as previously depicted in many atlases. The urogenital diaphragm exists only in humans because the
human pelvic outlet faces inferiorly, unlike that of quadrupeds.
Figure 72-16. A: The pelvic diaphragm (levator ani and the piriformis) and the urogenital diaphragm viewed from within the
pelvis. B: Hemisection of the pelvis revealing the levator ani, piriformis, obturator internus, and psoas muscles.
WHY DO HUMAN BEINGS DEVELOP ABDOMINAL WALL HERNIAS?
2 The most common hernias develop at sites where the abdominal wall has natural openings such as
the internal inguinal ring, the umbilicus, and the esophageal hiatus. Previous surgical entry sites
(incisional hernia) are also common areas where hernias develop. Factors that increase the pressure
in the abdominal cavity, such as obesity, heavy lifting, coughing with chronic lung disease, straining
during a bowel movement or urination (prostatism), chronic lung disease, and ascites, have
traditionally been considered important in the etiology, especially at these natural openings.
Developmental phenomena also play a role. For example, in the evolution from a quadruped to a
biped, the unprotected groin is more vulnerable to changes in intra-abdominal pressure, predisposing
to inguinal herniation. Major risk factors for the development of an abdominal wall hernias include
chronic obstructive pulmonary disease, smoking, high intra-abdominal pressure, collagen vascular
disease, thoracic or abdominal aortic aneurysm, peritoneal dialysis, matrix metalloproteinase (MMP)
abnormalities, and an increased type I: type III collagen ratio.
The role of heavy lifting, especially a single strenuous event, is an unsettled question and has
considerable medical–legal ramifications. There is minimal evidence that vigorous abdominal wall
activity is an independent risk factor for abdominal wall hernia development despite the overwhelming
opinion to the contrary in the lay literature.19–21 In a systematic review of existing evidence performed
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by Svendsen and colleagues, regarding the effects of occupational and mechanical exposures in relation
to inguinal hernias, a causal relationship could not be established between specific mechanical insults
and occurrence of inguinal hernia, hernia recurrence, and persistent pain after inguinal hernia
repair.22,23 According to the results of another register-based male cohort study in Denmark, increasing
cumulative exposure to daily lifting activities and prolonged standing or walking at work was associated
with an increased risk of having an indirect inguinal hernia repair.22,23 The authors hypothesized that
patent processus vaginalis may be more susceptible to changes in intra-abdominal pressures, whereas in
a direct hernia, other mechanisms may be involved in connective tissue degradation and weakening of
the transversalis fascia. Still, the role of mechanical activity in the development of abdominal wall
hernia is not completely clear, and further research is needed to determine if inguinal hernias can be
prevented and if the postoperative prognosis can be improved by reducing occupational mechanical
exposures.
Figure 72-17. The gluteal muscles and lateral rotators of the hip. External relations of the sciatic foramen are also evident.
Familial predisposition and the role of connective tissue diseases in hernia development have received
considerable attention in recent years. Particularly important for inguinal hernia is a family history as it
has been reported to increase the risk up to 8 times.24,25 Various connective tissue disorders, such as
osteogenesis imperfecta, Marfan syndrome, Ehlers–Danlos syndrome, and congenital hip dislocation, are
associated with hernias. Imbalances in collagen, the basic building block of the abdominal wall, are
believed to contribute to hernia disease. While type I collagen confers predominantly tensile strength,
type III collagen consists of thinner fibers and is regarded as a temporary matrix during tissue
remodeling. A decreased ratio of type I to type III collagens can be detected in fascial and skin
specimens obtained from patients with hernias. A similar phenomenon was discovered by Cannon and
Read in smokers when they performed biopsies of the rectus sheaths from adult smokers with inguinal
hernias and coined the term “metastatic emphysema.”26 The investigators also demonstrated
significantly greater levels of circulating serum elastolytic activity in patients who smoke.
Aside from primary defects in collagen synthesis, the imbalances in collagen in patients with hernia
can be attributed to altered extracellular matrix (ECM) which is maintained in a dynamic balance of
synthesis and degradation by a complex set of enzymes. MMPs,27 which are a group of 23 structurally
related zinc-dependent enzymes, protease with collagenolytic activity and have a pivotal role in the
integrity and composition of the ECM.
The association between MMP overexpression and abdominal wall hernia was initially demonstrated
by Bellon and colleagues, who studied the expression of MMP-1 and MMP-2 in the transversalis fascia of
patients with direct and indirect inguinal hernia. Since then, several studies have been conducted,
aiming at elucidating the role of MMPs in the development of primary and recurrent abdominal wall
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hernias. For this purpose, MMP levels in fascia, skin, hernia sac, and blood specimens of patients with
inguinal, incisional, and recurrent abdominal wall hernias have been measured. The expression of MMP
mRNA in cultured fibroblasts has also been investigated to evaluate cell–cell and cell–matrix interactive
mechanisms as causative factors for abnormal MMP production. In addition to this, in-vitro studies have
been performed to study the effect of different mesh materials on MMP expression on cultured
fibroblasts; in one such study, polypropylene has been shown to induce less MMP2 expression than
polygalactin. The function of MMPs is further regulated by a variety of endogenous regulators, the most
important ones are known as tissue inhibitors of MMPs (TIMPs).28–30 Studies have shown that an
imbalance between MMP and TIMP activity may have a role pathogenesis of abdominal wall hernias.31
Despite the increasing knowledge regarding MMPs in incisional and inguinal hernia, the exact role of
MMPs in the pathogenesis of hernia formation remains unclear. Most studies are small and not
completely controlled; and there is a remarkable heterogeneity among studies concerning the
characteristics of the study populations, the examined tissue specimens, and the biochemical assays
used. In addition to MMP and TIMPs, factors that have been implicated in hernia development include
deficiency of the elastic fiber system of the transversalis fascia, decreased tropoelastin and lysyl oxidaselike 1 synthesis, elastase overexpression and TGF-beta1 overexpression. It remains unclear whether
these alterations in hernia patients are a part of the “cause or effect” phenomenon. Another interesting
area of research are drug classes that can suppress MMP expression (e.g., tetracyclines, especially
doxycycline, aspirin, statins, and thiazolidinediones) and understanding their role in hernia prevention
and treatment.32
Figure 72-18. Reduction of a hernia by taxis. A: Applying pressure on the hernia directly occludes the neck. B: Elongating the neck
of the hernia while applying pressure allows reduction.
