Etiology

Inguinal hernia occurs because of a defect in the structure of the inguinal canal that may be either congenital or acquired.

  1. Congenital forms of indirect hernia occur because the processus vaginalis fails to undergo regression.

  2. Acquired defects occur because of degeneration and fatty changes in the tissues of the inguinal floor. Progressive myopectineal degeneration leads to weakness, resulting in dilation of the internal ring (an opening in the transversalis fascia) and/or direct weakness of the posterior wall of the inguinal canal.

There is a familial or hereditary predisposition to development of inguinal hernia.[15][16]

Connective tissue disorders such as Marfan syndrome and Ehlers-Danlos syndrome may predispose to hernia formation.[17][18] Groin herniation is also more likely among patients with acquired abnormalities of connective tissue, including lathyrism (a neurotoxic disease caused by ingestion of specific forms of legumes).[19]

Patients with inguinal hernia have been shown to have abnormal collagen metabolism and decreased collagen levels.[19][20] Biochemical and ultrastructural collagen abnormalities are also associated with inguinal hernias. Collagen may show altered salt precipitability and abnormal hydroxylation, with a reduced amount of mature, insoluble, thick (polymeric) forms. Electron microscope imaging of collagen fibrils may show swelling, irregular periodicity, variable width, and some intracellular positioning.[21] The reasons for these changes are unknown but studies of tissues obtained from hernia patients demonstrate blunted fibroblast proliferation rates in tissue culture as well as reduced rates of incorporation of proline into skeletal muscle collagen.[22][23][24]

Prior radical prostatectomy is an acquired risk for inguinal hernia.[25] Open radical prostatectomy has the highest incidence of inguinal hernia, followed by laparoscopic and robot-assisted radical prostatectomies.[26]

Pathophysiology

Indirect inguinal hernias usually occur because of a persistent processus vaginalis as a result of failure of normal regression, which leaves an empty peritoneal sac lying in the inguinal canal. The hernia becomes clinically evident when bowel or other abdominal content fills and enlarges the empty sac, creating a visible and palpable bulge. The hernia sac follows the spermatic cord (or round ligament in women) and may extend down into the scrotal sac in men. It follows the round ligament in women to the pubic tubercle. Indirect hernias may be congenital (closely adherent to the vas deferens) or acquired (within the cord structures but anatomically separate from the vas). Most hernias in women are indirect.

Direct hernias are always acquired and therefore unusual under the age of 25. A direct inguinal hernia occurs because of degeneration and fatty changes in the aponeurosis of the transversalis fascia that constitutes the inguinal floor or posterior wall in the Hesselbach triangle area. (Hesselbach's triangle is defined inferiorly by the inguinal ligament, laterally by the inferior epigastric artery and vein, and medially by the lateral border of rectus abdominis). Most direct hernias do not have a true peritoneal lining and do not contain bowel, but mainly preperitoneal fat, and occasionally bladder. However, a large, longstanding, direct hernia can both harbor bowel or abdominal content and extend into the scrotum.

Strangulation rarely occurs with a direct hernia because the structural defect in a direct hernia is usually a diffuse weakness and stretching of the inguinal floor tissues, rather than a discrete, sharply defined ring-like defect. Strangulation is more common with an indirect hernia, particularly if it passes through a narrow neck in the form of a tight internal ring. As segments of the intestine prolapse through the defect in the anterior abdominal wall, compression can cause sequestration of fluid within the lumen of the herniated bowel. This initially impairs the lymphatic and venous drainage, which further compounds the swelling. Over time this can impair the arterial supply and cause ischemia. Gangrene ensues and, if left untreated, perforation occurs. Peritonitis occurs initially within the sac and then spreads to the peritoneal cavity.

Classification

Inguinal hernias can be classified as either direct or indirect, based on the relationship of the hernia sac to the inferior epigastric artery. However, this classification is mainly used by anatomists, and is not clinically useful. The Nyhus classification and the European Hernia Society classification are more clinically useful.[1][2] 

Of these, the Nyhus classification tends to be easier to understand and use in clinical practice.

Nyhus classification[1]

Type 1 - indirect inguinal hernia with normal internal ring (congenital, as seen in infants and children).

Type 2 - indirect hernia with dilated internal ring but normal posterior inguinal wall (usually seen in children and young adults).

Type 3 - posterior wall (inguinal floor) defects:

  • 3A: direct hernia

  • 3B: indirect hernia with dilated internal ring associated with or caused by weakness of posterior wall; includes sliding hernia. Type 3B hernias are acquired, not congenital

  • 3C: femoral hernia.

Type 4 - recurrent inguinal hernia:

  • 4A: direct hernia

  • 4B: indirect hernia

  • 4C: femoral hernia

  • 4D: combination of 4A, 4B, and 4C.

European Hernia Society (EHS) classification[3][4]

The EHS classification is based on the following three factors:[3]

  • Type of hernia: primary or recurrent

  • Anatomic location hernia: lateral, medial, or femoral

  • Size of hernia orifice: <1.5 cm (one finger- EHS I), 1.5 cm to 3 cm (two fingers- EHS II), or >3 cm (more than two fingers- EHS III).

Anatomic

1. Direct - hernia sac comes through the inguinal floor medial to the inferior epigastric artery and the deep inguinal ring.

2. Indirect - hernia sac comes through the internal (deep) inguinal ring, lateral to the inferior epigastric artery. An important subclassification of indirect hernia is sliding hernia, in which colon fused to the peritoneum comes through the internal inguinal ring.

Inguinal hernia may be further subclassified into the following groups:

  • Reducible - the contents of the hernia may be reduced completely.

  • Irreducible or incarcerated - the contents may not be reduced. If bowel is incarcerated, it cannot be reduced into the peritoneal cavity, but its blood supply has not been compromised.

  • Strangulated - an incarcerated hernia in which the blood supply of the hernia contents is compromised, causing ischemia. Unless relieved, gangrene and perforation of the affected bowel segment ensues. A strangulated hernia can also contain omentum or other viscera, such as bladder.

Additional anatomic terms[5]

Bubonocele - inguinal hernia confined to the inguinal canal.

Funicular - hernial sac extending beyond the superficial ring but not reaching the scrotum.

Complete (scrotal) - hernial sac extending into the scrotum with the testis in the lower end of the hernial sac.

Obturator hernia - hernia protruding through the obturator foramen; mainly occurs in elderly and asthenic patients.

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