Inguinal Hernias

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Chapter 338 Inguinal Hernias

Inguinal hernias are one of the most common conditions seen in pediatric practice. The frequency of this condition in concert with its potential morbidity of ischemic injury to the intestine, testis, or ovary makes proper diagnosis and management an important part of daily practice for pediatric practitioners and pediatric surgeons. The overwhelming majority of inguinal hernias in infants and children are congenital indirect hernias (99%) as a consequence of a patent processus vaginalis. The incidence is up to 10 times higher in boys than in girls. Other types of inguinal hernias include direct or acquired (0.5-1.0%) and femoral (<0.5%). Approximately one half of inguinal hernias manifest clinically in the 1st year of life, most in the 1st 6 mo. Premature infants have an incidence of inguinal hernia approaching 30%. The risk of incarceration and possible strangulation of an inguinal hernia is greatest in the 1st year of life (30-40%) and mandates prompt identification and operative repair to minimize morbidity and complications.

Embryology and Pathogenesis

Indirect inguinal hernias in infants and children are congenital and result from an arrest of embryologic development, failure of obliteration of the processus vaginalis, rather than an acquired muscular weakness. The pertinent developmental anatomy of congenital indirect inguinal hernia relates to development of the gonads and descent of the testis through the internal ring and into the scrotum late in gestation. The gonads develop near the kidney as a result of migration of primitive germ cells from the yolk sac to the genital ridge, which is completed by 6 wk of gestation. Differentiation into testis or ovary occurs by 7 or 8 wk of gestation under hormonal influences. The testes descend from the urogenital ridge in the retroperitoneum to the area of the internal ring by about 28 wk of gestation. The final descent of the testes into the scrotum occurs late in gestation between weeks 28 and 36. The testis is preceded in descent to the scrotum by the gubernaculum and the processus vaginalis. The processus vaginalis is present in the developing fetus at 12 wk of gestation as a peritoneal outpouching that extends through the internal inguinal ring and accompanies the testis as it exits the abdomen and descends into the scrotum.

The gubernaculum testis forms from the mesonephros (developing kidney), attaches to the lower pole of the testis, and directs the testis through the internal ring and inguinal canal and into the scrotum. The testis passes through the inguinal canal in a few days but takes about 4 wk to migrate from the external ring to the scrotum. The cordlike structures of the gubernaculum occasionally pass to ectopic locations (perineum or femoral region), resulting in ectopic testes.

In the last few weeks of gestation or shortly after birth, the layers of the processus vaginalis normally fuse together and obliterate the patency from the peritoneal cavity through the inguinal canal to the testis. The processus vaginalis also obliterates just above the testes, and the portion of the processus vaginalis that envelops the testis becomes the tunica vaginalis. In girls, the processus vaginalis obliterates earlier, at about 7 mo of gestation. Failure of the processus vaginalis to close permits fluid or abdominal viscera to escape the peritoneal cavity and accounts for a variety of inguinal-scrotal abnormalities seen in infancy and childhood. The ovaries descend into the pelvis from the urogenital ridge but do not exit from the abdominal cavity. The cranial portion of the gubernaculum in girls differentiates into the ovarian ligament, and the inferior aspect of the gubernaculum becomes the round ligament, which passes through the internal ring and attaches to the labia majora. The processus vaginalis in girls extends into the labia majora through the inguinal canal and is also known as the canal of Nuck.

Androgenic hormones, adequate end-organ receptors, and mechanical factors such as increased intra-abdominal pressure influence complete descent of the testis through the inguinal canal. The testes and spermatic cord structures (spermatic vessels and vas deferens) are located in the retroperitoneum but are affected by increases in intra-abdominal pressure as a consequence of their intimate attachment to the processus vaginalis. The genitofemoral nerve also has an important role: It innervates the cremaster muscle, which develops within the gubernaculum, and experimental division or injury to both nerves in the fetus prevents testicular descent. Failure of regression of smooth muscle (present to provide the force for testicular descent) might have a role in the development of indirect inguinal hernias. Several studies have investigated genes involved in the control of testicular descent for their role in closure of the patent processus vaginalis, for example, hepatocyte growth factor and calcitonin gene-related peptide. Unlike in adult hernias, there does not appear to be any change in collagen synthesis associated with inguinal hernias in children (Fig. 338-1).

image

Figure 338-1 Hernia and hydroceles.

(Modified from Scherer LR III, Grosfeld JL: Inguinal and umbilical anomalies, Pediatr Clin North Am 40: 1121–1131, 1993.)

