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60 B.M. Stephenson
females than males with an average ratio of 2.5:1, but this is
also age dependent (see Figs.
other data that disputes this statistic (see Chap. 17 ). Maingot
states that femoral hernias in women are eight times more
common than in men [ 30 ] . Glassow, from the Shouldice Clinic
in Toronto Canada, reports more males than females in his
series, at a ratio of 5:3 [ 31 ] . However, it must be remembered
that Glassow’s large series is of patients undergoing elective
operation for inguinal hernia and many of the cases were
found as concomitant femoral hernias in men undergoing
elective inguinal hernia repair. Clearly this series, or similar
ones, does not fairly represent everyday general surgical
practice.
Over 30 years ago approximately 40% of femoral hernias
in the UK were admitted acutely with complications such as
strangulation or incarceration [ 32 ] . This is also still unfortu-
nately true in many other developed countries at the time of
writing [ 33, 34 ] . Women still however undergo three times as
many inguinal as opposed to femoral hernia repairs. Femoral
hernias are rare in those under 35, are most common in multiparous women, and surprisingly as common in men as in
multiparous women. The ratio of inguinal to femoral hernias
is between 10:1 and 8:1. In Accra, Ghana, femoral hernias are
rare, accounting for only 1.2% of groin hernias, with an inguinal to femoral ratio of 77:1. In Kampala, Uganda, the ratio is
very different, 22:1. It is interesting to observe that indirect
inguinal hernias outnumber direct inguinal hernias in Accra
and in Zaria, Nigeria, whereas in Kampala direct hernias are
more frequent. In Kampala there are nine women with femoral hernias to one man, whereas in West African Hausa the
male to female ratio of femoral hernias is 1.2:1 [ 35– 39 ] .
The surgical volume for rates of femoral hernia repair in
NHS hospitals in England has remained stable between 1975
and 1990, with 5,083 primary femoral hernia repairs and 299
recurrent femoral hernia repairs being performed in
1989/1990. The age-speci fi c data indicate an increasing rate
of repair through the decades with a peak in our elderly
female population (Fig.
There is also considerable variation in surgical rates for
both inguinal and femoral hernia repair in the districts of
English Regional Health Authorities. The range for primary
inguinal hernia repair is 0.57–24 per 10,000 and for primary
femoral hernia repair 0.16–2.3 per 10,000. Such unexplainable wide variations re fl ect the diversity of clinical practice
and the “demand and supply” of treatment options already
noted [
9 ] .
3.1 and 3.2 ). However, there is
3.5 ).
Etiology of Primary Groin Hernia
The pathogenesis of groin herniation is multifactorial. Sir
Astley Cooper’s “predispositions” to hernia, in 1827, and the
subsequent addition of chronic cough, obesity, constipation,
pregnancy, ascites, and prostatic hypertrophy are now only
of historic interest. These factors may reveal a hernia but certainly did not cause it ab initio.
As indirect inguinal hernias are so common in infancy,
the fi rst surgical speculation was that they were due to a
developmental defect. Indirect inguinal hernia arises from
incomplete obliteration of the processus vaginalis, the
embryological out pocketing of peritoneum that precedes
testicular descent into the scrotum. The testes originate along
the urogenital line in the retroperitoneum and migrate caudally during the second trimester of pregnancy to arrive at
the internal inguinal ring at about 6 months of intrauterine
life. During the last trimester they proceed through the
abdominal wall via the inguinal canal and descend into the
scrotum, the right slightly later than the left. The processus
vaginalis then normally obliterates postnatally except for the
portion surrounding and serving as a covering for the testes.
Failure of this obliterative process results in congenital indirect inguinal hernia. The modern epidemiological support
for this hypothesis has already been reviewed, while the differing familial and tribal incidences, and the coincidence of
hernias in twins, are supportive.
John Hunter, in the late eighteenth century, researched the
development and descent of the testis in men and domestic
animals. He showed that in some inguinal hernias, the sac
was continuous with the processus vaginalis [ 40 ] . The
Parisian surgeon Cloquet, of nodal fame, observed that the
processus vaginalis was frequently not closed at birth [ 41 ] .
Indeed a complete (or scrotal) indirect hernia in an adult man
has the same anatomy as that of the neonate—it is invested
by all the three layers of the spermatic cord as it transverses
the inguinal canal and its sac is continuous with the tunica
vaginalis of the testis. Additional support for the congenital
theory of indirect inguinal herniation is the fi nding at autopsy
that 15–30% of adult males without clinically apparent
inguinal hernias have a patent processus vaginalis at death
[ 42 ] . A Bedouin mother and her four daughters with indirect
inguinal hernia in whom there was no evidence of collagen
diseases, normal hormone pro fi le, and normal pelvic anatomy suggest that in adult females as well, there is genetic
heterogeneity [ 43 ] . Such an occurrence in females may be
associated with an alteration in the anatomy of the round
ligament, which normally terminates in a hernia sac and is
attached to the midportion of the fallopian tube near the
ovary [ 44 ] .
Review of the contralateral side in infantile inguinal hernias reveals a patent processus vaginalis in 60% of neonates
and a contralateral hernia in 10–20%. In slightly older
children (say 2 years or so) the rate of developing a
metachronous contralateral inguinal hernia is of the order of
5–7% with those children having a left-sided one at a higher
risk of later herniation than had the fi rst hernia been on the
other side [
45, 46 ] . In addition, at 20 years of follow-up after
613 Epidemiology and Etiology of Primary Groin Hernias
an infantile hernia repair, 22% of men will develop a
contralateral inguinal hernia, of which 41% occur if the initial hernia was on the left and 14% if the initial hernia was on
the right.
