- •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
Inguinal Hernias and Hydroceles |
17 |
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17.1Introduction
•Hippocrates used the Greek hernios for bud or bulge to describe abdominal hernias.
•Abdominal wall hernias are protrusions of abdominal contents through a defect or weakness in the abdominal wall.
•Abdominal wall hernias are among the most common of all surgical problems in infants and children.
•There are several different types of abdominal wall hernias in infants and children including:
–Inguinal hernia
–Umbilical hernia
–Paraumbilical hernia
–Epigastric hernia
–Femoral hernia
–Spigelian hernia
–Lumbar hernia
–Incisional hernia
–Other rare hernias
•The management of abdominal wall hernias are different and depend on the type of hernia, age of the patient and mode of presentation.
•All pediatric inguinal hernias require operative treatment to prevent the development of complications, such as inguinal hernia incarceration or strangulation.
17.2Inguinal Hernia
17.2.1 Incidence
•The exact incidence of indirect inguinal hernia in infants and children is unknown.
•The incidence of hernias is about 10–20 per 1,000 live births and is much more common in prematures.
•Indirect inguinal hernias are more common on the right side and about 60 % of hernias occur on the right side (Figs. 17.1 and 17.2).
•Premature infants are at increased risk for inguinal hernia, with incidence rates of 2 % in females and 7–30 % in males.
•Approximately 5 % of all males develop a hernia during their lifetime.
•Inguinal hernias are much more common in males than in females.
•The male-to-female ratio is estimated to be 4–8:1.
•Moreover, the risk of incarceration of inguinal hernia is more than 60 % in prematures.
•Inguinal hernias:
–60 % are on the right side.
–30 % are on the left side.
–10 % are bilateral (Figs. 17.3 and 17.4)
–Anatomically speaking, indirect and direct inguinal hernias differ in that the direct
© Springer International Publishing Switzerland 2017 |
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A.H. Al-Salem, An Illustrated Guide to Pediatric Urology, DOI 10.1007/978-3-319-44182-5_17 |
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17 Inguinal Hernias and Hydroceles |
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Figs. 17.1 and 17.2 Clinical photographs showing a large right and left inguinal hernia
Figs. 17.3 and 17.4 A clinical photograph showing bilateral inguinal hernias
hernia bulges through the inguinal floor medial to the inferior epigastric vessels and the indirect hernia arises lateral to the inferior epigastric vessels.
–Inguinal hernia can be complete where the whole sac descends into the scrotum and surrounds the tesis (Scrotal hernia) or incomplete where the hernial sac ends up in the inguinal canal above the testis (Inguinal hernia) (Fig. 17.5).
17.2.2 Etiology
•Inguinal hernias are congenital.
•Embryologically, the processus vaginalis is an outpouching of peritoneum attached to the testicle that trails behind as it descends retroperitoneally into the scrotum.
•Normally, the processus vaginalis obliterates.
•When obliteration of the processus vaginalis fails to occur, inguinal hernia results.
17.2 Inguinal Hernia |
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Fig. 17.5 Diagrammatic representation of the classic inguinal hernia and inguinal hernia extending into the scrotum (scrotal hernia)
INGUINAL
HERNIA
SCROTAL
HERNIA
•Increased intra-abdominal pressure is seen in a variety of conditions and also contribute to the appearance of inguinal hernia.
•Elevated intra-abdominal pressure is associated with chronic cough, ascites, increased peritoneal fluid from biliary atresia, peritoneal dialysis or ventriculoperitoneal shunts, intraperitoneal masses or organomegaly, and constipation.
•Other conditions with increased incidence of inguinal hernias are:
–Exstrophy of bladder.
–Neonatal intraventricular hemorrhage.
–Myelomeningocele.
–Undescended testes.
•The following conditions are associated with an increased risk of inguinal hernia:
–Prematurity and low birth weight.
–Urologic conditions:
•Cryptorchidism
•Hypospadias
•Epispadias
•Exstrophy of the bladder
•Ambiguous genitalia
•Cloacal exstrophy
–Patent processus vaginalis, which may be present because of increased intraabdominal pressure due to ventriculoperitoneal shunts, peritoneal dialysis, or ascites
–Abdominal wall defects
•Gastroschisis
•Omphalocele
–Family history
–Meconium peritonitis
–Cystic fibrosis
–Connective tissue disease
–Mucopolysaccharidosis
–Congenital dislocation of the hip
–Ehlers-Danlos syndrome
–Marfan syndrome
–Fetal hydrops
–Liver disease with ascites
–Ventriculoperitoneal shunting for hydrocephalus
17.2.3 Clinical Features
•The parents of infants and children with an inguinal hernia present with the history of a swelling that is commonly intermittent, in the inguino-scrotal region in boys and inguinolabial region in girls.
•The swelling commonly occurs after crying or straining.
