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62
Females
Males
Direct
emoral
Total: 263 Total: 3910
B.M. Stephenson
Indirect
125
47%
6%
15
Fig. 3.6 Groin hernia diagnoses in males and females (Truro 1974–
1992). Data from Williams et al. [9]
47%
Femoral
123
Indirect
2698
69%
2%
29%
F
94
Direct
1118
Statistics (NCHS) through its National Hospital Discharge
Survey, which has compiled data on the number of operations
performed annually in the USA, from a 5 to 8% sample of
patient records [18]. In the UK hernia surgery rates peak in the
55- to 85-year age group, at 600 operations per 100,000 population per year, and the incidence of strangulated hernia is
13/100,000 population, with a peak in the 80-year-old group.
A graphical analysis of hospital discharge data and demographic information guided by three hypotheses on urgency of
surgery, age, and evidence of discordance between population
prevalence of disease and rates of surgery has suggested that in
the last 10 years in Scotland, the rates of operation have
increased in over 65-year-olds but the rate of elective surgery
has decreased in the more socioeconomically deprived areas
[19]. It could be concluded from this data that more hernia
surgery is being carried out in an aging population and the
need for patient education is of particular importance, in terms
of health gains, in lower socioeconomic or uninsured population groups. Certainly in developing countries large, hernias in
the younger population place a significant economic burden
on society that is difficult to quantify [20].
In the USA the high rates of hernia surgery may have contributed to the reduction in mortality associated with strangulation. For instance, the mortality for hernia and intestinal
obstruction obtained by analysis of statistics data from the
NCHS shows a fall in the number of deaths per year per
100,000 population in patients over the age of 15 years, from
5 in 1968 to 3.1 in 1978, and stabilizing at 3.0 in 1988. This
was in spite of the fact that hernia patients with intestinal
obstruction were on average 15 years older in 1988 than in
1968. In 1971 Medicare discharges for inguinal hernia without intestinal obstruction showed 94% of patients having surgery, with a probability of death at 0.005 (5/100,000
population) [21]. Despite this low figure, uninsured patients
still seem five times more likely to present with complicated
hernias implying preventative measures still need to be
addressed even in well-developed countries [22].
Inguinal Hernias in Adults
Inguinal hernias are more common in males than females, in
a ratio of 8:1 or 20:1 in different series. However, there is
considerable incidence of under-reporting of inguinal hernia,
as illustrated by two validity checks in the US National
Health Surveys. In both studies half the hernias recorded
during the previous year were unreported on interview, and
in another study in Baltimore, positive reports were received
from only 21% of men found to have hernias on clinical
examination.
Incidence estimates in the literature vary widely and
depend on the source of the data. Approximately 94% of hernias among males are estimated to be in the inguinal region.
Ninety-five percent of inguinal hernia operations are on
males. Three times more females undergo femoral hernia
operations than males. By the age of 75 years, 10–15% of
males have already received inguinal hernia surgery. In the
period 1975–1990, mortality from inguinal hernia surgery in
the UK fell by 22% and for femoral hernia by 55%. In the
USA, for inguinal hernia with obstruction, 88% underwent
surgery with a mortality rate of 0.05% [21].
In a study of World War I British recruits, aged between
18 and 41 years, there was a marked variation in the reported
incidence of inguinal hernia. In Scotland 31/1000 were
found, whereas in London and the southeast of England, it
was 17–56/1000. In men aged 16–30 years, the rate was
6/1000, and in older men (aged 40–50), it was 24/1000. In
contrast, the overall rate in Stockport and Manchester was
125/1000. Sir Arthur Keith, in 1924, estimated the prevalence at 25/1000 males [23]. The figures for World War II
recruits are equally mystifying: the prevalence was about
26/1000 but ranged from 6 to 80/1000 men. Despite these
variations the overall incidence is probably much higher
given that these figures were recorded in young fit servicemen [24].
Sixty-five percent of inguinal hernias in adult European
males are indirect in type. Right-sided inguinal hernias in
adult males are slightly more frequent than left sided, 55%
occurring on the right, regardless of whether the hernia is
indirect or direct. Bilateral hernias are four times more often
direct than indirect. In Western series the peak incidence of
groin hernias is in the sixth decade [25].
