There are a number of urologic conditions that pediatric hospitalists will encounter in their care of pediatric inpatients. Primary urologic emergencies such as testicular torsion and urinary obstruction require prompt diagnosis and intervention to limit morbidity. In addition, several medical entities, such as recurrent urinary tract infection (UTI) and vesicoureteral reflux (VUR), may benefit from urologic consultation. Surgical intervention may be considered or required in some cases such as testicular torsion, high grade vesicoureteral reflux, or high grade ureteropelvic junction obstruction.
Testicular torsion is caused by twisting of the testicle and the spermatic cord resulting in hypoxia to the testicular parenchyma. Depending on the mechanism and degree of torsion, there is a variable period in which the testis is salvageable. Torsion can occur as a result of two mechanisms: extravaginal torsion and intravaginal torsion, terms referring to the tunica vaginalis, a structure that surrounds the testicle. In some regard, this distinction is clinically irrelevant because it cannot be determined clinically, nor does it alter treatment.
Although testicular torsion can occur at any age, it has a predominantly bimodal occurrence, namely, the neonatal and pubertal periods. The precise risk for the development of testicular torsion is not clearly established, but the approximate overall risk of testicular torsion developing by 25 years of age is 1 in 160. Testicular salvage rates have increased over the last 40 years, mainly as a result of early recognition and intervention. The undescended testis is also at risk for testicular torsion, presumably because of abnormal mesorchial attachments. Any child with a nonpapable testis and abdominal pain should be evaluated for intra-abdominal testicular torsion.
Neonatal torsion is usually the result of extravaginal torsion in which the testicle twists on the spermatic cord or outside the tunica vaginalis; it accounts for 12% of all cases. Neonatal torsion occurs in the prenatal and postnatal periods. Such occurrence does not appear to be correlated with prematurity, birth weight, method of delivery, or perinatal trauma. The condition is almost always asymptomatic and discovered on routine examination. The examination generally shows an edematous, erythematous hemiscrotum with a firm testis. The hemiscrotum does not usually transilluminate. Current ultrasound technology is very accurate in determining the presence or absence of testicular blood flow in neonatal torsion.1 However, ultrasound results and interpretation can vary due to operator experience and other technical factors and therefore clinical judgment remains relevant. Because of the imprecision of older ultrasound technology, nuclear scans to assess testicular blood flow were common but are now rarely performed. Neonatal torsion is thought to be secondary to the hypermobility of neonatal tissue, which does not firmly fix the testis to the scrotum. Controversy remains over the management of contralateral testis in neonates with torsion. Some believe that contralateral fixation is necessary and cite the occurrence of both synchronous and asynchronous torsion.2 Others believe that contralateral fixation is not necessary and note that the hypermobility of neonatal tissue quickly resolves and that most cases of neonatal torsion occur within the first 10 days of life. Nevertheless, bilateral testicular torsion does in fact occur, and the surgeon and family must weigh the options of observation versus intervention with regard to the contralateral testis. I prefer and continue to recommend contralateral scrotal fixation.
In contrast to neonatal torsion, pubertal torsion is symptomatic. Patients experience a sudden onset of hemiscrotal pain, abdominal pain, or both. Nausea and vomiting may also occur. Physical examination usually demonstrates an elevated testicle within the scrotal sac. If palpable, the spermatic cord is thickened or twisted. The cremasteric reflex is generally absent on the affected side. The cremasteric reflex is elicited by stroking the inner aspect of the thigh, which causes the cremasteric muscle within the scrotum to contract and thereby elevate the testis and scrotum. It is important to perform this test bilaterally because asymmetry is the key point. Some individuals do not demonstrate this reflex and it is therefore not useful in establishing the diagnosis of testicular torsion in these individuals. In general, manual detorsion should be attempted by a specialist (urologist) and does not preclude surgical intervention. If imaging is deemed necessary to help establish the diagnosis, scrotal ultrasound is the test of choice. Current ultrasound technology is highly sensitive in detecting testicular blood flow (Figure 164-1).3 In cases in which the diagnosis is not in question, proceeding directly to surgery is appropriate. The viability of the testis will be determined intraoperatively, and orchiectomy or orchiopexy will be performed. Viability is assessed after intraoperative manual detorsion and observation for a period. Contralateral scrotal fixation is performed to prevent a similar occurrence on the unaffected side. Some series have reported contralateral torsion in 40% of cases in which contralateral detorsion was not performed.
The prognosis refers to testicular salvage and fertility. The duration and degree of ischemia determine testicular salvage. Most of the precise experimental work regarding salvage rates relative to the duration of ischemia has been performed in dogs. Four hours of ischemia kills the germinal epithelium, whereas 8 to 10 hours kills the Sertoli cells (support cells for the germinal epithelium) and Leydig cells (testosterone production). The degree of torsion is also relevant. Intraoperatively, it is seen that some testicles contain one full twist whereas others have three or more twists. Obviously, the extent of torsion (i.e. hypoxia) will have an impact on the degree of ischemia and the duration of time after which salvage is not possible. Clinically, we use 4 to 6 hours as the time at which testicular salvage becomes questionable.
