Children’s Hospital of Eastern Ontario

Children’s Hospital of Eastern Ontario
Pediatric Urology Luis Guerra, MD University of Ottawa Children’s Hospital of Eastern Ontario

Evaluation Historically Recently
Urinalysis, IVP and cystoscopy Recently US, CT, MRI, and endourology Basic and most important approach starts with Complete history Thorough physical examination Attention to genitourinary system

History Extremely important Always address the child
Main complaint, past medical and family history Antenatal history Prenatal US (hydro, bladder distention, oligohydramnios) Delivery Uncomplicated, voided in the first 24 hrs, any metabolic unbalance Urologic Age toilet trained Enuresis or daytime incontinence UTI Intestinal constipation Dysfunctional voiding pattern Previous surgery Traumas

Physical Syndromes, social and psycho-emotional behavior
General aspect Syndromes, social and psycho-emotional behavior Abdomen Palpation (bladder, kidneys, masses) Lower back Skin dimples, hairy tufts, discolorations spots, gluteal cleft External genitals Girls Vulva- Inflammations, labial adhesions, wetness Boys Penis- Physiologic phimosis, hypospadias, chordee Testicles- Descended, size, texture, scrotal mass

Urinary infection in children

Urinary infection in children
What is UTI Bacterial infection in the urine May involve bladder and/or kidneys Incidence: UTIs more common First year of life Boys (peak at 6 months) >1 yr of life Girls (peak at 2-3 years) During school age 1.2% of boys and 5% of girls develop UTI

Most common etiology Organisms from bowel flora
E. Coli (most common) Less often Klebsiella, Proteus, Enterococcus, Staphylo saprophyticus Ascending route is the MC

Pathogenesis 3% of girls and 1% of boys will get a prepubertal UTI
(Winberg et al, 1974) Of these, 17% will get infection-related renal scarring Of those with scarring, 10% to 20% will become hypertensive, and a rare child will progress to renal failure

UTI – Clinical presentation
Kidney (pyelonephritis) Fever, abdominal or flank pain, vomit, diarrhea, child is ill Bladder (cystitis) Dysuria, sp pain, frequency, urgency, incontinence and foul urine Infants May be vague and without localization Fever 66%, irritability 55%, poor feeding 40%, vomiting 35%, diarrhea 31%, abdominal distension 10%

UTI - Diagnosis History – Symptoms Physical
There are no signs specific for UTI in the infant An abdominal mass may be palpated (hydro, bladder,etc) Abdominal, flank, sp, CVA tenderness in older child Active, febrile, dehydrated, septic shock

Methods of urine collection
Bag specimen Even after skin cleaning usually reflects perineal and rectal flora It is reliable if: Significant pyuria, grow only 1 bacteria and child is symptomatic May be useful to “rule out bacteriuria” Suprapubic aspiration (most reliable but less used) Catheterization (if bag urine is not definitive) Toilet trained children: Midstream void Diagnosis of UTI At least and preferably > colony-forming units/ml

Reliability of urinalysis
In a properly collected and processed urinary specimen, the combination of: Positive leukocyte esterase, Positive nitrite testing, and Microscopic confirmation of bacteria Has almost 100% sensitivity for detection of UTI When all (or the leukocyte esterase and nitrite tests) are negative: The negative predictive value approaches 100% ( Wiggelinkhuizen et al, 1988; Lohr et al, 1993) Combination of these 3 tests helps, however the urinalysis cannot replace urinary culture

UTI - Radiological evaluation
Recommended in all children < 5 yrs of age All boys, irrespective of age All girls with pyelonephritis (fever) After a 2nd UTI in a girls older than 5 yrs of age (Palmer, JS and Elder, JS 2003)

UTI - What kind of test? Ultrasound VCUG (voiding cystourethrogram)
Upper tract abnormalities (hydro, atrophic kidneys, cysts, renal scarring, etc) VCUG (voiding cystourethrogram) VUR and posterior urethral valve, assess bladder configuration If both test are normal, no other evaluation is necessary Renal scans For assess obstruction and renal function (DMSA, DTPA)

