- •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
Varicocele |
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25.1Introduction
•The testes are supplied by blood vessels that originate in the abdomen and course down through the inguinal canal as part of the spermatic cord to the testis.
•The testis is drained by a plexus of veins called the pampiniform venous plexus. These course upward and coalescence to form the testicular vein. The left testicular vein drains at right angle into the left renal vein while the right testicular vein drains directly into the inferior vena cava.
•Upward flow of blood in the veins is ensured by small one-way valves that prevent backflow.
•A varicocele is an abnormal enlargement and tortuosity of the pampiniform plexus of veins (Fig. 25.1).
•Varicoceles result from defective valves, or compression of the vein by a nearby structure. This leads to dilatation of the testicular veins and the formation of a varicocele.
•The true incidence of adolescent varicoceles is not known because most adolescent varicoceles are asymptomatic.
DILATED, TORSIOUS
PAMPINEFORM PLEXUS
TESTIS
Fig. 25.1 Diagrammatic representation of a varicocele
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25 Varicocele |
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•The initial presentation of varicoceles usually occurs during puberty, with an incidence in 13-year-old adolescent boys equal to that of adult men (15 %).
•Rarely, varicoceles are noted in the prepubertal period.
•Although varicoceles may be bilateral, they are usually unilateral and almost always on the left side.
•It has been estimated that 90 % of all varicoceles occur on the left side. This is attributed to the fact that the right testicular vein drain directly into the inferior vena cava while the left testicular vein drains at a right angle into the left renal vein. This predisposes to slower drainage in the left testicular vein.
•A unilateral right-side varicocele raises certain concerns and should prompt an investigation for an underlying obstructive cause such as:
–A tumor
–Retroperitoneal fibrosis
–Thrombosis or occlusion of the inferior vena cava
•These patients should be investigated radiographically including computed tomography (CT).
•Situs inversus is another rare cause of a rightside varicocele which must be kept in mind.
25.2Etiology
•The exact etiology of varicoceles is unknown and various theories have been proposed to explain this taking in consideration the fact that 90% of all varicoceles occur on the left side.
•Varicoceles are divided into two types depending on the etiology.
–Primary or idiopathic varicocele
–Secondary varicocele
•Primary or idiopathic varicocele:
–This is the commonest type.
–It occurs as a result of defective valves within the veins along the spermatic cord.
–This results in backflow of blood into the pampiniform plexus and causes its dilatation, tortuosity and increased pressures.
–The majority of idiopathic varicoceles occur on the left side.
–This is because the left testicular vein drains into the left renal vein (at a 90-degree angle), while the right testicular vein drains directly into the inferior vena cava.
–Isolated right sided varicoceles are rare.
–Increased length of the left testicular vein:
•The left vein is 8–10 cm longer than the right testicular vein. This may contribute to an increased pressure in the left testicular vein when compared to the right testicular vein.
•Secondary varicocele:
–This results from compression of the venous drainage of the testicle.
–This can develop as a result of pelvic or abdominal tumors that causes compression of the veins draining the testes.
–A unilateral right-sided varicocele that is newly diagnosed in a patient older than 40 years of age should raise the possibility of an underlying malignancy.
–The most common cause is renal cell carcinoma (hypernephroma) followed by retroperitoneal fibrosis or adhesions.
–In the pediatric age group, left-sided Wilms’ tumor with extension into the renal vein can cause obstruction of the testicular vein leading to left varicocele. In those with right-sided Wilms’ tumor, a varicocele can develop if the tumor extends into the inferior vena cava and leads to obstruction of the right renal vein.
–“The Nutcracker syndrome”:
•This is one non-malignant causes of a secondary varicocele.
•In this condition, the superior mesenteric artery compresses the left renal vein between it and the aorta, causing increased pressures which is transmitted retrograde into the left pampiniform plexus of veins.
25.3Pathophysiology
•The pampiniform plexus of veins is the network of veins that normally drain the testicle.
•Normally, the size of the veins that make up the pampiniform plexus range from 0.5 to 1.5 mm
25.4 Grading of Varicoceles |
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•This plexus of veins travels along the posterior portion of the testicle with the epididymis and vas deferens, and then into the spermatic cord and upwards where they coalesces to form the testicular vein.
•Upward flow of blood in the veins is ensured by small one-way valves that prevent backflow.
•The right testicular vein drains into the inferior vena cava, while the left testicular vein drains into the left renal vein at right angle to the renal vein, which then drains into the inferior vena cava.