The small embryologic appendages that occur on the testis and epididymis are subject to torsion. These small appendages serve no function and are vestigial remnants. Torsion of these appendages may cause scrotal pain and swelling. However, there are several characteristics that can help distinguish this diagnosis from testicular torsion. The pain and swelling are usually gradual in onset and are rarely associated with nausea or vomiting. Most boys are able to continue with most of their activities and note discomfort only when the area is touched. It most commonly occurs after the neonatal period but before puberty. Physical examination reveals tenderness of the upper pole of the epididymis or the superior aspect of the testis. The cremasteric reflex is generally intact. Sometimes the necrotic appendage is visible through the scrotum, a finding called the “blue dot” sign. Scrotal ultrasonography rarely identifies the necrotic appendages, but it does demonstrate normal blood flow to the testis and increased blood flow to the epididymis.4 This condition is treated conservatively with rest and analgesics. The prognosis is excellent with no known long-term sequelae.
Testicular torsion requires surgical consultation and treatment.
Transfer to a tertiary center is advisable only if anesthetic or surgical services are inadequate for treating the neonate.
KEY POINTS
Testicular torsion is a surgical emergency.
Scrotal ultrasonography is highly reliable in determining testicular blood flow.
Torsion of the appendages warrants conservative management.
Early detection of fetal hydronephrosis is commonplace with the widespread use of maternal ultrasonography. Fetal hydronephrosis is detectable at 15 weeks, shortly after the onset of fetal urine production. The internal renal architecture (differentiation between the renal cortex and the medullary pyramids) is best seen at 20 weeks gestation. Normal findings include sonolucent renal pyramids relative to the renal cortex and a renal cortex that is slightly less echogenic than the liver. It is also important to determine the status of amniotic fluid because polyhydramnios and oligohydramnios have renal origins and implications. Hydronephrosis is the most common finding during prenatal ultrasonography. The differential diagnosis, in order of frequency, includes transient hydronephrosis, VUR, obstruction of the ureteropelvic junction (UPJ), congenital megaureter or obstruction of the ureterovesical junction (UVJ), posterior urethral valves (PUV), ectopic ureter, and ureterocele.5 The obstructive processes (UPJ obstruction, megaureter, PUV, ectopic ureter, and ureterocele) are discussed in this chapter. The majority of antenatally detected cases are transient or physiologic and resolve spontaneously, particularly mild and moderate degrees of hydronephrosis. Severe prenatal hydronephrosis is more likely to represent as a true pathologic entity such as UPJ obstruction or high grade VUR. Controversy exists over the best method to classify prenatal hydronephrosis. The most common measurement is the anteroposterior (AP) diameter of the renal pelvis in the axial plane. No consensus has been reached on the AP diameter that will identify fetuses in which significant postnatal pathology and need for surgical intervention will ultimately develop. For this reason, others have proposed a qualitative assessment of mild, moderate, and severe hydronephrosis based on the appearance of the renal pelvis, calyces, and renal parenchyma. Hydronephrosis that is most likely associated with significant postnatal pathology is characterized by increasing hydronephrosis through pregnancy, oligohydramnios, increased renal cortical echogenicity, AP diameter greater than 10 mm, and calyceal dilation.
The vast majority of patients with hydronephrosis are asymptomatic. Infants and children rarely present with an abdominal mass. As noted earlier, most children with hydronephrosis are detected antenatally and monitored postnatally. In children not identified in this manner, some will remain undetected, whereas others will present with a febrile UTI or with complaints of episodic abdominal pain. Isolated hematuria is an unusual presentation.
In nearly all cases, prenatal hydronephrosis is monitored by serial ultrasonography until delivery. Postnatal management includes prophylactic antibiotics (amoxicillin, 25 mg/kg/day once daily) and a repeat renal/bladder ultrasound (Figure 164-2). Renal/bladder ultrasonography is performed after 48 hours because of the relative oliguria that occurs during this period. Voiding cystourethrography (VCUG) is indicated for moderate to severe hydronephrosis and any evidence of bladder wall thickening. In children with mild hydronephrosis, there is debate regarding the necessity for VCUG in the evaluation. Renal scans with mercaptoacetyltriglycine (MAG3) and dimercaptosuccinic acid (DMSA) are used to determine the degree of obstruction and renal scarring, respectively. Consultation with a pediatric urologist is advisable in children with postnatal hydronephrosis.
Pediatric urologic consultation is advisable in patients with moderate or greater hydronephrosis, VUR, bladder wall thickening or known PUV, and evidence of renal asymmetry or renal scarring.
KEY POINTS
Hydronephrosis is common and generally asymptomatic
As opposed to mild hydronephrosis, moderate to severe hydronephrosis requires a full evaluation and is more likely to represent a surgical etiology (reflux, UPJ, or UVJ obstruction).
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