Pathology

Closure of the processus vaginalis is often incomplete at birth; closure continues postnatally, and the rate of patency is inversely proportional to the age of the child. It has been estimated that ~40% close during the first months of life and that ~20% of boys have a persistent patency of the processus vaginalis at 2 yr of age. Patency of the processus vaginalis after birth is a potential hernia, but not all patients with a patent processus vaginalis develop a clinical hernia. An inguinal hernia occurs when intra-abdominal contents escape the abdominal cavity and enter the inguinal region through a patent processus vaginalis. Based on their location in the inguinal canal (lateral to the inferior epigastric vessels), they are indirect inguinal hernias but are rarely associated with a muscular weakness or defect, as is typical of an adult hernia. Depending on the extent of patency of the distal processus, the hernia may be confined to the inguinal region or pass down into the scrotum. Complete failure of obliteration of the processus predisposes to a complete inguinal hernia characterized by a protrusion of abdominal contents into the inguinal canal and possibly extending into the scrotum. Obliteration of the processus vaginalis distally (around the testis) with patency proximally results in the classic indirect inguinal hernia with the protrusion in the inguinal canal.

A hydrocele is when only fluid enters the patent processus vaginalis and the swelling may exist only in the scrotum (scrotal hydrocele), only along the spermatic cord in the inguinal region (hydrocele of the spermatic cord), or extend from the scrotum through the inguinal canal and even into the abdomen (abdominal-scrotal hydrocele). A hydrocele is termed a communicating hydrocele if it demonstrates fluctuation in size, often increasing in size after activity and, at other times, being smaller when the fluid decompresses into the peritoneal cavity. Occasionally, hydroceles in older children follow trauma, inflammation, or tumors affecting the testis. Although reasons for failure of closure of the processus vaginalis are unknown, it is more common in cases of testicular nondescent and prematurity. In addition, persistent patency of the processus vaginalis is twice as common on the right side, presumably related to later descent of the right testis and interference from the developing inferior vena cava and external iliac vein. Risk factors identified as contributing to the development of congenital inguinal hernia relate to conditions that predispose to failure of obliteration of the processus vaginalis and are listed in Table 338-1. Incidence of inguinal hernia in patients with cystic fibrosis is ~15%, believed to be related to an altered embryogenesis of the wolffian duct structures, which leads to an absent vas deferens in males with this condition. There is also an increased incidence of inguinal hernia in patients with testicular feminization syndrome and other forms of ambiguous genitalia. The rate of recurrence after repair of an inguinal hernia in patients with a connective tissue disorder approaches 50%, and often the diagnosis of connective tissue disorders in children results from investigation after development of a recurrent inguinal hernia.

Clinical Presentation

An inguinal hernia typically appears as a bulge in the inguinal region or extending through the inguinal region into the scrotum. In girls, the mass typically occurs in the upper portion of the labia majora. The bulge or mass is most visible at times of irritability or increased intra-abdominal pressure (crying, straining, coughing). It may be present at birth or might not appear until weeks, months, or years later. The bulge is most often 1st noted by the parents or on routine examination by the primary care physician. The classic history from the parents is of intermittent groin, labial, or scrotal swelling that spontaneously reduces but that is gradually enlarging or is more persistent and is becoming more difficult to reduce. The hallmark signs of an inguinal hernia on physical examination are a smooth, firm mass that emerges through the external inguinal ring lateral to the pubic tubercle and enlarges with increased intra-abdominal pressure. When the child relaxes, the hernia typically reduces spontaneously or can be reduced by gentle pressure, 1st posteriorly to free it from the external ring and then upward toward the peritoneal cavity.