•Sometimes, they present with an obvious swelling at the inguinal region or sometimes within the scrotum in boys (Fig. 17.6).
•The hernia may be bilateral (Figs. 17.7 and 17.8)
•The swelling is painless and reducible in a simple inguinal hernia.
•The presence of a painful swelling suggests an incarcerated inguinal hernia.
•Patients with an incarcerated hernia generally present with a tender firm mass in the inguinal canal or scrotum that is irreducible.
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17 Inguinal Hernias and Hydroceles |
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Fig. 17.6 |
A clinical |
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photograph showing an |
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incarcerated right inguinal |
INGUINAL |
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hernia. Note also the left |
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HERNIA |
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hydrocele |
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HYDROCELE
Figs. 17.7 and 17.8 Clinical photographs showing bilateral incarcerated inguinal hernia
•Silk sign: When the hernia sac is palpated over the cord structures, the sensation may be similar to that of rubbing two layers of silk together.
•This finding is known as the silk sign and is highly suggestive of an inguinal hernia.
17.2.4 Variants of Hernia
1.Indirect inguinal hernia:
•Indirect inguinal hernias occur when the abdominal contents protrude through the deep inguinal ring, lateral to the inferior epigastric vessels.
17.2 Inguinal Hernia |
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Fig. 17.9 Diagrammatic representation of a Littre’ hernia
MECKEL
DIVERTICULUM
IN A HERNIAL SAC
Fig. 17.10 Diagrammatic representation of a Richter’s hernia
PART OF THE
BOWEL WALL
•It is caused by failure of embryonic closure of the processus vaginalis.
2.Direct inguinal hernia:
•This type of inguinal hernia, enters through a weak point in the transversalis fascia of the abdominal wall, and its sac is noted to be medial to the inferior epigastric vessels.
•Direct inguinal hernias may occur in males or females, but males are ten times more likely to get a direct inguinal hernia.
•These hernias are capable of exiting via the superficial inguinal ring but, unlike indirect inguinal hernias, they cannot descend into the scrotum.
3.Littre’s hernia (Fig. 17.9):
•A Littre’s hernia is a hernia containing a Meckel’s diverticulum.
•Littre’s hernia was first described by the French surgeon Alexis Littré in 1700.
•He described three cases from cadaverous studies of incarcerated femoral hernias
containing a diverticulum of the small bowel.
4.Sliding inguinal hernia:
•A sliding inguinal hernia occurs when the wall of the hernia sac is made up of an organ like the urinary bladder or colon.
•It is a variant that is seen in 3% of hernia cases.
5.Richter’s hernia (Fig. 17.10):
•A Richter’s hernia occurs when the antimesenteric wall of the intestine protrudes through a hernial defect.
•The first scientific description of this hernia was by August Gottlob Richter in 1778.
•A Richter’s hernia can result in strangulation and necrosis in the absence of intestinal obstruction.
•It is a relatively rare but dangerous type of hernia.
6.Busse’s hernia (Fig. 17.11):
•An inguinal hernia in which the testicle is within the hernia sac.
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17 Inguinal Hernias and Hydroceles |
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7. Maydl’s hernia (Fig. 17.12): |
• This intervening portion of bowel becomes |
• This is seen when two adjacent loops of |
deprived of its blood supply and eventually |
small intestines are within a hernial sac |
becomes ischemic and necrotic. |
with a tight neck. |
• Perforation of this part of intestine will |
• The intervening portion of bowel lies |
lead to peritonitis and the patient present |
within the abdomen |
with an acute abdomen. |
8. |
Amyand’s hernia (Fig. 17.13): |
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• The content of the hernial sac is the vermi- |
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form appendix. |
17.2.5 Complications of Inguinal
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Hernias |
1. |
Incarceration: |
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• The herniated bowel in inguinal hernia can |
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become swollen, edematous and engorged |
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within the hernial sac. |
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• The hernia becomes irreducible and causes |
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intestinal obstruction in infants and chil- |
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dren (Figs. 17.14, 17.15, 17.16, and 17.17). |
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• Every attempt should be made to reduce it |
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manually. |
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• Incarceration occurs in 17 % of right-sided |
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hernias and 7 % of left-sided hernias. |
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• More than 50 % of cases of incarceration |
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occur within the first 6 months of life; |
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the risk gradually decreases after age |
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1 year. |
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• Premature infants have twice the risk of |
Fig. 17.11 Diagrammatic representation of Busse’s |
incarceration than the general pediatric |
hernia |
population. |
MAYDLE’S HERNIA
Fig. 17.12 A diagrammatic representation of Maydle’s hernia
17.2 Inguinal Hernia |
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Fig. 17.13 A diagrammatic representation of Amyand’s hernia
APPENDIX IN A
HERNIAL SAC
Figs. 17.14, 17.15, 17.16, and 17.17 Clinical photographs showing irreducible inguinal hernias