- •Preface
- •Acknowledgments
- •Contents
- •1.1 Introduction
- •1.2 Normal Embryology
- •1.3 Abnormalities of the Kidney
- •1.3.1 Renal Agenesis
- •1.3.2 Renal Hypoplasia
- •1.3.3 Supernumerary Kidneys
- •1.3.5 Polycystic Kidney Disease
- •1.3.6 Simple (Solitary) Renal Cyst
- •1.3.7 Renal Fusion and Renal Ectopia
- •1.3.8 Horseshoe Kidney
- •1.3.9 Crossed Fused Renal Ectopia
- •1.4 Abnormalities of the Ureter
- •1.5 Abnormalities of the Bladder
- •1.6 Abnormalities of the Penis and Urethra in Males
- •1.7 Abnormalities of Female External Genitalia
- •Further Reading
- •2.1 Introduction
- •2.2 Pathophysiology
- •2.3 Etiology of Hydronephrosis
- •2.5 Clinical Features
- •2.6 Investigations and Diagnosis
- •2.7 Treatment
- •2.8 Antenatal Hydronephrosis
- •Further Reading
- •3.1 Introduction
- •3.2 Embryology
- •3.3 Pathophysiology
- •3.4 Etiology of PUJ Obstruction
- •3.5 Clinical Features
- •3.6 Diagnosis and Investigations
- •3.7 Management of Newborns with PUJ Obstruction
- •3.8 Treatment
- •3.9 Post-operative Complications and Follow-Up
- •Further Reading
- •4: Renal Tumors in Children
- •4.1 Introduction
- •4.2 Wilms’ Tumor
- •4.2.1 Introduction
- •4.2.2 Etiology
- •4.2.3 Histopathology
- •4.2.4 Nephroblastomatosis
- •4.2.5 Clinical Features
- •4.2.6 Risk Factors for Wilms’ Tumor
- •4.2.7 Staging of Wilms Tumor
- •4.2.8 Investigations
- •4.2.9 Prognosis and Complications of Wilms Tumor
- •4.2.10 Surgical Considerations
- •4.2.11 Surgical Complications
- •4.2.12 Prognosis and Outcome
- •4.2.13 Extrarenal Wilms’ Tumors
- •4.3 Mesoblastic Nephroma
- •4.3.1 Introduction
- •4.3.3 Epidemiology
- •4.3.5 Clinical Features
- •4.3.6 Investigations
- •4.3.7 Treatment and Prognosis
- •4.4 Clear Cell Sarcoma of the Kidney (CCSK)
- •4.4.1 Introduction
- •4.4.2 Pathophysiology
- •4.4.3 Clinical Features
- •4.4.4 Investigations
- •4.4.5 Histopathology
- •4.4.6 Treatment
- •4.4.7 Prognosis
- •4.5 Malignant Rhabdoid Tumor of the Kidney
- •4.5.1 Introduction
- •4.5.2 Etiology and Pathophysiology
- •4.5.3 Histologic Findings
- •4.5.4 Clinical Features
- •4.5.5 Investigations and Diagnosis
- •4.5.6 Treatment and Outcome
- •4.5.7 Mortality/Morbidity
- •4.6 Renal Cell Carcinoma in Children
- •4.6.1 Introduction
- •4.6.2 Histopathology
- •4.6.4 Staging
- •4.6.5 Clinical Features
- •4.6.6 Investigations
- •4.6.7 Management
- •4.6.8 Prognosis
- •4.7 Angiomyolipoma of the Kidney
- •4.7.1 Introduction
- •4.7.2 Histopathology
- •4.7.4 Clinical Features
- •4.7.5 Investigations
- •4.7.6 Treatment and Prognosis
- •4.8 Renal Lymphoma
- •4.8.1 Introduction
- •4.8.2 Etiology and Pathogenesis
- •4.8.3 Diagnosis
- •4.8.4 Clinical Features
- •4.8.5 Treatment and Prognosis
- •4.9 Ossifying Renal Tumor of Infancy
- •4.10 Metanephric Adenoma
- •4.10.1 Introduction
- •4.10.2 Histopathology
- •4.10.3 Diagnosis
- •4.10.4 Clinical Features
- •4.10.5 Treatment
- •4.11 Multilocular Cystic Renal Tumor
- •Further Reading
- •Wilms’ Tumor
- •Mesoblastic Nephroma
- •Renal Cell Carcinoma in Children
- •Angiomyolipoma of the Kidney
- •Renal Lymphoma
