Lackgren G, Wahlin N, Skoldenberg E, Stenberg A. Long-term follow-up of children treated with dextranomer/hyaluronic acid copolymer for vesicoureteral reflux. J Urol 2001;166(5): 1887-92.

[18] Puri P, Chertin B, Velayudham M, Dass L, Colhoven E. Treatment of vesicoureteral reflux by endoscopic injection of dextranomer/hyaluronic Acid copolymer: preliminary results. J Urol 2003;170:1541-4 [discussion 1544].

[19] O’Regan S, Yazbeck S, Schick E. Constipation, bladder instability, urinary tract infection syndrome. Clin Nephrol 1985;23:152-4.

[20] Sher PK. Successful treatment of giggle incontinence with methylphenidate. Pediatr Neurol 1994;10(1):81.

[21] Sher PK, Reinberg Y. Successful treatment of giggle incontinence with methylphenidate. J Urol 1996;156:656-8.

Venkata R. Jayanthi, MDa,b,*

a Section of Pediatric Urology, Division of Urology, Department of Surgery, Children’s Hospital, 700 Children s Drive, Columbus, OH 43205, USA

b The Ohio State University, Columbus, OH 43210

* Children’s Hospital, 700 Children’s Drive, Columbus, OH 43205.

E-mail address: [email protected]

Copyright Hanley & Belfus, Inc. Oct 2004

Leave a Reply

Your email address will not be published. Required fields are marked *