Methods used to demonstrate the hernia on examination vary depending on the age of the child. A quiet infant can be made to strain the abdominal muscles by stretching him or her out supine on the bed with legs extended and arms held straight above the head. Most infants struggle to get free, thus increasing the intra-abdominal pressure and pushing out the hernia. Older patients can be asked to perform the Valsalva maneuver by blowing up a balloon or coughing. The older child should be examined while standing, and examination after voiding can also be helpful. With increased intra-abdominal pressure, the protruding mass is obvious on inspection of the inguinal region or can be palpated by an examining finger invaginating the scrotum to palpate at the external ring. In the female infant, the ovary and fallopian tube can be contained within the hernia sac, presenting as a firm, discrete, nontender mass in the labia. Another test is the “silk glove sign,” which describes the feeling of the layers of the hernia sac (processus vaginalis) as they slide over the spermatic cord structures, with rolling of the spermatic cord beneath the index finger at the pubic tubercle; this physical finding has a sensitivity of 91% and a specificity of 97.3%. If the bulge is located below the inguinal canal on the medial aspect of the thigh, a femoral hernia should be suspected. In the absence of a bulge, the finding of increased thickness of the inguinal canal structures on palpation also suggests the diagnosis of an inguinal hernia. It is important on examination to note the position of the testes because retractile testes are common in infants and young children and can mimic an inguinal hernia with a bulge in the region of the external ring. Because in the female patient ~20-25% of inguinal hernias are sliding hernias (the contents of the hernia sac are adherent within the sac and therefore not reducible), a fallopian tube or ovary can be palpated in the inguinal canal.

Evaluation of Acute Inguinal-Scrotal Swelling

Occasionally, an inguinal-scrotal mass appears suddenly in an infant or child and is associated with discomfort. The differential diagnosis includes incarcerated inguinal hernia, acute hydrocele, torsion of an undescended testis, and suppurative inguinal lymphadenitis. Differentiating between the incarcerated inguinal hernia and the acute hydrocele is probably the most difficult. The infant or child with an incarcerated inguinal hernia is likely to have associated findings suggesting intestinal obstruction, such as colicky abdominal pain, abdominal distention, vomiting, and cessation of stool, and might appear ill. The infant with an acute hydrocele might have discomfort but is consolable and tolerates feedings without signs or symptoms suggesting intestinal obstruction. When the diagnosis is incarcerated inguinal hernia, plain radiographs typically demonstrate multiple air-fluid levels.

On examination of the child with the acute hydrocele, the clinician may note that the mass is somewhat mobile. In addition, in the area between the suspected hydrocele mass and the internal ring, the cord structures can appear only slightly thickened. With the incarcerated hernia, there is a lack of mobility of the groin mass and marked swelling or mass extending from the scrotal mass through the inguinal area and up to and including the internal ring. An experienced clinician can use a bimanual examination to help differentiate groin abnormalities. The examiner palpates the internal ring per rectum, with the other hand placing gentle pressure on the inguinal region over the internal ring. In cases of an indirect inguinal hernia, an intra-abdominal organ can be palpated extending through the internal ring.

Another method is transillumination. It must be noted that transillumination can be misleading because the thin wall of the infant’s intestine can approximate that of the hydrocele wall and both might transilluminate. This is also the reason aspiration to determine the contents of a groin mass is discouraged. Ultrasonography can help distinguish between a hernia and a hydrocele. An expeditious diagnosis is important to avoid the potential complications of an incarcerated hernia, which can develop rapidly. Diagnostic laparoscopy has emerged as an effective and reliable tool in this setting but requires general anesthesia.

The occurrence of suppurative adenopathy in the inguinal region can be confused with an incarcerated inguinal hernia. Examination of the watershed area of the inguinal lymph node might reveal a superficial infected or crusted lesion. In addition, the swelling associated with inguinal lymphadenopathy is typically located more inferior and lateral than the mass of an inguinal hernia, and there may be other associated nodes in the area. Torsion of an undescended testis can manifest as a painful erythematous mass in the groin. The absence of a gonad in the scrotum in the ipsilateral side should clinch this diagnosis.

Incarcerated Hernia

With incarcerated hernia, the contents of the hernia sac cannot be reduced into the abdominal cavity. Contained structures can include small bowel, appendix, omentum, colon, or, rarely, Meckel diverticulum. In girls, the ovary, fallopian tube, or both are commonly incarcerated. Rarely, the uterus in infants can also be pulled into the hernia sac. A strangulated hernia is one that is tightly constricted in its passage through the inguinal canal and, as a result, the hernia contents have become ischemic or gangrenous.

Although incarceration may be tolerated in adults for years, most nonreducible inguinal hernias in children, unless treated, rapidly progress to strangulation with potential infarction of the hernia contents. Initially, pressure on the herniated viscera as they pass through the internal ring, inguinal canal, and external ring leads to impaired lymphatic and venous drainage. This leads, in turn, to swelling of the herniated viscera, which further increases the compression in the inguinal canal, ultimately resulting in total occlusion of the arterial supply to the trapped viscera. Progressive ischemic changes take place, culminating in gangrene and/or perforation of the herniated viscera. The testis is also at risk of ischemia because of compression of the spermatic cord structures by the strangulated hernia. In girls, herniation of the ovary places it at risk of strangulation and torsion. The incidence of incarceration of an inguinal hernia is between 12% and 17%. Two thirds of incarcerated hernias occur in the 1st year of life. The greatest risk is in infancy, with reported incidences of between 25% and 30% for infants <6 mo of age. The incidence of incarceration is slightly less in premature infants, although the reasons are unclear.