- •Ossifying Renal Tumor of Infancy
- •Metanephric Adenoma
- •Multilocular Cystic Renal Tumor
- •5.1 Introduction
- •5.2 Embryology
- •5.4 Histologic Findings
- •5.7 Associated Anomalies
- •5.8 Clinical Features
- •5.9 Investigations
- •5.10 Treatment
- •Further Reading
- •6: Congenital Ureteral Anomalies
- •6.1 Etiology
- •6.2 Clinical Features
- •6.3 Investigations and Diagnosis
- •6.4 Duplex (Duplicated) System
- •6.4.1 Introduction
- •6.4.3 Clinical Features
- •6.4.4 Investigations
- •6.4.5 Treatment and Prognosis
- •6.5 Ectopic Ureter
- •6.5.1 Introduction
- •6.5.3 Clinical Features
- •6.5.4 Diagnosis
- •6.5.5 Surgical Treatment
- •6.6 Ureterocele
- •6.6.1 Introduction
- •6.6.3 Clinical Features
- •6.6.4 Investigations and Diagnosis
- •6.6.5 Treatment
- •6.6.5.1 Surgical Interventions
- •6.8 Mega Ureter
- •Further Reading
- •7: Congenital Megaureter
- •7.1 Introduction
- •7.3 Etiology and Pathophysiology
- •7.4 Clinical Presentation
- •7.5 Investigations and Diagnosis
- •7.6 Treatment and Prognosis
- •7.7 Complications
- •Further Reading
- •8.1 Introduction
- •8.2 Pathophysiology
- •8.4 Etiology of VUR
- •8.5 Clinical Features
- •8.6 Investigations
- •8.7 Management
- •8.7.1 Medical Treatment of VUR
- •8.7.2 Antibiotics Used for Prophylaxis
- •8.7.3 Anticholinergics
- •8.7.4 Surveillance
- •8.8 Surgical Therapy of VUR
- •8.8.1 Indications for Surgical Interventions
- •8.8.2 Indications for Surgical Interventions Based on Age at Diagnosis and the Presence or Absence of Renal Lesions
- •8.8.3 Endoscopic Injection
- •8.8.4 Surgical Management
- •8.9 Mortality/Morbidity
- •Further Reading
- •9: Pediatric Urolithiasis
- •9.1 Introduction
- •9.2 Etiology
- •9.4 Clinical Features
- •9.5 Investigations
- •9.6 Complications of Urolithiasis
- •9.7 Management
- •Further Reading
- •10.1 Introduction
- •10.2 Embryology of Persistent Müllerian Duct Syndrome
- •10.3 Etiology and Inheritance of PMDS
- •10.5 Clinical Features
- •10.6 Treatment
- •10.7 Prognosis
- •Further Reading
- •11.1 Introduction
- •11.2 Physiology and Bladder Function
- •11.2.1 Micturition
- •11.3 Pathophysiological Changes of NBSD
- •11.4 Etiology and Clinical Features
- •11.5 Investigations and Diagnosis
- •11.7 Management
- •11.8 Clean Intermittent Catheterization
- •11.9 Anticholinergics
- •11.10 Botulinum Toxin Type A
- •11.11 Tricyclic Antidepressant Drugs
- •11.12 Surgical Management
- •Further Reading
- •12.1 Introduction
- •12.2 Etiology
- •12.3 Pathophysiology
- •12.4 Clinical Features
- •12.5 Investigations and Diagnosis
- •12.6 Management
- •Further Reading
- •13.1 Introduction
- •13.2 Embryology
- •13.3 Epispadias
- •13.3.1 Introduction
- •13.3.2 Etiology
- •13.3.4 Treatment
- •13.3.6 Female Epispadias
- •13.3.7 Surgical Repair of Female Epispadias
- •13.3.8 Prognosis
- •13.4 Bladder Exstrophy
- •13.4.1 Introduction
- •13.4.2 Associated Anomalies
- •13.4.3 Principles of Surgical Management of Bladder Exstrophy
- •13.4.4 Evaluation and Management
- •13.5 Cloacal Exstrophy
- •13.5.1 Introduction
- •13.5.2 Skeletal Changes in Cloacal Exstrophy