Vesicoureteric reflux

Vesicoureteric reflux
Wash back of urine to the kidneys (passive, active) Prevalence as high as 1 in 100 births 1:6 Male to female; present in 35-50% of children with UTI Boys are more likely to have high grades (IV and V) Causes Primary (congenital short intramural tunnel) Normal tunnel length and ureteral orifice is 2.5:1 Secondary (high pressure – PUV, neurogenic bladder,etc) Importance of diagnosis of VUR VUR + UTI can cause renal damage (scarring)

International classification VUR
International classification of vesicoureteral reflux. Copyright © 2003, Elsevier Science (USA)

VUR - Treatment Antibiotic prophylaxis and follow up Follow up
Annual US and cystogram Spontaneous cure rate 20% per year Depends on the grade of VUR, unilateral vs bilateral Surgery (open or endoscopic) in selected cases Breakthrough UTI (first year of life most likely to get scar) New onset or progressing of renal scarring Decreasing renal function Long follow up, parental preference

Treatment of an UTI: 10-14 days
Depends on age and severity of UTI Septic (pyelonephritis) Neonates or young infants Admission IV antibiotic (ampi or cephalosporin + genta) and then according to bacteria sensitivity (change to oral when discharged) Older children oral therapy may suffice (same as for cystitis) Clinically well (cystitis) Oral antibiotics (sulfa-trimethoprim, nitrofurantoin, amoxicillin, ampicillin, cephalosporin) Adequate oral intake for hydration

Should not be used < 2 mo of age
Sulfa derivatives (Sulfamethoxasole) Displaces protein-bound bilirubin and may interfere with bilirubin excretion, exacerbating neonatal physiologic jaundice Nitrofurantoin May cause hemolytic anemia because of glutathione instability in the erythorocyte

Management following a UTI
Adequate fluid intake Avoid intestinal constipation (fiber in the diet) Girls Proper hygiene (swipe front to back) Void spreading the legs (avoid vaginal voiding and incomplete voiding) Timed voiding (every 2 to 3 hours)

Who should have antibiotic prophylaxis?
Patients with abnormalities of the GU tract All VUR < 5 years of age Some risk factor for UTI (GU obstruction or urinary stasis) Select cases of PUV, megaureters, hydronephrosis, etc Patients with normal work-up More than 2 or 3 UTIs in 1 year Usually sulfamethoxasole-trimethoprim, nitrofurantoin or trimethoprim alone Little effect on stool’s bacterial flora Dose is 1/3 or 1/2 of the treatment dose Routine C+S should not be done Amoxicillin or cephalosporine can affect the intestinal flora

UTI.., Who I should refer? VUR, hydronephrosis, megaureters, etc
All daytime incontinence Diagnosed or suspected of GU abnormalities VUR, hydronephrosis, megaureters, etc Neurogenic features Abnormal lower back exam Established neurogenic entities Sacral agenesis, imperforate anus, tethered cord, etc Known syndromes (VACTERL, 21 trisomy) Child with recurrent UTIs after proper management of Intestinal constipation Adequate fluid ingestion Regular voiding (every 2-3 hours)

Scrotal mass in children

Causal conditions Inguino-scrotal hernia True scrotal swelling Cystic/Soft Epididymal cyst (spermatocele) Hydrocele Varicocele (MC on left side) Solid Benign or malignant tumors (testis, spermatic cord and adnexas ) Testicular torsion / appendix torsion Incarcerated/ strangulated hernias Trauma (hematocele, hematoma) Infectious (epididymitis)

Acute Testicular torsion Testicular/epidydimis appendix torsion Orchitis-epidydimitis Incarcerated / strangulated hernias Trauma Insect bits Non-acute Hydrocele Hernia Testicular tumor Varicocele Cysts (epididymis, testis, spermatic cord)

Inguinal hernias in children
Persistence of the peritoneal vaginalis conduct and insertion of abdominal contents into the inguinal canal Presentation may be Non-acute (inguinal lump, bulging) Incarcerated or strangulated (pain, vomiting, tenderness)

