Dysuria is defined as painful urination and can be related to uncomfortable contraction of the muscles of the bladder or when urine comes into contact with the inflamed genitourinary mucosa. The differential diagnoses for a patient presenting with dysuria are extensive ( Table 18.1 ) and can be due to infectious or noninfectious causes. The cause of dysuria varies based on age of the child or adolescent; therefore, specific elements of the patient history, potential causes, and diagnostic evaluation will vary with age. With every patient, the provider must elicit a history of signs and symptoms outside the genitourinary tract, including fever, weight loss, generalized rash, involvement of other mucosa, and joint pain or swelling. Physical examination for every patient should include temperature, blood pressure, inspection of the genitalia for skin lesions or discharge, abdominal palpation, pelvic examination when indicated, and neurologic examination in children with voiding dysfunction to exclude spinal cord pathology.
| Infectious causes |
|
| Urinary tract abnormalities (congenital and acquired) |
|
| Genital tract abnormalities |
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| Medications and irritants |
|
| Other |
|
* Vaginitis; chemical, nonspecific bacterial, Candida albicans , Trichomonas vaginalis , herpes simplex, gonorrhea, group A streptococcus, gram-negative organisms.
Neonates
Neonates and infants cannot complain of dysuria; however urinary tract infections (UTIs) are prevalent in this age group and a major source of morbidity. In this age group, it is difficult to distinguish between upper UTI (pyelonephritis) and lower UTI (cystitis) based on signs and symptoms alone. Unlike UTIs in older children, neonatal UTIs are more common in male neonates compared to females. In neonates, UTIs are associated with bacteremia and/or congenital abnormalities of the kidney and urinary tract. In term infants, infections tend to be community acquired and present in the 2nd to 3rd week after birth. UTIs can be caused by either hematogenous spread or an ascending infection. In preterm infants, infections are more likely to be hospital acquired.
The symptoms suggestive of a UTI in the neonate are the same as those for suspected sepsis ; therefore, major presenting symptoms include fever, poor feeding, weight loss, lethargy, and vomiting (see Chapter 39 ). Neonates may also present with jaundice or abdominal distention. A maternal urinary infection at or near term may increase the risk for neonatal pyelonephritis. A mother whose vaginal culture is positive for group B streptococci or who presents with fever, prolonged rupture of the amniotic membranes (>18 hours), uterine tenderness, or preterm labor is at an increased risk for delivering a premature baby with pyelonephritis as part of the neonatal sepsis syndrome. Family history is also important. There is a high genetic component to the presence of vesicoureteral reflux (VUR) ; the siblings of children with known VUR also have a significant risk of reflux, with or without infection. Children with a UTI and VUR are at increased risk of pyelonephritis and renal scarring. However, the screening for VUR in an asymptomatic sibling of an index case of VUR is controversial; a voiding cystourethrogram (VCUG) is recommended if there is evidence of renal scarring on ultrasound or if there is a history of UTI in the sibling who has not been tested. Given that the value of identifying and treating VUR is unproven in the absence of a UTI, an observational approach without screening for VUR may be taken for siblings of children with VUR, with the prompt treatment of any acute UTI and subsequent evaluation for VUR.
Physical examination of a neonate suspected of having a UTI should include the palpation of the abdomen to identify obstructive lesions or cystic kidneys. Urine culture should be obtained by suprapubic or bladder catheterization, as sterile bag collection has a high rate of contamination with perineal flora. Because of the associated risk of bacteremia, blood cultures and cerebrospinal fluid (CSF) cultures should be obtained in all neonates in whom UTI is suspected. Initial empirical therapy should be initiated after collection of urine, blood, and CSF cultures. The empirical therapy should provide broad coverage against probable uropathogens, and is initially administered parenterally, as the risk of urosepsis is higher in neonates than in other age groups. Common empirical therapy includes ampicillin in addition to either gentamicin or a 3rd-generation cephalosporin. Therapy is then tailored according to the specific uropathogen identified on culture and the antimicrobial sensitivity.
Ultrasound is the first-line imaging method in neonates after the first UTI. The main purpose of diagnostic imaging is the detection of risk factors, such as anomalies of the kidney and urinary tract or vesicoureteral reflux, as well as any renal damage acquired from the infection. Clinical practice guidelines from the American Academy of Pediatrics do not recommend DMSA (dimercaptosuccinic acid) scans as part of routine evaluation of infants with their first febrile UTI because the findings rarely affect acute clinical management.