- •13.5.3 Etiology and Pathogenesis
- •13.5.4 Prenatal Diagnosis
- •13.5.5 Associated Anomalies
- •13.5.8 Surgical Reconstruction
- •13.5.9 Management of Urinary Incontinence
- •13.5.10 Prognosis
- •13.5.11 Complications
- •Further Reading
- •14.1 Introduction
- •14.2 Etiology
- •14.3 Clinical Features
- •14.4 Associated Anomalies
- •14.5 Diagnosis
- •14.6 Treatment and Prognosis
- •Further Reading
- •15: Cloacal Anomalies
- •15.1 Introduction
- •15.2 Associated Anomalies
- •15.4 Clinical Features
- •15.5 Investigations
- •Further Reading
- •16: Urachal Remnants
- •16.1 Introduction
- •16.2 Embryology
- •16.4 Clinical Features
- •16.5 Tumors and Urachal Remnants
- •16.6 Management
- •Further Reading
- •17: Inguinal Hernias and Hydroceles
- •17.1 Introduction
- •17.2 Inguinal Hernia
- •17.2.1 Incidence
- •17.2.2 Etiology
- •17.2.3 Clinical Features
- •17.2.4 Variants of Hernia
- •17.2.6 Treatment
- •17.2.7 Complications of Inguinal Herniotomy
- •17.3 Hydrocele
- •17.3.1 Embryology
- •17.3.3 Treatment
- •Further Reading
- •18: Cloacal Exstrophy
- •18.1 Introduction
- •18.2 Etiology and Pathogenesis
- •18.3 Associated Anomalies
- •18.4 Clinical Features and Management
- •Further Reading
- •19: Posterior Urethral Valve
- •19.1 Introduction
- •19.2 Embryology
- •19.3 Pathophysiology
- •19.5 Clinical Features
- •19.6 Investigations and Diagnosis
- •19.7 Management
- •19.8 Medications Used in Patients with PUV
- •19.10 Long-Term Outcomes
- •19.10.3 Bladder Dysfunction
- •19.10.4 Renal Transplantation
- •19.10.5 Fertility
- •Further Reading
- •20.1 Introduction
- •20.2 Embryology
- •20.4 Clinical Features
- •20.5 Investigations
- •20.6 Treatment
- •20.7 The Müllerian Duct Cyst
- •Further Reading
- •21: Hypospadias
- •21.1 Introduction
- •21.2 Effects of Hypospadias
- •21.3 Embryology
- •21.4 Etiology of Hypospadias
- •21.5 Associated Anomalies
- •21.7 Clinical Features of Hypospadias
- •21.8 Treatment
- •21.9 Urinary Diversion
- •21.10 Postoperative Complications
- •Further Reading
- •22: Male Circumcision
- •22.1 Introduction
- •22.2 Anatomy and Pathophysiology
- •22.3 History of Circumcision
- •22.4 Pain Management
- •22.5 Indications for Circumcision
- •22.6 Contraindications to Circumcision
- •22.7 Surgical Procedure
- •22.8 Complications of Circumcision
- •Further Reading
- •23: Priapism in Children
- •23.1 Introduction
- •23.2 Pathophysiology
- •23.3 Etiology
- •23.5 Clinical Features
- •23.6 Investigations
- •23.7 Management
- •23.8 Prognosis
- •23.9 Priapism and Sickle Cell Disease
- •23.9.1 Introduction
- •23.9.2 Epidemiology
- •23.9.4 Pathophysiology
- •23.9.5 Clinical Features
- •23.9.6 Treatment
- •23.9.7 Prevention of Stuttering Priapism
- •23.9.8 Complications of Priapism and Prognosis
- •Further Reading
- •24.1 Introduction
- •24.2 Embryology and Normal Testicular Development and Descent
- •24.4 Causes of Undescended Testes and Risk Factors
- •24.5 Histopathology
- •24.7 Clinical Features and Diagnosis
- •24.8 Treatment
- •24.8.1 Success of Surgical Treatment
- •24.9 Complications of Orchidopexy