The symptoms of an incarcerated hernia are irritability, pain in the groin and abdomen, abdominal distention, and vomiting. A somewhat tense, nonfluctuant mass is present in the inguinal region and can extend down into the scrotum or labia majora. The mass is well defined, may be tender, and does not reduce. With the onset of ischemic changes, the pain intensifies, and the vomiting becomes bilious or feculent. Blood may be noted in the stools. The mass is typically tender, and there is often edema and erythema of the overlying skin, with fever and signs of intestinal obstruction. The testes may be normal or may be swollen and hard on the affected side because of venous congestion resulting from compression of the spermatic veins and lymphatic channels at the inguinal ring by the tightly strangulated hernia mass. Abdominal radiographs demonstrate features of partial or complete intestinal obstruction, and gas within the incarcerated bowel segments may be seen below the inguinal ligament or within the scrotum.

Ambiguous Genitalia

Infants with disorders of sexual development commonly present with inguinal hernias, often containing a gonad, and require special consideration. In female infants with inguinal hernias, particularly if the presentation is bilateral inguinal masses, testicular feminization syndrome should be suspected because >50% of patients with testicular feminization have an inguinal hernia (Chapter 577). Conversely, the true incidence of testicular feminization in all female infants with inguinal hernias is difficult to determine but is ~1%. In phenotypic females, if the diagnosis of testicular feminization is suspected preoperatively, the child should be screened with a buccal smear for Barr bodies and appropriate genetic evaluation before proceeding with the hernia repair. The diagnosis of testicular feminization is occasionally made at the time of operation by identifying an abnormal gonad (testis) within the hernia sac or absence of the uterus on rectal examination. In the normal female infant, the uterus is easily palpated as a distinct midline structure beneath the symphysis pubis on rectal examination. Preoperative diagnosis of testicular feminization syndrome or other disorders of sexual development such as mixed gonadal dysgenesis and selected pseudohermaphrodites enables the family to receive counseling, and gonadectomy can be accomplished at the time of the hernia repair.

Management

The presence of an inguinal hernia in the pediatric age group constitutes the indication for operative repair. An inguinal hernia does not resolve spontaneously, and early repair eliminates the risk of incarceration and the associated potential complications, particularly in the 1st 6-12 mo of life. The timing of operative repair depends on several factors including age, general condition of the patient, and comorbid conditions. In infants <1 yr of age with an inguinal hernia, repair should proceed promptly because as many as 70% of incarcerated inguinal hernias requiring emergency operation for reduction and repair occur in the 1st year of life. In addition, the incidence of testicular atrophy after incarceration in infants <3 mo of age has been reported as high as 30%. In children >1 yr, the risk of incarceration is less and the repair can be scheduled with less urgency. For the routine reducible hernia, the operation should be carried out electively shortly after diagnosis. Elective inguinal hernia repair can be safely performed in an outpatient setting with an expectation for full recovery within 48 hr. The operation should be performed at a facility with the ability to admit the patient to an inpatient unit as needed. Certain conditions can dictate postponement of repair, such as marked prematurity, intercurrent pneumonia (especially respiratory syncytial virus [RSV]), other infections, or severe congenital heart disease. In cases of marked prematurity (1,800-2,000 g), repair is typically performed before discharge from the neonatal intensive care unit.

The operation is most often performed under general anesthesia, but it can be performed under spinal or caudal anesthesia if avoidance of intubation is preferable due to chronic lung disease or bronchopulmonary dysplasia. Prophylactic antibiotics are not routinely used except for associated conditions such as congenital heart disease or the presence of a venticuloperitoneal shunt. Preterm infants mandate special consideration because of their higher risk for apnea and bradycardia after general anesthesia (Chapter 70). Infants <44 wk postconceptional age and full-term infants <3 mo of age and with comorbid conditions should be observed overnight with appropriate apnea and cardiorespiratory monitors.