The introduction of continuous ambulatory peritoneal
dialysis (CAPD) in the management of renal failure has
demonstrated that a persistent processus vaginalis, if subjected to intra-abdominal pressure, will dilate to give a
hydrocele or hernia [
47– 49 ] . Indeed this has been docu-
mented as late as 2 years after commencing CAPD. In addition the development of an inguinal hernia in female CAPD
patients adds further support to this premise [ 49– 51 ] .
Russell, an Australian pediatric surgeon, in 1906 advanced
the “saccular theory” of the formation of hernia, a theory that
“rejects the view that any hernia can ever be “acquired” in
the pathological sense and maintains that the presence of a
developmental peritoneal diverticulum is a necessary antecedent condition in every case … We may have an open
funicular peritoneum and we may have them separately or
together in in fi nitely variable gradations” [ 52 ] . In recent
years, with the increasing use of “diagnostic” laparoscopy,
some light has been shed on this debate. When the inguinal
anatomy of 600 patients undergoing diagnostic laparoscopy
for other reasons was carefully recorded, the prevalence of a
sac or remnant of a patent processus vaginalis did not seem
to increase with age [ 53 ] . However and interestingly, when
these patients were followed for over 5 years, those in whom
an asymptomatic patent processus vaginalis had been noted
were four times more likely to have undergone a later hernia
repair [ 54 ] .
It would be apparent from the above that the problem of
indirect inguinal hernia may not be simply one of a congenital defect, that is, there is more to the story than just a persistent patent processus vaginalis. The high frequency of
indirect inguinal hernia in middle-aged and older people
suggests a pathological change in connective tissue of the
abdominal wall to be a contributory factor. Indeed, simple
removal of the sac in adults results in an unacceptably high
recurrence rate and clearly is inappropriate. Thus the susceptibility to herniation is based on both the presence of a con-
genital sac and failure of the transversalis fascia. In direct
inguinal hernia there is no peritoneal sac and the prevalence
parallels aging and other factors including smoking [ 55, 56 ] .
Furthermore the absence of an adequate musculoaponeurotic
support for the fascia transversalis and the medial half of the
inguinal canal has been described in about a quarter of individuals [ 24 ] . In these men there is de fi ciency of the lower
aponeurotic fi bers of the internal oblique muscle, coupled
with a narrow insertion of the transversus abdominis onto the
superior pubic ramus [
57, 58 ] . Because such a congenital
anomaly would be symmetric, this explanation is consistent
with the clinical fi nding that direct hernias are frequently
bilateral and often surprisingly asymptomatic.
Fig. 3.7 The European pelvis is relatively wide with a less deep arch
than the Negro pelvis. This ensures that the internal oblique muscle
origin from the lateral inguinal ligament is broad, so that the internal
oblique muscle “protects” the deep ring
The anatomic disposition of the pelvis, and particularly
the height of the pubic arch, may also be a signi fi cant and
possibly ethnic characteristic predisposing to inguinal hernia
formation. The height of the pubic arch is measured as the
distance of the pubic tubercle from the bispinous line between
the innermost parts of the two anterior superior iliac spines.
African (Negro) peoples have lower pubic arches than
Europeans and a higher incidence of inguinal hernia. In West
and East Africa the “lowness” of the pubic arch is greater
than 7.5 cm in 65% of males; in Europeans and in Arabs the
arch is less low, 65% of males having a height of between 5
and 7.5 cm (Fig.
3.7 ). In European females 80% have an arch
between 5 and 7.5 cm, and they have the lowest incidence of
groin hernias [ 39, 59, 60 ] .
This “low” arch is associated with a narrower pelvis and
with a narrower origin of the external oblique muscle from
the lateral inguinal ligament. With these anatomic variations
the inguinal canal is shorter with the deep inguinal ring left
uncovered by the internal oblique. The canal may then be so
short that no signi fi cant muscular “shutter mechanism” is
apparent [ 59 ] as illustrated by Fig. 3.8 . There is another
much rarer form of direct hernia where a narrow peritoneal
diverticulum comes directly through the conjoint tendon lateral to the rectus and pyramidal muscles to project at the
super fi cial inguinal ring. In addition there are numerous
unusual types of interparietal hernias where the sac may be
mono- or bilocular and associated or not with a patent indirect sac.
It must be concluded that there are congenital, anatomical, and genetic factors that render individuals more likely to
manifest direct as opposed to indirect inguinal hernias.
Over 80 years ago Sir Arthur Keith, a Scottish anatomist
and anthropologist, observed: “There is one other matter,
which requires further observation. We are so apt to look on
62 B.M. Stephenson
Fig. 3.8 The Negro pelvis is narrower than the European, which means
that the lowness of the arch of the pelvis is greater in the Negro and the
origin of the internal oblique relatively narrower. Hence the internal
oblique will not cover the deep ring during straining, and the “shutter
mechanism” of the inguinal canal is de fi cient. Negroes have a ten times
greater incidence of indirect inguinal hernia than Europeans
tendons, fascial structures and connective tissues as dead
passive structures. They are certainly alive, and the fact that
hernias are so often multiple in middle aged and old people
leads one to suspect that a pathological change in the connective tissues of the belly wall may render certain individuals particularly liable to hernia.” He concluded his
argument with a statement regarding “the importance of a
right understanding of the etiology of hernia … If they
occur only in those who have hernial sacs already formed
during fetal life then we must either excise the sacs at birth
or stand by and do nothing but trust to luck. But if … the
occurrence of hernia is due to circumstances over which we
have control then the prevention of hernia is a matter worthy of our serious study” [ 23 ] .