- •24.10 Infertility and Undescended Testes
- •24.11 Undescended Testes and the Risk of Cancer
- •Further Reading
- •25: Varicocele
- •25.1 Introduction
- •25.2 Etiology
- •25.3 Pathophysiology
- •25.4 Grading of Varicoceles
- •25.5 Clinical Features
- •25.6 Diagnosis
- •25.7 Treatment
- •25.8 Postoperative Complications
- •25.9 Prognosis
- •Further Reading
- •26.1 Introduction
- •26.2 Etiology and Risk Factors
- •26.3 Diagnosis
- •26.4 Intermittent Testicular Torsion
- •26.6 Effects of Testicular Torsion
- •26.7 Clinical Features
- •26.8 Treatment
- •26.9.1 Introduction
- •26.9.2 Etiology of Extravaginal Torsion
- •26.9.3 Clinical Features
- •26.9.4 Treatment
- •26.10 Torsion of the Testicular or Epididymal Appendage
- •26.10.1 Introduction
- •26.10.2 Embryology
- •26.10.3 Clinical Features
- •26.10.4 Investigations and Treatment
- •Further Reading
- •27: Testicular Tumors in Children
- •27.1 Introduction
- •27.4 Etiology of Testicular Tumors
- •27.5 Clinical Features
- •27.6 Staging
- •27.6.1 Regional Lymph Node Staging
- •27.7 Investigations
- •27.8 Treatment
- •27.9 Yolk Sac Tumor
- •27.10 Teratoma
- •27.11 Mixed Germ Cell Tumor
- •27.12 Stromal Tumors
- •27.13 Simple Testicular Cyst
- •27.14 Epidermoid Cysts
- •27.15 Testicular Microlithiasis (TM)
- •27.16 Gonadoblastoma
- •27.17 Cystic Dysplasia of the Testes
- •27.18 Leukemia and Lymphoma
- •27.19 Paratesticular Rhabdomyosarcoma
- •27.20 Prognosis and Outcome
- •Further Reading
- •28: Splenogonadal Fusion
- •28.1 Introduction
- •28.2 Etiology
- •28.4 Associated Anomalies
- •28.5 Clinical Features
- •28.6 Investigations
- •28.7 Treatment
- •Further Reading
- •29: Acute Scrotum
- •29.1 Introduction
- •29.2 Torsion of Testes
- •29.2.1 Introduction
- •29.2.3 Etiology
- •29.2.4 Clinical Features
- •29.2.5 Effects of Torsion of Testes
- •29.2.6 Investigations
- •29.2.7 Treatment
- •29.3 Torsion of the Testicular or Epididymal Appendage
- •29.3.1 Introduction
- •29.3.2 Embryology
- •29.3.3 Clinical Features
- •29.3.4 Investigations and Treatment
- •29.4.1 Introduction
- •29.4.2 Etiology
- •29.4.3 Clinical Features
- •29.4.4 Investigations and Treatment
- •29.5 Idiopathic Scrotal Edema
- •29.6 Testicular Trauma
- •29.7 Other Causes of Acute Scrotum
- •29.8 Splenogonadal Fusion
- •Further Reading
- •30.1 Introduction
- •30.2 Imperforate Hymen
- •30.3 Vaginal Atresia
- •30.5 Associated Anomalies
- •30.6 Embryology
- •30.7 Clinical Features
- •30.8 Investigations
- •30.9 Management
- •Further Reading
- •31: Disorders of Sexual Development
- •31.1 Introduction
- •31.2 Embryology
- •31.3 Sexual and Gonadal Differentiation
- •31.5 Evaluation of a Newborn with DSD
- •31.6 Diagnosis and Investigations
- •31.7 Management of Patients with DSD
- •31.8 Surgical Corrections of DSD
- •31.9 Congenital Adrenal Hyperplasia (CAH)
- •31.10 Androgen Insensitivity Syndrome (Testicular Feminization Syndrome)
- •31.13 Gonadal Dysgenesis
- •31.15 Ovotestis Disorders of Sexual Development
- •31.16 Other Rare Disorders of Sexual Development
- •Further Reading
- •Index
2.7 Treatment |