An incarcerated, irreducible hernia without evidence of strangulation in a clinically stable patient should initially be managed nonoperatively. Unless there is clear peritonitis or bowel compromise, incarcerated hernias can usually be reduced manually using a technique called taxis. Manual reduction is performed first with traction caudad and posteriorly to free the mass from the external inguinal ring, and then upward to reduce the contents back into the peritoneal cavity. The attempt should not be continued if the infant is crying and resisting the pressure on the hernia. The use of sedation or analgesia before attempting reduction can be helpful; this reduces intra-abdominal pressure and relieves the pressure on the neck of the hernia sac at the inguinal ring. Care must be taken to avoid respiratory depression, especially in the premature infant. Other techniques advocated to assist in the nonoperative reduction of an incarcerated inguinal hernia include elevation of the lower torso and legs and brief exposure to an ice pack. Many practitioners do not favor the use of an ice pack in infants because of the risk of hypothermia. If reduction is successful but difficult, the patient should be observed to ensure that feedings are tolerated and there is no concern that necrotic intestine was reduced. Because of the high risk for early recurrent incarceration, surgical repair is performed 24-48 hr later, by which time there is less edema, handling of the sac is easier, and the risk of complications is reduced.

A common presentation in female patients is an irreducible ovary in the inguinal hernia in an otherwise asymptomatic patient. The inguinal mass is soft and nontender to gentle exam, and there is no swelling or edema; thus, there are no findings suggesting strangulation. This represents a “sliding” hernia with the fallopian tube and ovary fused to the posterior-medial wall of the hernia sac. Overzealous attempts to reduce the hernia are unwarranted and potentially harmful to the tube and ovary. The risk that incarceration of the ovary in this setting will lead to strangulation is not known. Most pediatric surgeons recommend elective repair of the hernia within 24-48 hr. For any patient who presents with a prolonged history of incarceration, signs of peritoneal irritation, or small bowel obstruction, surgery and operative reduction and repair of the hernia should be performed.

Operative Management

When the hernia cannot be reduced or is strangulated, immediate operation is indicated to prevent further damage to the contents of the hernia sac or testis. If there are signs of intestinal obstruction or strangulation, initial management includes nasogastric intubation, intravenous fluids, and administration of broad-spectrum antibiotics. When fluid and electrolyte imbalance has been corrected and the child’s condition is satisfactory, exploration is undertaken. The operation consists of reduction of the contents of the hernia sac, separation of the hernia sac from the spermatic cord vessels and vas deferens in the inguinal canal, and high ligation of the hernia sac at the internal ring. Resection of nonviable structures within the hernia sac or of an infarcted testis may be indicated based on the experience and judgment of the surgeon. Although the testis might appear ischemic, most patients recover after the incarceration is relieved and do not require removal.

The elective operative repair of a congenital indirect inguinal hernia is straightforward and consists of high ligation of the hernia sac (patent processus vaginalis) at the level of the internal ring, thus preventing protrusion of abdominal contents into the inguinal canal. In boys, this requires careful separation of the sac from the spermatic cord structures and avoidance of injury to these vital structures. An associated hydrocele, present ~20% of the time, is released anteriorly to avoid injury to the spermatic cord structures located posteriorly. In girls, surgical repair is simpler because the hernia sac and round ligament can be ligated without concern for injury to the ovary and its blood supply, which generally remain within the abdomen. The fallopian tube is routinely visualized to rule out testicular feminization syndrome. If the ovary and fallopian tube are within the sac and not reducible, most often the sac is ligated distal to these structures and the internal ring is closed after reducing the sac and its contents to the abdominal cavity.

Contralateral Inguinal Exploration

Controversy exists regarding when to proceed with contralateral groin exploration in infants and children with a unilateral indirect inguinal hernia. The only purpose of contralateral exploration is to avoid the occurrence of a hernia on that side at a later date (metachronous hernia). The incidence of a contralateral patent processus vaginalis is ~60% at 2 mo of age and decreases to ~20% at 2 yr of age. A patent processus represents only a potential hernia, and many risk factors influence the likelihood of development of an actual inguinal hernia.