Inguinal hernias in children
Treatment Elective surgery to prevent strangulation Urgent exploration if strangulated Dissection of the hernia sac up to internal ring and closure Repair of the posterior wall is generally not necessary in children but adolescents may need it (or mesh)

Hydrocele - characteristics
Is an accumulation of fluid within the tunica vaginalis Usually communicating in children All hydroceles in infants and children result from persistence of or delayed closure of the processus vaginalis Present in 1-3% of all children Greater in premature children Males (85%)

Hydrocele - Anatomy

US - Hydrocele

Hydrocele - diagnosis Adequate history and physical examination are the hallmarks of diagnosis Assess the presence of Characteristic of scrotal swelling (soft or tense) Positive transillumination Inguinal bulge or incarceration (hernia) Important to feel a normal testis (US if necessary) More frequent on the right and 10% is bilateral Ultrasound is not usually necessary

Hydrocele - Management
Scrotal hydroceles common in newborn Usually resolve first year of life No evidence of testicular injury (even if tense) Older child Secondary to minor trauma or inflammation Observation is reasonable

Surgical management Hernias Hydroceles Repaired when recognized
Emergently if it is strangulated Hydroceles Usually repaired after 18 months of age, electively

Acute scrotum

Testicular torsion

Testicular torsion (TT)
Most common in Neonates (extravaginal) Peripubertal (intravaginal) 16-42% of boys with acute scrotum have TT Extremely challenging condition One of the true Urologic Emergencies Diagnostic tests are not entirely reliable Must rule out in patient with acute scrotal pain/swelling Diagnosis usually determined from history and physical

Testicular torsion - History
Can begins abruptly in early morning/during resting Severe pain from onset History of scrotal trauma is common Pain that persists >1 hr after minor trauma is not normal Often previous episode/s of similar pain

TT – Physical exam Scrotum/ position of testes
Cremasteric reflex - rarely intact in patients with TT “Hard mass” or “swelling” Depending on how long the onset Check for flank tenderness and bladder distension Inguinal region for hernia/spermatic cord Prehn’s sign Lack of pain relief with elevation suggests TT Manual detorsion (controversy)

Bell clapper

Testicular torsion Don’t delay proper treatment
Most of the TT can be saved before 6 hrs of onset Urinalysis – Not reliable to rule out Color Doppler U/S: Operator dependant May not demonstrate flow in very young boys Reduced flow may indicate torsion Gold standard diagnosis of TT – Surgical exploration

Doppler US - Arterial flow

True testicular torsion

Testicular/epididymal appendix
Wolfian duct remnant Mullerian duct remnant

Testicular appendix torsion

Testicular appendix torsion
Clinical presentation Usually less severe pain and swelling Upper pole “blue dot” However, it may be mimic TT Management Reassurance Relative rest Analgesic (acetaminophen, codeine) It takes 1-2 weeks to improve Return to ER if any change in symptoms/findings

Testicular tumors

(paratesticular rhabdomyosarcoma)

Testicular tumors Uncommon disease 0.5-2 / 100.000 children
1% to 2% of all pediatric solid tumors Incidence of childhood testicular tumors Peaks at age 2 years Tapers after age 4 years Rises again at puberty Germ cell tumors account for 65% of prepubertal tus Rare among black and Asian children

Diagnosis Painless firm testicular mass is the MC presentation of a child with a testicular tumor Negative transillumination Disorders that must be excluded: Epididymitis Hydrocele Hernia Spermatic cord torsion

Investigation High in 90% of Yolk sac tumor
US testis Alpha-fetoprotein High in 90% of Yolk sac tumor Single polypeptide chain amino acid produced by the fetal yolk sac, liver, and gastrointestinal tract Half-life: 5 days (25-30 days) β-hCG Made by syncytiotrophoblast Is rarely increased in preadolescent tumors Half-life: 24 hrs (5-7 days) Serum LDH (lactate dehydrogenase) Chest x-ray and abdominal CT Retroperitoneal lymph nodes are the 1st site of meta Lung (MC distant site of meta)