Some 50 years later, Read, an American surgeon, made a
crucial clinical observation which further advanced our
thoughts as to the etiology of inguinal hernia. In 1970 he
noted, when using an open preperitoneal approach to the
inguinal region, that the rectus sheath is thinner and has a
“greasy” feel in those patients who turned out to have direct
inguinal defects. This observation was con fi rmed by weighing samples of a constant cross-sectional area; specimens
from controls weighed signi fi cantly more than those from
patients with indirect, pantaloon, and direct hernias (in that
order). Bilateral hernias were associated with more severe
atrophy. Adjustments for age and muscle mass con fi rmed the
validity of this observation [ 56 ] . Further evidence in support
of a collagen derangement in the transversalis fascia was presented by Peacock and Madden in 1974, who observed that
satisfactory repair of adult inguinal herniation depended on
the local extent of any collagen de fi ciency. And, if surgical
technical failure can be excluded, the logical treatment of
recurrent herniation is a fascial graft or prosthetic repair [ 61 ] .
This concept was enthusiastically promoted by Irving
Lichtenstein, one of the earliest pioneers of prosthetic repair
for primary inguinal hernia [ 62 ] . We now all know how this
revolutionized modern hernia practice [
17 ] .
Hernias “Under the Microscope”
Let us start with some basic science that we may have forgotten! Surgical wound healing is a controlled cascade in which
there are sequential cellular and molecular events allowing
ordered tissue repair. After the initial wound there is a phase
of healing characterized by hemostasis and in fl ammation
followed by one of proliferation, which is predominantly one
of increased fi broblastic activity with extracellular deposition and increased angiogenesis. Collagen is the end product
of fi broblast activity, and while there are many types of collagen, type I and type III are those most implicated in wound
healing. Subsequent remodeling involves collagen bundle
organization to give rise to a mature scar. Now, before moving on, let us remind ourselves that the inguinal canal and
transversalis fascia comprise tissues made up of collagen,
elastic fi bers consisting of elastin and micro fi brils, and the
glycosaminoglycan component of the extracellular matrix.
Following the earlier observations regarding the “greasy”
feel of the rectus sheath [ 56 ] , Read and coworkers showed
that hydroxyproline, which comprises 80% of the dry weight
of collagen, was strikingly decreased in the rectus sheath of
inguinal hernia patients especially if the hernia was of a direct
type [ 63, 64 ] . The extracted collagen revealed a reduced
hydroxyproline:proline ratio. Intermolecular cross-linking is
unaffected, but synthesis of hydroxyproline is inhibited, and
there is variability in the diameter of the collagen fi brils in
hernia patients [ 65 ] . Similar electron microscopic fi ndings
are also present in pericardial and skin biopsies from these
patients [ 65 ] and have also been described in connective tissue tumors [
[
68 ] . Based upon these observations and the results of later
similar studies, the prosthetic repair of inguinal hernias was
promoted as the new “gold standard” of surgery. These
fi ndings also changed the approach to the repair of ventral
(including incisional) hernias such that the vast majority are
now also augmented with prosthetic biomaterials.
The above observations led Read, in 1978, to the postulate that inguinal herniation is not a localized defect of the
groin fascia but is in fact a manifestation of a generalized
connective tissue disorder similar to emphysema, a 1 -antit-
rypsin de fi ciency, osteogenesis imperfecta, scurvy, varicose
veins, and experimental nicotine de fi ciency [
was then tested with a computerized suction device to assess
the biomechanical properties of the transversalis fascia and
rectus abdominis so as to measure any functional connective
66 ] , pulmonary emphysema [ 67 ] , and scurvy
67 ] . This hypothesis
633 Epidemiology and Etiology of Primary Groin Hernias
tissue abnormalities in the groin [ 69 ] . The study was unable
to demonstrate any differences in the properties of aponeurosis between hernia patients and controls. There was, however, a difference in collagen ultrastructure when it was
examined under an electron microscope and in its physicochemical properties as observed by altered perceptibility and
de fi ciency in hydroxyproline content. It appears thus that the
fundamental problem in the aponeurosis of men with direct
inguinal herniation is failure of hydroxylation of the collagen
molecule.
Berliner in 1984 con fi rmed these fi ndings by studying
biopsies from three sites in patients with inguinal hernia
[
70 ] . Degenerative changes in the musculoaponeurotic fi bers
were found not only in the transversalis fascia/transversus
abdominis of patients with direct inguinal hernias but also in
the transversalis fascia at the superior aspect of the internal
ring in patients with indirect inguinal hernia and also distant
from the hernia site in grossly normal transversus abdominis
aponeurosis. The main changes observed were reduction in
elastic tissue with a paucity and fragmentation of elastic fi ber
similar to that seen in Marfan and Ehlers–Danlos syndrome
(EDS). The implication from these fi ndings is that collagen
malsynthesis and enzymolysis mutually but not necessarily
equally play a major role in the etiology of both direct and
indirect inguinal hernia. Indeed, this was supported when the
in vitro synthesis of types I and III collagens (and their procollagen mRNAs) was studied from isolated skin fi broblasts
in patients with inguinal hernia. Fibroblasts incubated with
radiolabeled tritiated proline secreted increased amounts of
type III procollagen, suggesting that an altered fi broblast
phenotype in patients with inguinal hernia could result in
reduced collagen fi bril assembly and defective connective
tissue formation [ 71 ] . Further support for this suggestion
comes from a case–control (fresh cadavers) study where both
the total and type I collagen were decreased in fi t young men
with indirect inguinal hernias [ 72 ] .