A possible genetic link has been postulated in the Inuit living
in the western Arctic of Greenland. Hernia is common in males
and thought to be due to a high prevalence of disorders associated with instability of mesenchymal tissues, such as spondylolisthesis, arthritis, and heart block. The Inuit have been living in
almost complete genetic isolation for 150–200 generations and
have a high incidence and frequency of the HLA-B27 allele.
Such polymorphism could result in the observed frequency of
hernia in this closed knit population [26].
3 Epidemiology and Etiology of Primary Groin Hernias
Table 3.3 Percentage of age group with inguinal hernia
Age (years)
25–34 35–44 45–54 55–64 65–74 75 Total
No. examined 620 438 300 322 156 47 1883
Current prevalence (excluding
successful repairs)
“Obvious” hernias
Unoperated swellings 0.7 3.7 5.7 10.9 13.5 23.4 5.5
Recurrences 0.3 1.4 3.7 3.4 5.8 6.4 2.2
Palpable impulse only 11.0 10.3 10.7 11.8 10.3 4.3 10.7
Lifetime prevalence (including
successful repairs)
“Obvious” hernias
Data from Abramson et al. [28]
a
“Obvious” hernias included swellings and repaired hernias and excluded those presenting with a palpable impulse only. The current prevalence of
obvious hernias may be less than the combined prevalences of unoperated swellings and recurrences, since a person may have for example an
unoperated swelling in one groin and a recurrence in the other
a
a
11.9 15.1 19.7 26.1 29.5 34.1 18.3
1.0 4.8 9.0 14.3 19.2 29.8 7.6
15.2 19.4 28.0 34.5 39.7 46.8 24.3
4.7 9.6 18.3 24.2 30.8 44.7 14.5
63
The difference between the ratios of indirect to direct
inguinal hernia in different geographical locations supports a
polygenic predisposition to herniation. In Japan hernias are
seen twice as frequent in twins. In Ghana, West Africa, one in
every five live births is a twin (twice the rate seen in nonAfricans), a fact that may account for the higher incidence of
hernias recorded in Ghanaian men [27]. Comparing the age
structure of the patients with inguinal hernia operated in
Accra (the capital of Ghana) with the age structure found in a
field study shows that all age groups are equally represented
in the Accra hospital population, whereas in rural Ghana the
prevalence of groin hernia rises with increasing age [27].
It is impossible to compare these findings. Clearly the
results of the two large-scale surveys of fit uncomplaining
males, drawn from recruits of the British and American
forces in two world wars, do not represent fair and unbiased
sampling. The only field study is from southern Ghana and
confirms that inguinal hernias are at least three times more
common in Africans than Europeans.
The true prevalence of inguinal hernias can be estimated
only by community-based epidemiological studies, the
validity of which will depend on the diagnostic criteria used.
The presence of a visible, palpable lump may be supplemented by such diagnostic criteria as cough impulse at the
internal or external ring and the presence of an incision in the
groin. The latter, of course, may represent another form of
surgery, such as orchidopexy, rather than hernia. Moreover,
recurrent inguinal hernias may not be adequately ascertained. These drawbacks are well illustrated by the two studies alluded to above, carried out on British Army recruits in
the first and second world wars. The prevalence of groin hernias in recruits aged 30–40 years in World War I was 1.6% as
compared to 11% in World War II [9, 23].
Perhaps the most rigorous epidemiological study carried
out was that of Abramson in Western Jerusalem between
1969 and 1971 [28]. Males from differing ethnic and social
backgrounds were studied, although young males were
largely excluded because of national service. The study
involved interviewing subjects in their own homes where the
response rate approached 90%. Of these, 91% participated in
the second stage of the study, that is, of a physical examination. Both interviewers and examiners had been trained in
the use of questionnaires and diagnostic criteria. The results
are shown in Table 3.3. The prevalence increased with age in
all cohorts studied with the majority diagnosed on the basis
of a visible swelling. An important finding from the
Abramson study was the concordance between interview and
examination findings: only 50% of men reported a swelling
in the groin on interview, which is in close agreement with
the 50% under-reporting revealed from validity checks by
the US National Health Surveys [29]. It is obvious from
these studies that questionnaire-based data must be augmented by clinical examination if the true prevalence is to be
ascertained, although this may be confounded by problems
with diagnostic criteria. Clearly data regarding the incidence
statistics of hernia patients are difficult to ascertain accurately and are probably all underestimates.