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Figs. 2.54 and 2.55 Abdominal CT-scan showing hydronephrosis secondary to PUJ obstruction. Note the difference in the renal parenchyma thickness between the
two patients. I the second picture, there is hardly any renal tissue remaining
Figs. 2.56 and 2.57 MRU showing bilateral severe hydroureteronephrosis. Note the marked dilated ureters
2.7Treatment
•The aim of treatment is to remove the obstructive cause and allow free drainage of the urine.
•The specific treatment of patients with hydronephrosis depends on the etiology and site of obstruction.
•The presence of infection should be treated aggressively as infection with hydronephrosis may progress rapidly to sepsis.
•The presence of bilateral hydronephrosis or hydronephrosis in a solitary kidney calls for urgent evaluation and management.
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Figs. 2.58 and 2.59 MRU showing severe right hydronephrosis secondary to pelvi-ureteric junction obstruction. Note the compressed renal tissue
Figs. 2.60, 2.61, 2.62, and 2.63 Percutaneous nephrostograms showing unilateral and bilateral hydronephrosis secondary to PUJ obstruction
2.8 Antenatal Hydronephrosis |
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• A nephrostomy tube is a very valuable procedure to relieve acute hydronephrosis (Figs. 2.60, 2.61, 2.62, and 2.63).
•The use of ureteral stent can bypass an obstruction and temporarily relieve the pressure on the affected kidney.
•Lower urinary tract obstruction can be relieved by insertion of a urinary catheter or a suprapubic catheter.
•Fetal surgery:
–Fetal surgery is indicated in those with antenatal severe hydronephrosis in an attempt to preserve renal function and improve the clinical outcome.
–It is however not readily available and require expertise.
•Indication of surgical interventions in those with PUJ obstruction:
–Conservative management is appropriate for infants with an obstructive pattern on diuretic renography and differential function exceeding 40 %.
–While most experts suggest that pyeloplasty be considered in patients showing obstructed drainage and differential function below 40 %, others propose surgery at differential function below 35 %, or an obstructed renogram with prolonged t1/2 >20 min.
–In those with PUJ, a reduction of differential renal function by more than 5–10 % correlates with declining renal function, and the need for pyeloplasty.
–The presence of symptoms including pain, palpable renal mass or recurrent febrile UTI.
–The presence of large anteroposterior
diameter of renal pelvis exceeding 20–30 mm predicts the need for surgery in 50–55 % patients.
–Surgery allows preservation of renal function in the majority of patients.
–Predictors of unsatisfactory outcome include baseline renal differential function <30 % and anteroposterior diameter of renal pelvis >50 mm with dilated calyces.
•Antibiotic Prophylaxis
–While there is increased risk of UTI, there is lack of evidence that antibiotic prophylaxis
in patients with mild VUR confers clinical benefit.