•The pampiniform plexus of veins not only drains the blood from the testes, vas and epididymis but also has an important function to lower the temperature of the testes.
•A varicocele develops when there is dilatation and tortuosity of the veins of the pampiniform plexus.
•It has been estimated that a varicocele devel-
ops when the size of these veins exceeds
2 mm.
•The development of a varicocele with these dilated veins leads to an increase in the temperature around the testes resulting in testicular atrophy, reduction in the quality and the quantity of the sperms and infertility. This effect on sperm quantity and quality is progressive.
•It has been shown also that blood from the testes that cannot drain via the pampiniform plexus may drain via communicating vessels through the prostate. The increased flow of blood to the prostate can lead to congestion and enlargement of the prostate gland secondary to cell proliferation resulting from the high concentration of free testosterone reaching directly from the testes to the prostate.
•It has been shown that a varicocele that persists will lead to histopathological changes in the testis which include:
– The affected testis is abnormally small as compared with the contralateral testis.
– Seminiferous tubule sclerosis
– Small vessel degenerative changes
– Abnormalities of Leydig, Sertoli, and germ cells
–The subsequent effects of a varicocele on semen include:
•Decreased sperm motility
•Lower total sperm counts
•Increased number of abnormal sperm forms
•These changes may be reversed with corrective surgery.
•The reasons for altered sperm production, testicular size, and morphologic changes in the testis are not clearly understood. The proposed pathophysiologic mechanisms include the followings:
–The dilated veins in the pampiniform plexus with pooling of venous blood results in increased scrotal and testicular temperature.
–The increase in testicular temperature will lead to morphologic changes in sperm and testicular tissue.
–It is suggested that the renal and adrenal metabolites that reflux into dilated spermatic veins affect testicular tissue leading impaired spermatogenesis and compromised testicular hormone production and function.
–The low oxygen tension in the dilated veins of the testis may result in local tissue hypoxia which could also affect both testicular function and sperm production.
–As a result of this, there will be a paracrine imbalances in the testicle which may lead to impaired testicular function.
25.4Grading of Varicoceles
•Dubin and Amelar graded varicoceles into four grades based on physical examination findings as follows:
–Grade 0:
•This is a subclinical varicocele which cannot be detected during physical examination and diagnosed with ultrasonography or venography
–Grade 1:
•This is detected clinically with difficulty (<1 cm) and increases in size with Valsalva maneuver
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–Grade 2:
•This is easily detected without Valsalva maneuver (1–2 cm)
–Grade 3:
This a large varicocele that is palpable and can be seen from a distance (>2 cm)
•The degree of testicular atrophy correlates with the varicocele grade.
•No patients with grade 1 varicoceles were noted to have testicular atrophy while 80 % with grade 3 and 30 % with grade 2 varicoceles have testicular atrophy.
–Dragging-like or aching pain within scrotum
–Feeling of heaviness in the testicle
–Atrophy of the testicle
•There may be a difference in testicular sizes without a palpable varicocele.
•Varicoceles may present as an incidental finding on scrotal ultrasonography done for other reasons.
•Varicoceles are considered as one of the leading causes of adult male infertility and are detected in 35 % of adult males with primary infertility.
25.5Clinical Features
•Varicoceles are most frequently diagnosed when a patient is 13–30 years of age, and rarely develop after the age of 40.
•They are reported to occur in 15–20 % of all males.
•The prevalence of varicoceles in individuals aged 10–19 years is reported to be approximately 15 % and is similar to the prevalence reported for adults.
•Varicoceles are extremely rare in patients younger than 9 years (Fig. 25.2)
•The vast majority of varicoceles are asymptomatic.
•Varicoceles mat present with:
–Testicular pain
–A scrotal mass
–Acute or chronic scrotal discomfort
–Visible or palpable enlarged vein
25.6Diagnosis
•The diagnosis of a varicocele is made clinically.
•This is made by carefully palpating the scrotum while the patient is standing.
•Sometimes, the distended veins can be seen on the lateral aspect of the scrotum.
•A small varicocele may feel like a thickened spermatic cord.
•A larger varicocele feels like a bag of worms.
•A varicocele is a non-tender mass.
•When the patient is asked to perform a Valsalva maneuver, the veins of the pampiniform plexus becomes more distended and accentuates the physical findings.
•When the patient is asked to lie down, gravity may allow the drainage of the pampiniform plexus and thus make the mass smaller and
DILATED,
TORSIOUS
PAMPINEFORM
PLEXUS
Fig. 25.2 A clinical photograph of a child with left varicocele