Could an uninhibited elastolytic enzyme system cause
groin herniation—a similar mechanism to low serum levels
of the protease inhibitor a 1-antitrypsin globulin allowing
endogenous enzymes to destroy alveoli? [ 73 ] . Experimental
evidence certainly supports the biochemical hypothesis that
the pulmonary connective tissue disorder in emphysema is an
imbalance between proteolytic enzyme levels and their inhibitors. Evidence of raised elastolytic enzyme has been found in
smokers, and in smokers with inguinal herniation there is a
close association between raised elastolytic levels and raised
white counts. Neutrophils carry proteolytic and elastolytic
enzymes and are actively involved in the lung in fl ammatory
response to cigarette smoke. Could they not also deliver the
same proteolytic insult to the transversalis fascia? The neutrophil-derived enzyme metalloproteinase (MMP-2 and
MMP-9) has been identi fi ed as one that breaks down collagen, elastin, and other components of the extracellular matrix.
They have been found in transversus abdominis biopsies of
patients with direct but not indirect inguinal hernias. MMP-2
overexpression has been measured in fi broblasts of patients
with direct hernias, and MMP-13 overexpression detected in
recurrent inguinal hernias [ 74, 75 ] . While these studies are
best described as observational they are important indicators
of the pathological process at the cellular level. Although it is
unclear whether a deteriorating groin expresses increased
MMP levels, it is of interest to see that transforming growth
factor beta1 (TGF- b 1) is overexpressed in the transversalis
fascia of young patients with direct hernias [ 76 ] . Such growth
factors are known to play a role in tissue remodeling and are
presumably doing so or attempting to counterbalance the
microscopic problems of a failing groin.
On a “macroscopic” or clinical scale, is there evidence
that collagen is at fault? The prevalence of inguinal hernia
(41%) in 119 patients with infrarenal aortic aneurysms was
signi fi cantly higher when compared with 81 patients with
aortic–iliac occlusive disease (18.5%) and 293 patients with
coronary artery disease (18.1%). In addition, the number of
patients who had undergone a recent hernia repair (16%) or
were still waiting for repair (19%) was very high [ 77 ] . Also
following elective aortic reconstruction for aneurysmal or
occlusive aortic disease, at 1 year follow-up, incisional hernias were found in 31% of patients with aneurysm and 12%
with occlusive disease, and inguinal hernias were found in
19% of patients with aneurysm and 5% with occlusive disease further supporting the concept of a biochemical abnormality [ 78 ] . The smoking habits of the three groups were
not different, and again the fi ndings support the concept of
systemic fi ber degeneration [ 79 ] . Although the enzymatic
elastase content of the wall of abdominal aortic aneurysms
has been shown to be increased, the concept of high levels
of circulating elastase has not been con fi rmed. Nevertheless,
overall patients with aneurysmal disease have a fourfold
increased risk of inguinal and incisional herniation [ 80, 81 ] .
Similar fi ndings have been found in patients examined by a
magnetic resonance imaging of the abdominal wall following aortic surgery [ 82 ] . These fi ndings indicate that 50% or
more of patients with nonocclusive infrarenal aortic aneurysm suffer from inguinal hernia. Indeed, it has been suggested that an inguinal hernia in certain high-risk age groups
be used as an index for ultrasonic screening for aneurysmal
disease [ 83 ] . However as the ultrasonography would have to
be performed and repeated over a substantial period of time,
the results of a small ( n = 70) prospective study go some
way to point out this is not going to be a useful screening
tool [ 84 ] .
A number of years ago the term “metastatic emphysema”
was coined by Cannon and Read [
67 ] for the concept of a
generalized connective tissue disorder, which was maybe
due to a leakage of proteases from the lungs of heavy smokers
[ 85 ] . Read emphasized that the data indicate that more than
64 B.M. Stephenson
Fig. 3.9 Persistent
herniation in Ehlers–
Danlos syndrome. Note the
unusual skin appearance
one factor can cause systemic metabolic disease of collagen
leading to abdominal herniation including the imbalanced
expression of different collagens. Subsequent results have
con fi rmed this in the transversalis fascia of patients with
inguinal hernia by direct measurement of the important collagens (types I and III) [ 72, 86 ] . Nevertheless we must be
cautious in interpreting the experimental data about a proteolytic defect in inguinal hernia patients and then relating it to
the proven association with abdominal aortic aneurysm. It is
however tempting to relate this “metastatic emphysema theory of inguinal herniation” to Hunt’s and Tilson’s ideas that
aortic aneurysm is a copper transport collagen disorder
enhanced by cigarette smoking [ 87, 88 ] .
With all the available data [ 89– 91 ] , it seems probable and
indeed highly likely that primary inguinal hernias are a connective tissue disorder as opposed to recurrent ones, which
are due to a combination of this underlying innate problem
and a technical failure of wound healing/repair. This further
supports the need for a well-dissected prosthetic repair in the
fi rst instance. Whether biological meshes will play a part in
the elective repair of primary inguinal hernias, other than in
a few very selected cases, remains to be seen [ 92 ] .