–Multiple studies and a systematic review suggest that the severity of antenatal hydronephrosis does not correlate with the grade of reflux, and that patients with VUR may have normal postnatal ultrasound.
–Infants with postnatally confirmed moderate or severe hydronephrosis (SFU 3–4; renal APD >10 mm) or dilated ureter receive antibiotic prophylaxis while awaiting evaluation.
•There are those who recommend that all patients detected to have VUR receive antibiotic prophylaxis through the first year of life.
•Antibiotics that are preferred include cephalexin (10 mg/kg/day) during the first 3 months of life, and cotrimoxazole (1–2 mg/kg/day) or nitrofurantoin (1 mg/kg/day) later.
•Patients with moderate or severe hydronephrosis and/or dilated ureter should receive antibiotic prophylaxis while awaiting investigations.
•Since the risk of UTI is low with mild hydronephrosis, antibiotic prophylaxis is not necessary in these infants.
2.8Antenatal Hydronephrosis
•The widespread use of antenatal ultrasound has resulted in an increase in the early detection of antenatal hydronephrosis.
•Fetal hydronephrosis (dilatation of the renal pelvis with or without dilation of the renal calyces) is a common, readily diagnosed finding on antenatal ultrasound examination and can be detected as early as the 12th–14th week of gestation.
•Although antenatal hydronephrosis is most often transient or clinically insignificant, urinary tract obstruction or vesicoureteral reflux (VUR) are important causes that should be diagnosed soon after birth because they may result in renal impairment or cause further renal damage.
•The risk of significant renal and urinary tract abnormality in those with hydronephrosis increases with:
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–The severity of hydronephrosis
–Persistence of hydronephrosis into the third trimester
–Bilateral involvement
–The presence of oligohydramnios
•Once fetal hydronephrosis is detected, the following parameters need to be evaluated using ultrasonography:
–Severity of hydronephrosis
–Whether hydronephrosis is unilateral or bilateral
–Dilatation of the ureter
•The risk of postnatal renal pathological changes correlates with the degree of antenatal hydronephrosis as follows:
–The risk for those with mild hydronephrosis is 12 %
–The risk for those with moderate hydronephrosis is 45 %
–The risk for those with severe hydronephrosis is 88 %
•The severity of antenatal hydronephrosis correlates positively with:
–Persistent postnatal hydronephrosis
–The need for surgical intervention
–The risk of UTI
•Grading the severity of antenatal hydronephrosis is important as this enables identification of infants that require close follow-up.
•About 88 % of mild antenatal hydronephrosis resolve in utero or in the neonatal period.
•It has been estimated that one in three neonates with moderate to severe hydronephrosis persisting in the third trimester required postnatal surgery.
•Hence, an ultrasound in the third trimester is valuable for identifying fetuses that require postnatal evaluation, follow up and possibly surgery.
•A systematic review concluded that:
–98 % of patients with SFU grade 1–2 or antero-posterior diameter (APD) of the renal pelvis <12 mm resolved.
–51 % of patients with APD >12 mm or SFU 3–4 resolved.
•All newborns with history of antenatal hydronephrosis should have postnatal ultrasound examination within the first week of life.
•Ultrasonography should be performed early, within 24–48 h of birth for neonates with:
–Suspected posterior urethral valves
–Oligohydramnios
–Severe bilateral hydronephrosis
–Severe hydronephrosis in a solitary kidney
Pathological Causes of Antenatally
Diagnosed Hydronephrosis
•Isolated Unilateral hydronephrosis
–PUJ
•Unilateral hydronephrosis with hydroureter
–Uretro-esical junction obstruction
–Uretrocele
–Vesicoueteric reflux
–Posterior urethral valve
•Isolated bilateral hydronephrosis
–Bilateral PUJ
•Bilateral hydronephrosis with hydroureter
–Bilateral uretro-vesical obstruction
–Bilateral vesicoureteric reflux
–Posterior urethral valve
–Bilateral uretrocele
–Urethral stricture
•In all other cases, the ultrasound should be performed preferably within 3–7 days, or before hospital discharge.