Children 2-24 Months of Age
Like neonates, children 2-24 months of age cannot report dysuria. Nonetheless, urinary tract infections (UTIs) are common (see Chapter 39 ). The main risk factor for febrile infant males is whether or not they are circumcised; other individual risk factors for UTI in males include nonblack race, temperature >39°C, fever for at least 24 hours, and absence of another source of infection. Individual risk factors for UTI in infant females include white race, age less than 12 months, temperature of at least 39°C, fever for at least 2 days, and absence of another source of infection.
The method of collecting urine for testing is dependent on the risk factors of the child. Culture of a urine specimen from a sterile bag attached to the perineal area has a high false-positive rate; this method of urine collection is not suitable for diagnosing UTI. However, a culture of a urine specimen from a sterile bag that shows no growth is strong evidence that UTI is absent; if growth of a single uropathogen is present, it may represent a UTI. Nonetheless, a clinical practice guideline from the American Academy of Pediatrics outlines several recommendations in testing and treatment of UTIs in febrile infants:
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If a febrile infant with no apparent source for fever requires antibacterial therapy, a urine specimen should be obtained via suprapubic aspiration or catheterization for both culture and urinalysis (UA) prior to the initiation of antibacterials.
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If the clinician determines that the patient is at low risk for having a UTI, clinical monitoring without urine testing is acceptable.
- •
If the febrile infant is not in the low-risk category:
- •
Clinician should obtain urine sample for UA and culture through catheterization or suprapubic aspiration.
- •
Or clinician can obtain clean-void bagged urine sample. If UA results suggest UTI ( Table 18.2 ), then an additional urine specimen for culture should be obtained via catheterization or suprapubic aspiration.
TABLE 18.2
Sensitivity and Specificity of Components of Urinalysis, Alone and in Combination
Test
Sensitivity (Range) (%)
Specificity (Range) (%)
LE test
83 (67-94)
78 (64-92)
Nitrite test
53 (15-82)
98 (90-100)
LE or nitrite positive
93 (90-100)
72 (58-91)
Microscopy (WBCs)
73 (32-100)
81 (45-98)
Microscopy (bacteria)
81 (16-99)
83 (11-100)
LE, nitrite, or microscopy positive
99.8 (99-100)
70 (60-92)
LE, leukocyte esterase; WBC, white blood cell.
Modified from Subcommittee on Urinary Tract Infection, Steering Committee on Quality Improvement and Management: Clinical practice guideline. Urinary tract infection: clinical practice guideline for the diagnosis and management of the initial UTI in febrile infants and children 2 to 24 months. Pediatrics. 2011;128:595-610.
- •
Diagnosing a UTI in young children requires both a positive UA (for white cells and/or bacteria) and >50,000 CFU/mL of a single urinary pathogen on urine culture from a suprapubic or catheterized urine specimen. The usual choices for empirical antibacterial therapy include a 3rd-generation cephalosporin, amoxicillin plus clavulanic acid, or trimethoprim-sulfamethoxazole. The clinician should base choice of antibacterial on local antimicrobial sensitivity patterns if available and should adjust according to sensitivity results of the isolated uropathogen. Most infants can be treated orally.
The rationale for imaging infants with UTI is to identify abnormalities of the genitourinary tract. Renal ultrasound is the first-line imaging modality to identify anatomic abnormalities. Voiding cystourethrogram (VCUG) to detect vesicoureteral reflux (VUR) should not be performed after the first febrile UTI. It is indicated if the ultrasound reveals hydronephrosis, renal scarring, or other findings that suggest high-grade VUR or obstructive uropathy.
Preschool Children
A young child may or may not be able to verbalize dysuria; however, they may show signs of urethral irritation including delayed toilet training (especially during the day), secondary enuresis, dribbling, and frequent squatting. Due to the large variability in the time of achievement of daytime dryness (15 months-4 years), delayed toilet training may be an unreliable sign of dysuria; however, primary diurnal enuresis should be evaluated if the child is older than 48 months of age. Nocturnal enuresis is rarely a sign of UTI, but urine cultures should probably be obtained in children who do not stay dry at night by 5 years of age. A more significant symptom in young children is the acute onset of daytime enuresis after a period of continence.
