Pediatric Abdominal Wall Hernias

INGUINAL HERNIAS

Inguinal hernias were first described in the Ebers Papyrus in 1550 BC.
In AD 150, Galen defined hernias as a rupture of the peritoneum, and in the 16th century, Ambrose Paré documented the need for repair of hernias in childhood.¹
In the 1800s, the involved anatomic structures were discovered and surgical techniques for repair were developed.
Gross performed a large series of hernia repairs in 1953, reporting a recurrence rate of 0.45%.¹

EMBRYOLOGY

The processus vaginalis forms during the third month of gestation from an outpouching of the peritoneum, creating a diverticulum at the internal ring.
In males, the processus vaginalis obliterates spontaneously after the descent of the testes, usually by 2 years of age.
In females, the processus vaginalis correlates to the diverticulum of Nuck and normally obliterates at 7 months’ gestation.

RELEVANT ANATOMY

The inguinal canal is a channel through the abdominal wall through which
- The spermatic cord extends from the abdomen into the scrotum in males (Figure 28.1).
- The round ligament extends from the abdomen into the labia majora in females.
The canal is bordered by the aponeurosis of the external oblique muscle anteriorly and the transversus abdominus muscle and the transversalis fascia posteriorly.
Hesselbach triangle is an area of risk for direct herniation and is bounded by the inferior epigastric vessels, the inguinal ligament, and the rectus abdominus.
The external inguinal ring, formed by the external oblique muscle, is located superior and lateral to the pubic tubercle.
The internal inguinal ring is located in the transversalis fascia.
In infants the external ring lies almost directly over the internal ring, which leads to increased risk of herniation.
A congenital indirect inguinal herniation is the protrusion of fat or bowel through the processus vaginalis through the internal and external rings.
A direct inguinal herniation is the protrusion of fat or bowel through the Hesselbach triangle and through the external ring.
An incarcerated hernia is one that can no longer be reduced, while a strangulated hernia is one that has a compromised vascular supply.

Figure 28.1 Inguinal hernia anatomy. (Reprinted with permission from Moore KL, Dalley AF, Agur AMR. Clinically Oriented Anatomy. 6th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2010:213.)

EPIDEMIOLOGY AND ETIOLOGY

Incidence: The overall incidence of inguinal hernias in children is 4/100 live births.

Males are affected approximately 10 times more frequently than females.
Of inguinal hernias, 60% to 75% occur on the right side, and 15% to 20% of cases are bilateral.
Preterm infants also have an increased risk with 30% of infants weighing less than 1 kg developing inguinal hernias.²
The rate of incarceration is between 5% to 15% in the pediatric hernia population, with preterm infants having higher rates of up to 31%.²
Peak incidence is during the first 3 months of life.⁴
Most inguinal hernias are indirect; direct hernias are rare at this age.

Etiology:

The predominance of congenital inguinal hernias is due to failure of the proximal processus vaginalis to close (Figure 28.2).
This closure is thought to be hindered by the persistence of smooth muscle.³

CLINICAL PRESENTATION

Classic presentation: An infant presents with an intermittent bulge in the groin, scrotum, or labia.

The bulge is often exacerbated by increased intra-abdominal pressures, for example, when an infant cries or has a bowel movement.
Examiners should palpate the external ring with 1 finger to feel for the spermatic cord and associated structures.
If a hernia is present, often the “silk glove sign” or thickening of the spermatic cord/associated structures will be evident.
This clinical sign has a diagnostic sensitivity of 91% and a specificity of 97.3%.²
Diagnosis of an inguinal hernia is often a clinical diagnosis.

DIAGNOSIS

Laboratory Findings

Routine laboratory work is not helpful in the evaluation of patients with inguinal hernias.
One study of 69 infants with incarcerated hernias found no correlation between white blood cell count and degree of vascular compromise.³

Figure 28.2 Patent processus vaginalis. A, When the uterus forms, the caudal ligament is interrupted in its course by growth of the uterus and becomes attached to the uterine wall. The part of the ligament from the ovary to this wall forms the proper ligament of the ovary, while the part extending from the wall to the labia majora forms the round ligament of the uterus. In addition, a cranial ovarian ligament, the suspensory ligament, forms from urogenital ridge mesoderm to hold the ovary in place at this pole. In males, the caudal genital ligament becomes surrounded by a band of mesenchyme tissue called the gubernaculum testis. B, Initially, this tissue band terminates in the inguinal region, but later it grows down to the floor of the scrotum. The gubernaculum is largely responsible for pulling the testes into the scrotum. Thus, outgrowth of the gubernaculum from the inguinal region to the scrotum pulls the testes to the inguinal area; then, as organ growth occurs and intra-abdominal pressure increases, the testes are pushed into and through the inguinal canal. The testes reach the inguinal region by 12 weeks, pass through the inguinal canal by 28 weeks, and reach the scrotum by 33 weeks. To pass from their intraabdominal position of origin to the scrotum, the testes must migrate through the abdominal wall via the inguinal canal. They are preceded in this maneuver by an outpocketing of peritoneum called the processes vaginalis (B). (Reprinted with permission from Sadler TW, Langman J, Sadler TW. Langman’s Essential Medical Embryology. Philadelphia, PA: Lippincott Williams & Wilkins; 2005.)

Only gold members can continue reading. Log In or Register to continue