•A single ultrasound in the first few days of life might not detect all abnormalities of the kidneys or urinary tract, due to low urine flow secondary to dehydration and low glomerular filtration rate. An ultrasound at 6 weeks is more sensitive and specific for obstruction, than that in the first week of life.
•Postnatal radiologic studies:
–Postnatal radiologic evaluation of a newborn with antenatal hydronephrosis begins with an ultrasonography examination.
–The timing of ultrasonography and the need for other studies depend on the severity of postnatal hydronephrosis and whether
2.8 Antenatal Hydronephrosis |
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there is bilateral involvement or an affected solitary kidney.
–The timing of the study depends on the severity of the antenatal hydronephrosis.
•In general, examination should be avoided in the first 2 days after birth because hydronephrosis may not be detected because of extracellular fluid shifts that underestimate the degree of hydronephrosis.
•However, infants with bilateral hydronephrosis and those with a severe hydronephrotic solitary kidney require urgent evaluation on the first or second postnatal day because of the increased likelihood of significant disease and a possible need for early surgical intervention.
•For those with unilateral hydronephrosis without antenatal bladder pathology,
performing postnatal sonography 1–4 weeks after birth is recommended.
–A voiding cystourethrography (VCUG) is performed to detect VUR and, in boys, to evaluate the posterior urethra.
Postnatal Hydronephrosisultrasound
Evaluation
•The severity of hydronephrosis postnatally is determined by a renal ultrasound performed after 48 h of life in a full term infant and is based on anterior posterior pelvic diameter as follows:
–<7 mm should be considered normal
–7–8 mm: Mild hydronephrosis
–9–15 mm: Moderate hydronephrosis
–>15 mm: Severe hydronephrosis. These infants are at the greatest risk for significant renal disease, which requires surgical correction.
–Diuretic renography:
•This is used to diagnose urinary tract obstruction in infants with persistent hydronephrosis.
•It is usually ordered after a VCUG has demonstrated no vesicoureteral reflux.
•It measures the drainage time from the renal pelvis and assesses total and individual kidney function.
•The preferred radioisotope is technetium Tc 99m-mercaptoacetyltriglycine (Tc99m MAG3), which is taken up by the renal cortex, filtered across the glomerular basement membrane to the renal tubules, and excreted into the renal pelvis and urinary tract.
•The management of infants with antenatal hydronephrosis depends on:
– Confirmation of persistent postnatal hydronephrosis
– The severity of hydronephrosis: Fetuses with a renal pelvic diameter greater than 15 mm during the third trimester are at the greatest risk for significant renal disease
– Whether hydronephrosis is bilateral or unilateral
– Whether hydronephrosis is in a solitary kidney or not
•Bilateral hydronephrosis:
– Infants with severe bilateral antenatal hydronephrosis and/or bladder distension are at increased likelihood of having significant disease.
– These infants and those with a severe hydronephrotic solitary kidney should be evaluated initially by ultrasonography on the first postnatal day.
– Bilateral hydronephrosis suggests an obstructive process at the level of or distal to the bladder, such as uretrovesical obstruction, ureterocele or posterior urethral valves (PUV) in a male infant, which can be associated with impaired renal function and ongoing renal injury.
– If postnatal ultrasonography demonstrates persistent hydronephrosis, voiding cystourethrography (VCUG) should be performed. In male infants, the posterior urethra should be fully evaluated to detect possible PUVs.