A Curious Case of Recurrent Recurrence
A 45-year-old otherwise asymptomatic man developed an
incisional hernia following a lower midline laparotomy for
peritonitis from a perforated appendix. This was repaired but
recurred and did so again when this recurrence was repaired
with preperitoneal mesh. Wound healing seemed attenuated
and the hernia unmanageable. After a further repair using the
component separation technique (again augmented with onlay mesh) failed, a diagnosis of EDS was contemplated and
later established (Fig. 3.9 ).
This unusual inherited connective tissue disorder, also
known as “cutis hyperelastica,” is caused by a defect in the
synthesis of collagen (type III). There are numerous recognized types of EDS [ 93 ] with the genetic mutations (auto-
somal dominant mode of inheritance) altering the structure,
production, or processing of collagen or the proteins that
interact with collagen to varying degrees. Even in established
EDS, now known to be more prevalent than previously
thought, the symptoms and presentation vary widely.
Treatment is generally supportive and the prognosis dependent on the type of EDS.
Could “milder” defects in collagen synthesis/metabolism
be even more prevalent in the population than otherwise contemplated with other factors such as smoking accelerating
the general wear and tear process that we subject ourselves
too? Interestingly inguinal hernia occurs more frequently in
patients with milder EDS phenotypes.
Genetics in Pediatric Surgical Practice
Inguinal hernia may be associated with many different
genetic syndromes including single gene and chromosomal
disorders. Given the known constituents of the inguinal canal
and transversalis fascia, one would expect such disorders to
be associated with a higher risk of inguinal hernia [
Indeed genetic diseases of the micro fi bril (Marfan syndrome),
94 ] .
653 Epidemiology and Etiology of Primary Groin Hernias
elastin (Costello syndrome and Menkes disease), and
collagen (EDS and osteogenesis imperfecta) are all associated with an increased risk of inguinal hernia.
While the vast majority of childhood inguinal hernias do
not have a genetic basis warning signs that a hernia may
have, a genetic basis includes a direct hernia, a recurrent hernia, or a hernia in girls as well as the more commonly recognized features associated with genetic disorders such as
developmental delay.
The Genetics of Inheritance of the “Common” Indirect Inguinal Hernia
Although there is considerable evidence suggesting the role
of genetic factors in the etiology of inguinal hernia, its mode
of inheritance remains controversial [
hypotheses have been suggested:
1. Autosomal dominant inheritance with incomplete pene-
trance [
96 ]
2. Autosomal dominant inheritance with sex in fl uence [ 97, 98 ]
3. X-linked dominant inheritance [ 99 ]
4. Polygenic inheritance [ 100, 101 ]
In a study from Budapest [ 100 ] , the parents of 707 index
patients with operated indirect congenital inguinal hernia
born during the years 1962–1966 were studied for their frequency of indirect inguinal hernia. There was a 2 and 5.6
times higher incidence respectively in the fathers and mothers than in the general population, and the rate of affected
siblings was higher than that of parents but was generally
dependant on the sex of the index patient. In twins the hereditability was 0.77. These data suggested a multifactorial
threshold model involving dominant variance.
A study of 280 families with congenital indirect inguinal
hernia in the Shandong province of China has indicated that
the mode of transmission in these families is autosomal dominant with incomplete penetrance and sex in fl uence. There is
preferential paternal transmission of the gene, suggesting a
role for genomic imprinting in the etiology of indirect inguinal hernias [ 102 ] . In this study the probands (index cases)
had all been operated on by 5 years of age, with the hernia
occurring on the right side in 138 and on the left side in 84.
This is consistent with the known embryological facts that
the right testis descends later than the left and that the processus vaginalis is therefore obliterated later on the right side
than on the left side; hence hernia is more frequent on the
right than on the left side.
In a record linkage study from the UK reported in 1998, of
the risk of congenital inguinal hernia in siblings, 1921 male
and 347 female cases born during 1970–1986 and who were
operated on for inguinal hernia at the ages of 0–5 years were
matched against 12,886 male and 2,534 female controls
103 ] . The relative risk for inguinal hernia was found to be
[
5.8 for brothers of male cases and 4.3 for brothers of female
95 ] . A number of
cases, while the relative risk was 3.7 for sisters of male cases
and 17.8 for sisters of female cases. This pattern of sex-dependant risk suggests a multifactorial threshold model for the
disease. In essence as girls have a much lower incidence of
inguinal hernia, those girls who do develop the disease might
have a potentially larger contribution to susceptibility from
genetic or intrauterine risk factors unrelated to their sex.
More recently a study from Hong Kong has examined the
strength of a positive family history as a risk factor for developing an inguinal hernia [
using multivariate logistic regression analyses, a positive
family history was the only truly independent predictor for a
hernia; indeed a man with a positive family history is eight
times more likely to develop a primary inguinal hernia.
Indirect inguinal hernia arises from incomplete obliteration of the processus vaginalis, the embryological protrusion of peritoneum that precedes testicular descent into the
scrotum. The testes originate along the urogenital line in the
retroperitoneum and migrate caudally during the second trimester of pregnancy to arrive at the internal inguinal ring at
about 6 months of intrauterine life. During the last trimester
they proceed through the abdominal wall via the inguinal
canal and descend into the scrotum, the right slightly later
than the left. The processus vaginalis then normally obliterates postnatally except for the portion surrounding and serving as a covering for the testes. Failure of this obliterative
process results in congenital indirect inguinal hernia.