Femoral Hernias in Adults
The prevalence and incidence of femoral hernias in the population cannot be determined accurately for a number of reasons. However, the demand incidence can be estimated from
the general practitioner morbidity survey of 1981/1982,
which is summarized in Table 3.1. An incidence figure for
England derived from these data is approximately 7000/year
[3], but the 95% confidence intervals are very wide indeed
(1500–24,000).
Femoral hernias are less common than inguinal and
account for only 10% of all groin hernias. They are more
frequent in females than males with an average ratio of 2.5:1,
64
B.M. Stephenson
but this is also age dependent (see Figs. 3.1 and 3.2).
However, there is other data that disputes this statistic (see
Chap. 20). 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 unfortunately 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 and 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 5083 primary femoral hernia repairs and 299
recurrent femoral hernia repairs being performed in
1989/1990 (Table 3.1). The age-specific data indicate an
increasing rate of repair through the decades with a peak in
our elderly female population (Fig. 3.5).
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 0.57–24/10,000 and for primary femoral hernia repair 0.16–2.3/10,000. Such unexplainable wide
variations reflect the diversity of clinical practice and the
“demand and supply” of treatment options already noted [9].
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
first 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 finding at autopsy that
15–30% of adult males without clinically apparent inguinal
hernias have a patent processus vaginalis at death [42]. In a
Bedouin mother and her four daughters with indirect inguinal
hernia in whom there was no evidence of collagen diseases,
normal hormone profile 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 mid
portion 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 first hernia been on the other
side [45, 46]. In addition, at 20 years of follow-up after 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
3 Epidemiology and Etiology of Primary Groin Hernias
65
subjected to intra-abdominal pressure, will dilate to give a
hydrocele or hernia [47–49]. Indeed this has been documented 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
infinitely 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 fol-
lowed 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 simply be one of a congenital defect, i.e., 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 congenital 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 deficiency of the lower
aponeurotic fibers 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 finding that direct hernias are frequently
bilateral and often surprisingly asymptomatic.
The anatomic disposition of the pelvis, and particularly
the height of the pubic arch, may also be a significant 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 significant muscular “shutter mechanism” is
apparent [59] as illustrated in Fig. 3.8. There is another much
rarer form of direct hernia where a narrow peritoneal diver-
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
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
66
B.M. Stephenson
ticulum comes directly through the conjoint tendon lateral to
the rectus and pyramidal muscles to project at the superficial
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
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 confirmed by weighing samples of a constant cross-sectional area; specimens
from controls weighed significantly 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 confirmed 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 deficiency. 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 inflammation
followed by one of proliferation, which is predominantly one
of increased fibroblastic activity with extracellular deposition and increased angiogenesis. Collagen is the end product
of fibroblast activity, and while there are many types of collagen, types I and 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 fibers consisting of elastin and microfibrils, 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 to proline ratio. Intermolecular
cross-linking is unaffected, but synthesis of hydroxyproline
is inhibited, and there is variability in the diameter of the collagen fibrils in hernia patients [65]. Similar electron microscopic findings are also present in pericardial and skin
biopsies from these patients [65] and have also been
described in connective tissue tumors [66], pulmonary
emphysema [67], and scurvy [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 findings 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 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, α1-antitrypsin deficiency,
osteogenesis imperfecta, scurvy, varicose veins, and experimental nicotine deficiency [67]. This hypothesis 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 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 deficiency
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 confirmed these findings by studying
biopsies from three sites in patients with inguinal hernia
[70]. Degenerative changes in the musculoaponeurotic fibers
3 Epidemiology and Etiology of Primary Groin Hernias
67
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 fiber
similar to that seen in Marfan and Ehlers–Danlos syndrome.