The advantages of contralateral exploration include avoidance of parental anxiety and possibly a second anesthesia, the cost of additional surgery, and the risk of contralateral incarceration. The disadvantages include potential injury to the spermatic cord vessels, vas deferens, and testis; increased operative time; and the fact that, in many infants, it is an unnecessary procedure. The relevant issues in the debate revolve around the frequency of occurrence of contralateral hernias after one-sided hernia repair and the relation of this to age, gender, and side of the clinically apparent hernia. Historically, most large series noted a chance of developing a contralateral hernia as 30-40% in children <2 yr of age, leading most pediatric surgeons to recommend routine contralateral exploration in this age group. The risk of injury to the spermatic cord or vas deferens with inguinal exploration has been estimated in some studies to be as low as 1% and by others as high as 30%. When boys were studied 8 to 20 yr after inguinal hernia repair, 5.8% of them had decreased testicular size on the side of the repair and 1% had testicular atrophy. Most pediatric surgeons believe that routine open contralateral exploration is indicated selectively in high-risk patients for contralateral hernia. In girls, because of the higher incidence of bilateral inguinal hernias and elimination of concern for injury to the spermatic cord or testis, routine contralateral exploration has been recommended up to age 5 or 6 yr. Infants and children with risk factors for development of an inguinal hernia or with medical conditions that increase the risk of general anesthesia should be approached with a low threshold for routine contralateral exploration.

Laparoscopy enables assessment of the contralateral side without risk of injury to the spermatic cord structures or testis. This procedure can be performed through an umbilical incision or by passing a 30-degree or 70-degree oblique scope through the open hernia sac just before ligation of the hernia sac on the involved side. If patency of the contralateral side is demonstrated, the surgeon can proceed with bilateral hernia repair, and if the contralateral side is properly obliterated, exploration and potential complications are avoided. The downside of this approach is that laparoscopy cannot differentiate between a patent processus vaginalis and a true hernia (Figs. 338-2 and 338-3).

Direct Inguinal Hernia

Direct inguinal hernias are rare in children. Direct hernias appear as groin masses that extend toward the femoral vessels with exertion or straining. The etiology is from a muscular defect or weakness in the floor of the inguinal canal medial to the epigastric vessels. Thus, direct inguinal hernias in children are generally considered an acquired defect. In one third of cases, the patient has a history of a prior indirect hernia repair on the side of the direct hernia, which suggests a possible injury to the floor muscles of the inguinal canal at the time of the first herniorrhaphy. Patients with connective tissue disorders such as Ehlers-Danlos syndrome or Marfan syndrome and mucopolysaccharidosis such as Hunter-Hurler syndrome are at increased risk for the development of direct inguinal hernias either independently or after indirect inguinal hernia repair.

Operative repair of a direct inguinal hernia involves strengthening of the floor of the inguinal canal, and many standard techniques have been described, similar to repair techniques used in adults. The repair can be performed through a single limited incision and, therefore, laparoscopic repair does not offer any significant advantage. Recurrence after repair, in contrast to that in adults, is extraordinarily rare. Because typically the area of muscular weakness is small and pediatric tissues have greater elasticity, primary repair is usually possible. Prosthetic material for direct hernia repair or other approaches, such as preperitoneal repair, are rarely required in the pediatric age group. The older child with a direct inguinal hernia and a connective tissue disorder may be the exception, and a laparoscopic approach and prosthetic material in such a case can be useful for repair.

Complications

Complications after elective inguinal hernia repair are uncommon (1.5%) but significantly higher in association with incarceration (10%). Some complications are related to technical factors (recurrence, iatrogenic cryptorchidism), whereas others are related to the underlying process, such as bowel ischemia, gonadal infarction, and testicular atrophy related to an incarcerated hernia. The majority of complications are related to episodes of incarceration or occur after emergency operative reduction and hernia repair.

Injury to the Vas Deferens and Male Fertility

Similar to the gonadal vessels, the vas deferens can be injured as a consequence of compression from an incarcerated hernia or during operative repair. This injury is almost certainly underreported because it is unlikely to be recognized until adulthood and, even then, possibly only if the injury is bilateral. Although the vulnerability of the vas deferens has been documented in many studies, no good data exist as to the actual incidence of this problem. One review reported an incidence of injury to the vas deferens of 1.6% based on pathology demonstrating segments of the vas deferens in the hernia sac specimen; this may be overstated, because others have shown that small glandular inclusions found in the hernia sac can represent müllerian duct remnants and are of no clinical importance.

The relationship between male fertility and previous inguinal hernia repair is also unknown. There appears to be an association between infertile males with testicular atrophy and abnormal sperm count and a previous hernia repair. A relationship has also been reported between infertile males with spermatic autoagglutinating antibodies and previous inguinal hernia repair. The proposed etiology is that operative injury to the vas deferens during inguinal hernia repair might result in obstruction of the vas with diversion of spermatozoa to the testicular lymphatics, and this breach of the blood-testis barrier produces an antigenic challenge, resulting in formation of spermatic autoagglutinating antibodies.

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