It is plausible to speculate that morphogenesis may be
determined by single genes and complicated by environmental factors. In the case of indirect inguinal hernia, an autosomal dominantly inherited gene with reduced penetrance
and sex in fl uence would therefore be susceptible to environmental factors in fl uencing its expression as a clinical inguinal hernia. In most families, however, a monogenic mode of
inheritance is not apparent. Therefore the maternal allele (of
a/the gene?) may protect against failure of closure of the patent processus vaginalis.
In conclusion, the fact that most affected males have
inherited an indirect inguinal hernia gene(s) from their father
implicates a role of genomic imprinting (i.e., the paternal
allele) in the etiology of the indirect inguinal hernia phenotype. Finally it may be of interest to note that certain chromosomal loci have been identi fi ed as genetic susceptibility
targets in pigs at known “high risk” of developing inguinoscrotal hernias [ 105 ] . We all have to start somewhere!
104 ] . As compared to controls and
Intra-abdominal Diseases Causing Hernias
Ascites due to liver, heart disease (failure), and more rarely
abdominal or peritoneal carcinomatosis can present as recent
onset groin and umbilical herniation. The mechanism is
similar to that already described in CAPD patients, with
increasing hydrostatic pressure dilating a preexisting sac
66 B.M. Stephenson
irrespective of its earlier size. Intra-abdominal contents may
then follow into this enlarged space. Clearly the sudden onset
of a hernia in middle-aged or elderly patients should thus
arouse diagnostic suspicion. It is a sound policy to subject
hernial sacs to histological examination, especially in older
patients, where ascites (blood stained or not) is found or
when the sac is thickened or indurated. However, the routine
histological examination of “normal” hernial sacs is not
justi fi ed. Indeed the chance of unexpected “pathology” in an
otherwise normal hernial sac has been estimated (!) to be
0.00098% [
106 ] . Routine histology is certainly unnecessary
and obviously uneconomical.
Interestingly the histological examination of sacs obtained
from children with hernia, hydrocoele, or undescended testis
revealed that in the inguinal hernia patients during childhood, smooth muscle was found within the wall of the sac
but not in sacs associated with undescended testis. This suggests that this smooth muscle may have played a role in the
prevention of obliteration and clinical outcome [ 107 ] .
Thickening of a hernial sac per se is not necessarily due to
signi fi cant pathology; peritoneum is active tissue and particularly in children and young adults can exhibit overexuberant tumor-like reaction to mechanical injury. This
so-called mesothelial hyperplasia may follow wearing a truss
or occur simply after repeated attacks of near-incarceration.
Microscopically there are atypical mesothelial cells that are
either free or attached to the wall of the sac. Mitoses and
multinucleated cells are frequently seen but despite this
mesothelial hyperplasia are reactive and certainly not neoplastic [ 108 ] .
The development of an abdominal wall hernia may be a
rare but initial sign of decompensated heart or liver disease.
Whereas good surgical practice is to repair an uncomplicated
hernia, the question of repair in cirrhotics raises other issues.
Leonetti et al. [ 109 ] reported that repair of umbilical hernias
in uncontrolled unshunted cirrhotics led to a mortality of
8.3%, a morbidity of 16.6%, and a recurrence rate of 16.6%.
However umbilical herniorrhaphy in patients with a functioning peritoneovenous shunt was associated with minimal
morbidity (7%). The authors suggested that peritoneovenous
shunting should be a prerequisite to hernia repair [ 109 ] .
While this may not now always be necessary, these patients
clearly need medical optimization before surgery [ 110 ] .
There is now little doubt that elective surgery has signi fi cantly
[ 111, 112 ] improved the quality of life of these patients with
mesh repairs well tolerated and outcomes similar to patients
without cirrhosis [ 113 ] .
Intra-abdominal pus can also collect in and distend an
empty hernial sac, as with any peritoneal recess, at the initial
peritonitis. It may also collect in a long-standing hernia even
after successful emergency surgery (Fig. 3.10 ). In a review of
32 examples of this phenomenon, 19 were right inguinal, fi ve
right femoral, three left inguinal, one epigastric, and one
Fig. 3.10 Residual collection in a large long-standing hernia after
emergency surgery for gastric perforation
umbilical. Acute appendicitis accounted for 16 examples,
perforated peptic ulcers for three, one followed pneumococcal
peritonitis in a 2-week-old male child, one an acute pyosalpinx,
and one followed a biliary leak after removal of a common
bile duct drain [ 114 ] . Every patient with this complication
was originally diagnosed as having a strangulated hernia,
which is not surprising. If pus is found in a hernial sac,
abdominal exploration is usually mandatory with acute appendicitis being the commonest diagnosis, especially in rightsided hernias [ 115 ] . When confronted with a tender
incarcerated hernia, the diagnosis remains primarily a clinical
one, but appropriate and recently more immediately available
radiological investigations can usefully augment ones suspicions allowing a tailored minimally invasive staged approach
when appropriate [ 116, 117 ] . A tender inguinal mass may not
represent a hernia as demonstrated by Fig. 3.11 !
Inguinal Hernia and Appendectomy
Over a hundred years ago Hoguet fi rst reported the development of inguinal hernia in patients who had undergone previous appendectomy [ 118 ] . He found eight right inguinal
hernias in a series of 190 patients who had undergone appendectomy and suggested a causal relationship. Other authors
have supported this contention [ 119– 121 ] .