COMPLICATIONS OF HERNIAS
Hernia Accident
For years, surgeons have been taught that all hernias should be repaired at diagnosis to prevent a hernia
accident, which is defined as a bowel obstruction or incarceration with strangulation, because of the
perception that patients presenting with these complications have an unacceptable increase in mortality.
This thinking, however, has not stood up when tested in randomized controlled trials. For example, for
men with asymptomatic inguinal hernias, randomized controlled trials have shown that a strategy of
watchful waiting is safe.33
Incarceration
Incarcerated means “trapped” or “imprisoned.” Clinically, an incarcerated hernia is an irreducible hernia.
An incarceration is not in and of itself a surgical emergency. Many hernias are chronically incarcerated
due to adhesions of contents (e.g., omentum, bowel, ovary, etc.) to the hernia sac. The hernia itself is
not necessarily tense to palpation, and the overlying skin appears normal. Normal bowel sounds may be
heard within the hernia. It is important to differentiate an incarcerated hernia from a hydrocele of the
cord. One can get above the hydrocele with the examining fingers. One cannot get above a hernia,
however, as it communicates with the abdominal cavity. Hydroceles will transilluminate clearly, but a
hernia will not.
An acutely incarcerated, painful hernia must be managed carefully. An attempt at reduction is
reasonable unless there are signs of strangulation, which is not always obvious by clinical examination.
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Immediate surgical exploration is the safest approach when the diagnosis is not clear. The advantage of
reduction followed by elective repair is that edematous tissue associated with an acute incarceration can
return to normal, which presumably will translate into a better repair with less chance of infection.34 If
an attempt at reduction seems reasonable, the patient is sedated and placed in bed. The Trendelenburg
position should facilitate reduction of a groin hernia. An attempt should be made at the initial
examination to reduce the hernia. The maneuver of taxis entails grasping the neck of the hernia with the
fingers of one hand and then applying intermittent pressure on the most distal part of the hernia with
the other hand. Taxis has the effect of elongating the neck of the hernia so that the contents of the
hernia may be guided through this area back into the abdominal cavity with a rocking movement. Mere
pressure on the most distal part of the hernia causes bulging of the hernial sac around the neck, which
can occlude the neck and prevent it from being reduced (Fig. 72-18). The maneuver of taxis should not
be performed with excessive pressure or too vigorously. If the hernia is strangulated, gangrenous bowel
might be reduced into the abdomen or perforated in the process. One or two gentle attempts should be
made at taxis. If they are unsuccessful, this procedure should be abandoned. Rarely, the hernia together
with its peritoneal sac and constricting neck may be reduced into the abdomen (reduction en masse).
The patient would then have persistent obstruction after reduction of the hernia.
Intestinal Obstruction
One hundred years ago, the most common cause of intestinal obstruction was a hernia. At the present
time, hernia is third, after adhesive obstructions and cancer. Hernia is an important cause of obstruction
that is not infrequently missed on clinical examination. When a patient with an intestinal obstruction is
examined, great emphasis should be placed on adequate exposure of the entire abdominal wall and
groin area (from nipples to knees). Proper lighting is essential because previous scars can fade with
time and become barely perceptible. The patient with intestinal obstruction as a result of a hernia will
have a tense hernia that is irreducible. The abdomen itself will be distended, and high-pitched bowel
sounds with frequent rushes will be heard. If the process continues to the complication of strangulation,
these signs will disappear. Unlike adhesive small-bowel obstructions, partial small-bowel obstructions
secondary to hernia are rare. Most patients will have had vomiting and obstipation.
A plain roentgenogram of the abdomen will reveal the signs of an intestinal obstruction – dilated
loops of bowel with air–fluid levels and no bowel gas distal to the obstruction. Frequently on a plain
roentgenogram, one can see bowel shadows in the region of the hernia. A lateral view is often useful to
demonstrate this feature more clearly. Contrast studies are not usually necessary in this instance.
Computed tomography (CT) reliably demonstrates the hernia with characteristic features of obstruction
and should be considered if the clinical diagnosis is not certain (Fig. 72-19) because a distal intestinal
obstruction secondary to another cause (e.g., adhesions) may result in significant distention of a
coincidental nonobstructing hernia of the abdominal wall. Should the examiner focus attention
exclusively on the hernia, the real cause of the obstruction may be missed when the hernia is repaired.
Figure 72-19. Computed tomogram showing a left-sided inguinal hernia.
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