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Infants with mild or moderate hydrone- |
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phy findings or in those with mild |
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phrosis can be evaluated after |
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days |
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hydronephrosis. |
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of life. |
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It was found that infants with high-grade |
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Severe unilateral hydronephrosis: |
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hydronephrosis receiving continuous anti- |
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In newborns with severe antenatal unilat- |
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biotic prophylaxis had significantly lower |
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eral hydronephrosis (renal pelvic diameter |
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urinary tract infections when compared to |
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>15 mm in the third trimester), ultrasonog- |
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those who did not receive prophylactic |
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raphy should be performed after age 48 h |
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antibiotics (14.6 % vs 28.9 %). |
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and within the first 2 weeks of life). |
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This however is not the case for infants |
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• Moderate and mild unilateral hydronephrosis: |
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with low-grade hydronephrosis were the |
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– In newborns with less severe antenatal uni- |
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frequency of urinary tract infections were |
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lateral hydronephrosis (renal pelvic diam- |
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similar (2.2 % vs. 2.8 %). |
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eter <15 mm during third trimester), |
– Other indications for prophylactic antibiot- |
||||
|
|
ultrasonography can be performed after |
|
ics include: |
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|
|
age 7 days to see whether the hydronephro- |
|
• The presence of ureteral dilation |
|||
|
|
sis has persisted postnatally. |
|
|
|
• |
Associated high-grade VUR |
|
– Moderate hydronephrosis (renal |
pelvic |
|
• |
Ureterovesical junction obstruction |
||
|
|
diameters between 10 and 15 mm) resolves |
– In patients with low-grade hydronephrosis |
||||
|
|
by age 18 months in most cases. Resolution |
|
(SFU grades I and II), there was no differ- |
|||
|
|
was defined as renal pelvic |
diameter |
|
ence in the rate of UTI between patients |
||
|
|
≤5 mm on two consecutive ultrasounds. |
|
treated with continuous antibiotic prophy- |
|||
• |
Antibiotic prophylaxis: |
|
|
|
laxis and those who were not treated. |
||
|
– |
The frequency of urinary tract infections |
– Patients with high-grade hydronephrosis |
||||
|
|
has been reported to be higher in children |
|
(SFU grades III and IV) who received con- |
|||
|
|
with prenatally diagnosed hydronephrosis |
|
tinuous antibiotic prophylaxis had a lower |
|||
|
|
when compared with the general pediatric |
|
rate of UTI compared with those who were |
|||
|
|
population. |
|
|
|
not treated with antibiotics. |
|
|
– |
The risk of urinary tract infection rises if |
– Infants with persistent severe postnatal |
||||
|
|
there is an underlying urologic abnormal- |
|
hydronephrosis should have a VCUG to |
|||
|
|
ity, such as VUR or obstructive uropathy. |
|
detect VUR. |
|||
|
– The risk of urinary tract infection is greater |
|
• VUR accounts for approximately 9 % of |
||||
|
|
in girls than boys. |
|
|
|
|
cases of antenatal hydronephrosis, but it |
|
– |
Infants with severe hydronephrosis are at |
|
|
is more common and severe in infants |
||
|
|
greater risk for an underlying urologic |
|
|
with persistent postnatal hydronephro- |
||
|
|
abnormality and should receive antibiotic |
|
|
sis (13–30 %). |
||
|
|
prophylaxis after delivery until the diagno- |
|
• Infants who have VUR demonstrated on |
|||
|
|
sis of VUR or obstructive uropathy is |
|
|
VCUG should remain on antibiotic |
||
|
|
excluded. |
|
|
|
|
prophylaxis. |
|
– |
Children with mild or moderate hydrone- |
|
• If the VCUG does not show reflux, anti- |
|||
|
|
phrosis confirmed postnatally should also |
|
|
biotics are discontinued. |
||
|
|
receive antibiotic prophylaxis (amoxicillin, |
• Surgical management: |
||||
|
|
12–25 mg/kg given orally per day) until the |
– |
The specific treatment of an infant with |
|||
|
|
diagnosis of VUR has been made or |
|
hydronephrosis and hydroureter depends |
|||
|
|
eliminated. |
|
|
|
on the etiology. |
|
|
– |
Antibiotic prophylaxis is not indicated in |
– There is no good evidence to support that |
||||
|
|
infants with normal postnatal ultrasonogra- |
|
antenatal surgery in fetuses with sono- |