MC types in children Yolk sac tumor Teratoma
Most common type in childhood - 60% Mostly in < 2 years of age Persistent AFP elevation post orchiectomy suggests mets Teratoma Usually benign in children Second most common in childhood (21%) Mean age: 18 months US usually contain complex cysts Germ cell tumor with more than one germ cell layer Endoderm, ectoderm, and mesoderm Cartilage, bone, mucous glands or muscle

Testicular tumor - Treatment
Initial treatment is radical inguinal orchiectomy Stage I disease do not receive additional adjuvant Routine RPLND and/or adjuvant chemotherapy is not indicated (only if metastasis) Partial orchiectomy in selected cases Teratoma: No report of metastases in prepubertal males

Timely surgery

Testicular mass… Who and when I should refer?
All cases of testicular mass should be referred as soon as diagnosed Even before US is obtained In testicular cancer, time matters

Abdominal mass in children

Abdominal mass in neonates
Abdominal mass (75% arise in the GU tract) 1-Hydronephrosis is the MC (UPJO, VUR, UVJO, PUV) 2-Multicystic dysplastic kidney (MCDK) 3-Tumors account for 12 % MC abdominal tumors: Neuroblasoma, congenital mesoblastic nephroma and teratoma (sacrococcygeal) Hydronephrosis MCDK

Abdominal mass in neonates
Neuroblastoma is the MC malignance in neonate Wilms tumor is extremely rare Abdominal mass + hematuria: renal vein thrombosis Girl with abd mass + interlabial bulging: hydrocolpos CMN is the MC renal tumor

Abdominal mass after neonatal period
From 1 month to 1 year of age Hydronephrosis – 40% Solid masses and tumor – 40% Older than 1 year Tumor is the MC cause of abdominal mass

Neuroblastoma Wilms Tumor (Nephroblastoma)

Neuroblastoma (NB) MC malignant tumor of infancy
8% to 10% of all childhood cancers Annual incidence 10 cases per 1 million Median age at diagnosis: 22 mo 50% of cases < 2 years of age (75% <4yrs) (Fortner et al, 1968)

NB- What and Where? Tumor of the neural crest cell origin
Cells that form the adrenal medulla and sympathetic ganglia 75% are retroperitoneal 50% adrenal 25% sympathetic chain (from neck to pelvis)

NB - Presentation Often has systemic symptoms (different from WT)
Fever, abdominal pain or distension, abd mass, weight loss, anemia, bone pain, proptosis and periorbital ecchymoses (retro-orbital metastasis) Metastases are present in 70% at diagnosis VMA (vanilmandelic acid), HMA (homovanillic acid) Are elevated in > 90% of the neuroblastomas 24 hs urine collection (catecholamine metabolites)

NB - Imaging US is usually the first exam in child with abdominal mass CT or MRI Both detect extension beyond midline and hepatic involvement MRI: better displays the relationship with great vessels and detects intraspinal extension (tumor of sympathetic chain) CT may show calcifications (rare in Wilms tumor)

NB - Treatment Generally based on risk assessment
Tumor stage Grade Biochemical risk factors Genetic risk factors Low-stage favorable Sx alone Higher risk tumor Adj chemo +/- Rt Very aggressive tumor Autologous bone marrow transplantation

Wilms’ tumor (Nephroblastoma)

Wilms' Tumor MC primary malignant renal tumor of childhood
Embryonal tu develops from remnants of immature kidney Annual incidence 7 to 10 cases per million Median age 3.5 yrs 80% diagnosed < 5 yrs of age Worldwide sex ratio is close to 1 (North America girls slightly > boys)

Congenital anomalies and WT
Genitourinary anomalies in 4.5% of WT Renal fusion anomalies Cryptorchidism Hypospadias (Breslow et al, 1993) These are common disorders and screening for WT is not necessary in most children with genital anomalies

Syndromes associated with WT
Without overgrowth Denys-Drash syndrome (DDS) Male pseudohermaphroditism, renal mesangial sclerosis and WT ( Drash et al, 1970) Aniridia (Found in 1.1% of patients with WT) WAGR syndrome (W ilms' tumor, a niridia, g enital anomalies, mental r etardation (Clericuzio , 1993) Horseshoe kidney (NWTSG found 7 times incidence of WT) With overgrowth Hemihypertrophy, which may occur alone or with syndromes Beckwith-Wiedemann (BWS), Perlman, Soto, Simpson-Golabi-Behmel ( Perlman et al, 1975; Neri et al, 1998)