UTIs are the most common cause of dysuria in preschool children. It may be difficult to distinguish between pyelonephritis and cystitis in these young children. Both urine and stool withholding have a role in causing UTIs in young children. Constipation is associated with large residual urine volumes after voiding, thus the treatment of constipation leads to a reduction in UTIs. Females are at increased risk of UTI due to the ease at which pathogens can migrate from the gastrointestinal tract to the periurethral area and urethra, and ultimately ascend to the bladder. Improper toileting habits can further increase the risk of UTI. Uncircumcised males, patients with neurogenic bladders (spina bifida), patients with indwelling catheters, and patients with renal or bladder anomalies (e.g., cysts, obstructed hydronephrosis, double collecting systems, ectopic ureter, horseshoe kidney, posterior urethral valves, VUR) are at increased risk for UTI.
Children who are toilet-trained can give a clean-void urine sample. Those that are not toilet-trained can give a urine specimen from a sterile bag attached to the perineal area, although this has a high false-positive rate.
Preschool children may also have irritant urethritis.
School-Aged/Prepubertal Children
Dysuria in school-aged children can be due to infectious and noninfectious causes ( Table 18.1 ). Most children with a UTI present with dysuria, frequency, or fever. It is worthwhile to ask about any urine color change, which suggests the presence of hematuria. The child should be questioned about the frequency, character, and size of his or her bowel movements. Constipation may predispose the school-aged child to a UTI; stool softeners, such as mineral oil or fiber, may be indicated. Pyelonephritis can be clinically distinguished from cystitis by presence of systemic features (fever, vomiting) and signs (flank pain, costovertebral angle tenderness).
A careful inspection of the genitalia is important in the diagnosis of the cause of dysuria. Boys may have nonspecific bacterial infection of the glans penis ( balanitis ); uncircumcised boys can have infection of both the glans and the prepuce ( balanoposthitis ). Both of these are usually accompanied by painful swelling and inflammation. Irritants can cause a nonspecific urethritis in males, with dysuria being the main symptom.
Prepubertal females can have dysuria as the presenting symptom of vaginitis , along with other symptoms including vaginal discharge. In prepubertal females, the vulvar mucosa is thin and susceptible to inflammation from chemicals and mechanical irritation. Because the labia are not well developed, the vulvar mucosa is not anatomically shielded and is thus vulnerable to irritation. Vaginitis in prepubertal females can be nonspecific, due to irritants (soaps, detergents) or may be due to the presence of a foreign body ( Table 18.3 ). Whereas vulvovaginal candidiasis is common in postpubertal females, the vaginal environment in prepubertal females is not typically conducive to Candida species growth, unless she has an immunodeficiency or recent antibacterial use. In the majority of cases, vulvovaginitis in prepubertal females is a mixed, nonspecific bacterial infection secondary to contamination by urine and feces. The responsible bacteria are usually normal flora ( Table 18.4 ). Bloody vaginal discharge in young females may be caused by Shigella species or group A streptococcal infections, a foreign body (e.g., toilet paper), neoplasm (such as rhabdomyosarcoma), or trauma. Most cases of prepubertal nonspecific vaginitis can be managed with hygiene; some vulvovaginitis may require a course of antibacterial agents or topical estrogen vaginal cream ( Table 18.5 ).
| Condition | Historical Cues |
|---|---|
| Poor hygiene | Infrequent bathing, hand washing, and clothing changes, soiled underwear, toilet independence |
| Poor perineal aeration | Tight clothing, nylon underwear, tights, leotards; wet bathing suits, hot tubs, obesity |
| Frictional trauma | Tight clothing, sports, sand from sandbox or beach, obesity, excessive masturbation or sexual abuse |
| Chemical irritants | Bubble baths, harsh or perfumed soaps or detergents, powders, perfumed and/or dyed toilet paper, ammonia, perfumed and/or dyed sanitary products; douches and feminine hygiene products |
| Contact dermatitis | Topical creams or ointments |
| Vaginal foreign bodies | Wiping habits, excessive masturbation or self-exploration, sexual abuse |
| Parasites, insect bites, infestations | Home environment, pets, sandboxes, travel, camping, exposure to woods or beach |
| Medications | Topical steroid or hormone creams, antibiotics, chemotherapy |
| Generalized skin disorders | History of pruritus, chronic skin lesions, prior diagnosis |
| Anatomic anomalies | Vesicovaginal or rectovaginal fistula, ectopic ureter, spina bifida, cloacal anomalies, urogenital anomalies |
| Neoplasms | Discharge, bleeding, bulging abdomen, change in bowel or bladder function, premature puberty |
| Systemic illness (Stevens-Johnson syndrome, Crohn disease, toxic shock syndrome) | Tampon use, systemic evidence of inflammatory bowel disease including rash, oral ulcers, failure to gain weight or height, abdominal pain |
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