Right inguinal hernias are more frequent when appendectomy is performed through a lower, “more cosmetic” incision,
which is placed below the anterior superior iliac spine and in
which the iliohypogastric nerve is injured. Electromyographic
studies have shown con fl icting results. While some investiga-
121 ] have shown that denervation of the transversus
tors [
abdominis muscle in the groin does occur and could therefore
interfere with the shutter mechanism of the deep ring and be a
factor in the subsequent development of inguinal hernia, other
673 Epidemiology and Etiology of Primary Groin Hernias
Fig. 3.12 Herniography on a 40-year-old man who had sustained a
Fig. 3.11 A diverticular abscess presenting as a hernia. Fortunately a
colocutaneous fi stula did not develop in this frail 78-year-old lady
fracture of both pubic rami. The patient developed a “pantaloon” inguinal hernia
investigators have failed to detect any signi fi cant denervation
of the musculature in and around the right groin [ 122 ] .
Using the standard McBurney (introduced by Charles
McBurney in 1894) appendectomy incision (at right angles to
a line from the umbilicus to the anterior superior iliac spine, at
a point at the junction of its lateral third and medial two-thirds
and parallel to the iliohypogastric nerve which is rarely injured
if the fl ank muscles are opened by splitting in their fi ber line),
there is no evidence that inguinal herniation is a consequence
of appendectomy. In a series of 549 patients who had undergone inguinal hernia repair, the percentage incidence of previous appendectomy in right-sided hernias was 8.9 ± 1.7% and
in left-sided inguinal hernias 11.2 ± 2.1% [ 123 ] .
It is the lower and “more cosmetic” incisions, which carry
a particular hazard to the iliohypogastric nerve and a propensity to subsequent inguinal herniation. The introduction of
effective antibiotics and the consequent reduction in wound
complications are also clearly important. If and when laparoscopic appendectomy is fully embraced as a standard
approach (with reasons for and follow-up of converted cases)
will we know if this technique also contributes to a lower
incidence of subsequent inguinal herniation. The debate
regarding open or laparoscopic appendectomy will no doubt
continue for sometime before this becomes universal surgical practice even in the developed world [
124 ] .
Hernias Related to Trauma and Pelvic Fracture
Abdominal hernias related to trauma and blunt injuries are
rare and are only reported following lower abdominal and
pelvic injuries. To diagnose a traumatic hernia there must be
immediate signs of local soft-tissue injury, bruising, hematoma,
etc., and then there must be the early presentation of the
symptoms of the hernia. The aponeuroses close to their pelvic attachments are most at risk.
Disruption of the inguinal canal and complete ruptures of
the conjoint tendon are recorded but are very rare [ 125 ] .
Ryan, from the Shouldice clinic, reported only fi ve hernias
related to pelvic fractures in 8,000 hernia repairs [ 126 ] .
Figure 3.12 illustrates an unusual case of a patient whose
hernia was related to a pelvic fracture: A 40-year-old man
developed a “pantaloon” hernia after fracture of both rami of
the pubis in a traf fi c accident. Such “traumatic” hernias are
also recognized after pelvic diastasis in the absence of fracture and often present late and may contain bladder or small
bowel alone (supravesical).
Hernias related to iatrogenic pelvic fractures, for example, an osteotomy for congenital dislocation of the hip, are
well described in the literature. Ryan classi fi es these
fracture-related hernias according to the mechanism of the
fracture [
126 ] :
68 B.M. Stephenson
Fig. 3.13 Diagram to show how innominate osteotomy predisposes to
inguinal herniation
1. Due to acute anteroposterior forces acting on the pelvis:
In these instances there is tearing of the rectus abdominis
origin from the pubic crest. The tearing is maximal on the
side opposite to that on which maximum bony displacement had occurred. The damage to the muscle is usually
more severe medially than laterally, leading to the development of a broad-necked sac just suprapubically from
Fig. 3.14 An external femoral hernia (Hesselbach’s) passing deep into
the thigh below the inguinal ligament lateral to the femoral vessels.
Note the previous incision for corrective hip surgery of uncertain
nature
the midline extending laterally across the attachment of
the rectus to the pubic crest.
2. Due to lateral or lateral/vertical forces: These fractures
involve the superior pubic ramus with consequent tearing
of the fascial and aponeurotic attachments of the
inguinofemoral region. In these circumstances a direct
inguinal hernia develops through the fascia transversalis
immediately above the bony fracture line. A repair of the
direct hernia corrects the situation.
3. Due to surgical innominate osteotomy: This hernia occurs
in children with congenital dislocated hips. The hernia
following innominate osteotomy is either a direct inguinal
hernia, a prevascular femoral (Narath’s) hernia, or a combination of the two [ 127 ] .
Following innominate or Salter’s osteotomy, there is a
downward lateral and forward displacement of the lower fragment of the pelvis produced by a combination of hinging and
Fig. 3.15 An earlier anterior bone graft site complicated by groin herniation. The sac contained incarcerated omentum
rotation at the symphysis pubis [ 128 ] . This procedure leads to
an increase in the distance between the edge of the rectus
abdominis muscle and the inguinal and pectineal ligaments.
There is a consequent weakening in the posterior wall of the
inguinal canal. The angle between the midline (and, therefore,
the lateral edge of the rectus muscle) and the superior ramus
of the pubis is increased by a minimum of 5° when compared
to the opposite side, and there is also an increase in the distance from the pubic tubercle to the anterior superior iliac
spine. These changes alter the anatomy of the inguinofemoral
region predisposing to hernia. It must be stressed that a consequent hernia is rare and undoubtedly compensatory remodeling of the soft tissues occurs as the child develops after the
traumatic procedure (Fig. 3.13 ). Any earlier musculoskeletal
surgery, iatrogenic or not, in the region of the groin can lead
to the later unusual groin herniation (Fig.