Imaging in WT Ultrasound is the first study performed in most children with an abdominal mass. (solid nature of the lesion) CT shows the relationship with other organs MRI is the study of choice if extension of tumor into the inferior vena cava cannot be excluded by ultrasound (Weese et al, 1991)

Treatment of WT Surgical Radical nephrectomy
Accurate staging for determination need Rt +/- chemo Exploration of the abdominal cavity Liver and nodal metastases and peritoneal seeding Formal exploration of the contralateral kidney Should be performed before nephrectomy Formal retroperitoneal lymph node dissection Is not recommended Surgery The renal vein and inferior vena cava are palpated to exclude intravascular tumor extension before vessel ligation Wilms' tumor extends into the inferior vena cava in approximately 6% of cases and may be clinically asymptomatic in more than 50% (Ritchey et al, 1988) Selective sampling of suspicious nodes is an essential component of local tumor staging. Formal retroperitoneal lymph node dissection is not recommended (Othersen et al, 1990; Shamberger et al, 1999) Complete removal of the tumor without contamination of the operative field Gentle handling of the tumor throughout the procedure is mandatory to avoid tumor spillage, which leads to a sixfold increase in local abdominal relapse Risk factors for local tumor recurrence Tumor spillage Unfavorable histology Incomplete tumor removal Absence of any lymph node sampling The 2-year survival after abdominal recurrence was 43%, emphasizing the importance of a careful and complete tumor resection. Complications NWTS-4 patients undergoing primary nephrectomy had an 11% incidence of surgical complications ( Ritchey et al, 1999) The most common complications encountered are hemorrhage and small bowel obstruction SIOP investigators reported a lower rate of complications when nephrectomy was performed after preoperative chemotherapy ( Godzinski et al, 1998)

Urinary incontinence - Definitions

Urinary incontinence Normal voiding
Activation of the micturition reflex The micturiction reflex Under voluntary control Coordinated by the pontine micturiction center Two neurological systems involved Sympathetic system (relaxes detrusor and closes internal sphincter) Parasympathetic system (detrusor contraction) Somatic – Pudendal nerve (external urethral sphincter) Continence Learned behavior

Physiology of micturition
From Blaivas JG: Pathophysiology of lower urinary tract dysfunction. Clin Obstet Gynaecol 1985; 12(2):295–309.) Copyright © 2003, Elsevier Science (USA). All rights reserved.

Transition from childhood to adult pattern of urine control
Many children transiently presents Voiding disturbances or Urinary incontinence that suggest dysfunction But they are simply a normal transition phase They are in fact a process of bladder function maturation and self limited

What is urinary incontinence?
Is the involuntary loss of urine A careful history may determine the cause Four main categories Continuous Stress Urgency Overflow

Nocturnal enuresis

Enuresis, Is it a… night or daytime problem?
Nocturnal enuresis Involuntary loss of urine during sleep Neurological maturation and improve over time Daytime incontinence Involuntary loss of urine during the day (awake) Need to rule out Neurological causes Dysfunctional elimination syndrome Other causes (anatomical GU abnormalities)

Nocturnal enuresis 15 % at 5 yrs and 1% at 15 yrs of age
It is considered normal until 6 years of age Often children > 6 yrs should be investigated Exam of lower back Skin dimple, hairy tufts, discolorations Ultrasound Urinalysis and urine culture Vast majority these tests will be normal

Nocturnal enuresis Number of theories tried to explain the cause
Behavioral, genetic, developmental, neurologic, psychological, urodynamic, and organic causes There is no single explanation for this symptom Multiple factors may be involved Neurological maturation theory is the MC accepted MNE is a symptom rather than a disease

Urodynamics in MNE Not indicated Research studies
Urodynamics don’t show increased bladder instability Involuntary contractions are not the cause MNE Therapy aiming at eliminating uninhibited contractions is generally ineffective (anticholinergic)

Vasopressin levels In normal children Theory
Increased production of vasopressin at night 50% less urine is normally excreted at night Theory Vasopressin deficiency is the cause for NE Controversy, contradictory studies However, many children with MNE have similar levels of vasopressin during both the day and the night

Hereditary Factors Likelihood of MNE Twin studies
77% if it occurred in both parents 43% if 1 parent had NE 15% if neither parent had NE Twin studies Monozygotic 65-70% Dizygotyic %

Evaluation Sufficient evaluation for most children with primary MNE
A carefully history Physical examination Urinalysis Check for a history of Urinary infection Diurnal incontinence Obstructive GU symptoms or signs of neuropathy In their absence of above risk factors There is generally no indication for radiographic studies or cystoscopy The incidence of associated uropathology is low However, some authors recommend U/S in children older than 6 yrs

Treatment - Enuresis Controversy
Some authors recommend treatment in children after the age of 5-6 years of age Others wait to treat until the child seems bothered by the problem Treatment should be individualized

Pharmacologic Therapy
Anticholinergic therapy has low effectiveness ranging from only 5% to 40% (Person-Junemann et al, 1993; Kosar et al, 1999) Imipramine (tricyclic antidepressant) Increases functional bladder capacity Good result in 40% to 50% of cases However, discontinuation causes relapse in up to 60%

DDAVP - Desmopressin Rationale - Reduction of urine output at night
Some enuretics have reduced nocturnal vasopressin concentrations and have nocturnal polyuria (Norgaard et al, 1989c) The therapeutic effect of DDAVP is temporary 50% to 90% of children relapse after stop treatment (Kahan et al, 1998)

Behavior Modification
Should be considered the first-line approach Bladder training (increase bladder capacity) Responsibility reinforcement Classic conditioning therapy with a urinary alarm Varied success rate (40-60%) Most effective and reproducible rate of cure

Daytime Incontinence

Daytime incontinence MC causes of daytime incontinence in children
Dysfunctional voiding Neurological conditions Rarely – Obstructive (PUV or urethral stenosis), fistulas, sphincteric incontinence, etc Daytime wetting is of more concern than nocturnal enuresis May be caused by an organic problem Complete physical Lower back, palpable bladder, neurogenic conditions Girls: Vulvo-vaginitis, labial adhesion (vaginal voiding), ectopic ureter Boys: Urethral meatal stenosis, fistulas

Daytime incontinence, Non-neurological cause
Dysfunctional voiding is the MC cause Part of a “behavioral elimination syndrome” Intestinal constipation Holding urine for too long Abnormal spastic pelvic floor Voiding and stoolling calendars (3 days record) Other causes Ectopic ureter, urethral stenosis (overflow), external sphincter insufficiency, vaginal or rectal fistulas

Daytime incontinence, Neurologic causes
Tethering of the spinal cord (TC) is the MC cause Occult spinal dysraphism (primary TC) Stigmata (skin dimple, discoloration, hairy tufts, gluteal asymmetry) Open spina bifida (secondary TC) Lipomyelomeningocele, dermal sinus tract, split cord malformations, syringomyelia, etc Post-operative (myelomeningocele repair) Other neurological causes Down syndrome, sacral agenesis, VACTERL complex, imperforate anus, cloacal anomalies, etc The VACTERL complex refers to anomalies of the bony spinal column (V), atresias in the gastrointestinal tract (A), congenital heart lesions (C), tracheoesophageal defects (TE), renal and distal urinary tract anomalies (R) and limb lesions (L).

Evaluation if Neurogenic cause is suspected
Urodynamics US kidneys and bladder MRI of the spinal cord EMG of the legs and perineum Complete neurological assessment (neurosurgeon)

Tx of daytime incontinence
Dysfunctional voiding Increase fluid and fiber in the diet Prompt to void every 2-3 hours Maintain soft and non-painful BM Stool softener if necessary Neurogenic According the underlying cause Release of tethered cord Anticholinergic, Clean intermittent bladder catheterizations Bladder augmentation

Who I should refer? All cases of daytime incontinence should be referred to urological assessment

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