3.14 ).
The use of autologous bone grafts from the iliac crest is
also troublesome. When full thickness grafts are taken from
the posterior iliac crest, the inferior lumbar triangle is enlarged
693 Epidemiology and Etiology of Primary Groin Hernias
Table 3.4 Severity of abdominal wall injury
Description Grade Incidence (%)
Tissue bruising/contusion I 54
Muscle(s) hematoma II 28
Single-layer disruption III 8
Complete-layer disruption IV 8
IV with herniation V 2
IV with evisceration VI 0
Data from Dennis et al . [
blunt trauma
130 ] based on CT scans in 1,549 patients with
predisposing to herniation. These “iatrogenic” lumbar hernias
cause backache and can be complicated by irreducibility and
strangulation and should be repaired [ 129 ] . Bone grafts from
the anterior iliac crest are similarly complicated by later herniation and require corrective surgery (Fig.
3.15 ).
Truly blunt traumatic abdominal wall hernias may occur
after both low- (falls) or high-“energy” (motor vehicle
accidents) impact injuries. Despite the use of early CT scanning,
the mechanism of injury is vitally important, and a high index
of suspicion is necessary when managing such patients. Highenergy trauma cases may need urgent laparotomy for concomitant intra-abdominal injuries, whereas in low impact injuries
local wound toilet, debridement, and immediate repair may
suf fi ce. In a review of 1,549 CT scans from a level I trauma
center, abdominal wall injuries were graded as to their severity
with respect to the documented disruption of the layers of the
abdominal wall [
130 ] . Overall abdominal wall injuries occurred
in 9% of cases (Table 3.4 ) with those at risk of later herniation
(not necessarily in the groin) estimated to be 16%. The role of
subsequent follow-up CT scanning may well de fi ne the place
of “early vs . late” repair of these injuries. To date the later
repairs of such hernias should probably be undertaken through
a preperitoneal approach so that the anatomy, or lack of it, can
be best appreciated.
Exertion and Groin Herniation
There is no fi rm evidence that strong muscular or strenuous
athletic exertion causes inguinal hernia in the absence of a
fascial and/or muscular abnormality—either acquired connective tissue disease or congenital anomaly of the abdominal wall. Indeed, inguinal hernias (as opposed to sliding
hiatal hernias) are rare in weight lifters [ 131 ] . However, in
a study of inguinal hernia and a “single strenuous event,” in
which 129 patients with a total of 145 inguinal hernias were
included, in 7% the hernia was subjectively attributable to
a single muscular strain [
gested guidelines to assist in assessing “causation” in workrelated compensation claims in such patients, which
included the following four recommendations:
132 ] . Indeed these authors sug-
1. The patient should have made an of fi cial report of the
incident of muscular strain.
2. Severe groin pain must have been experienced at the time
of the strain.
3. The diagnosis of hernia should preferably have been made
within 3 days of the incident (or certainly within 30 days).
4. There should be no previous history of inguinal hernia.
Interestingly, a recent similar study, using structured
postal questionnaires, suggested that inguinal herniation may
be attributed to a single event in a similar proportion of
patients [
133 ] , but another report questions the appearance
of a hernia (of any type) after such an event [ 134 ] .
At the moment, the relative importance of genetic, ana-
tomic, and environmental (smoking and heavy manual work)
factors cannot be construed in each case. Manual work or
strain is never, or very rarely, the sole cause of inguinal her-
niation; it may however reveal an underlying previously
asymptomatic one of which our patient was “clearly”
unaware of.
Recent research suggests that persistent straining and
heavy work is relevant (but not causal) to the development of
groin hernia. Recent European research has stressed these
environmental factors rather than congenital defects in hernia
development [ 135, 136 ] . In man and many mammalian quadrupeds, there is an abstinence of the posterior rectus sheath
below the arcuate line (of Douglas) and an “ineffectual” transversalis fascia in the groin. Gravitational stresses, while in the
erect posture, amplify this hindrance of weakness, which is an
evolved anatomical defect [ 137 ] . The etiology of groin hernia
also has importance in terms of prevention; smoking is a
causal agent but possibly less so in women [ 138 ] .
In medicolegal terms, the situation remains somewhat
confused—an accident or heavy strain at work is generally
construed as a causal factor in the onset of a hernia, and in
British courts damages are usually awarded. Our current
understanding of the etiology of inguinal hernias casts
doubt on judicial reasoning in many cases. The legal foundation for compensating a workman who develops a hernia
after an accident at his workplace is the commission of a
tort or breach of contract by his employer. The heads of
damages awarded are for pain or suffering, loss of amenities (usually sex life), pecuniary loss, medical expenses,
and loss of later earning capacity. The role of a preexisting
disability, patent processus vaginalis or metastatic emphysema, will need offsetting against these “damages.” This is
de fi nitely a task for the judiciary, being largely unrelated to
the observations of natural science [ 139 ] . Nevertheless in
preparing a medicolegal report, surgeons and other medical
experts must carefully examine all the contemporaneous
medical records to support a claim. If there is insuf fi cient
evidence to support a claim, they have a duty to the court to
nullify the plaintiff’s claim and associated litigation [ 134, 140 ] .
Finally the risk of a “work-related” hernia causes many