The implication from these findings 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) were studied from isolated skin fibroblasts in
patients with inguinal hernia. Fibroblasts incubated with
radiolabeled tritiated proline secreted increased amounts of
type III procollagen, suggesting that an altered fibroblast
phenotype in patients with inguinal hernia could result in
reduced collagen fibril 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 fit young men
with indirect inguinal hernias [72]. In addition when patients
who had had at least three previous hernia repairs were compared to controls, venous biomarkers of collagen turnover
(“synthesis,” P4NP and P5CP; “breakdown,” C4M and CM5)
were significantly different [73].
Could an uninhibited elastolytic enzyme system cause
groin herniation—a similar mechanism to low serum levels
of the protease inhibitor α1-antitrypsin globulin allowing
endogenous enzymes to destroy the alveoli [74]?
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 inflammatory 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
identified 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 fibroblasts of patients with
direct hernias and MMP-13 overexpression detected in
recurrent inguinal hernias [75, 76]. 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 (TGFβ1) is overexpressed in the transversalis
fascia of young patients with direct hernias [77]. 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 significantly 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 [78]. 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 [79].
The smoking habits of the three groups were not different,
and again the findings support the concept of systemic fiber
degeneration [80]. 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 confirmed. Nevertheless, overall patients with
aneurysmal disease have a fourfold increased risk of inguinal
and incisional herniation [81, 82]. Similar findings have been
found in patients examined by a magnetic resonance imaging
of the abdominal wall following aortic surgery [83]. These
findings 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 [84]. 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 goes some way to point out this is not going to
be a useful screening tool [85].
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 [86]. Read emphasized that the data indicate that more
than one factor can cause systemic metabolic disease of collagen leading to abdominal herniation including the imbalanced expression of different collagens. Subsequent results
have confirmed this in the transversalis fascia of patients
with inguinal hernia by direct measurement of the important
collagens (types I and III) [72, 87]. 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
68
aortic aneurysm is a copper transport collagen disorder
enhanced by cigarette smoking [88, 89].
With all the available data [90–92], 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
first 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 debatable [93]. Indeed a
recent meta-analysis of nearly 400 patients from five randomized controlled trials showed no superiority of biologic
mesh over a prosthetic one in terms of either recurrence or
chronic pain [94]. They are more expensive and lead to a
longer operating time, and such repairs are more often complicated by seroma formation.
B.M. Stephenson
Fig. 3.9 Persistent herniation in Ehlers–Danlos syndrome. Note the
unusual skin appearance
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 Ehlers–Danlos syndrome
(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 Ehlers–Danlos syndrome [95] with the genetic
mutations (autosomal 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 [96]. Indeed
genetic diseases of the microfibril (Marfan syndrome), elastin
(Costello syndrome and Menkes disease), and collagen
(Ehlers–Danlos syndrome 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 include 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 [97]. A number of
hypotheses have been suggested:
1. Autosomal dominant inheritance with incomplete pene-
trance [98]
2. Autosomal dominant inheritance with sex influence [99,
100]
3. X-linked dominant inheritance [101]
4. Polygenic inheritance [102, 103]
In a study from Budapest [102], 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
dependent on the sex of the index patient. In twins the hered-
3 Epidemiology and Etiology of Primary Groin Hernias
69
itability 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 influence. There is
preferential paternal transmission of the gene, suggesting a
role for genomic imprinting in the etiology of indirect inguinal hernias [104]. 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 2534 female controls
[105]. The relative risk for inguinal hernia was found to be
5.8 for brothers of male cases and 4.3 for brothers of female
cases, while the relative risk was 3.7 for sisters of male cases
and 17.8 for sisters of female cases. This pattern of sexdependent 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 [106]. As compared to controls and
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 autosomally dominantly inherited gene with reduced penetrance
and sex influence would therefore be susceptible to environmental factors influencing 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
were identified as genetic susceptibility targets in pigs at
known “high risk” of developing inguinoscrotal hernias [107].
All geneticists have to start somewhere, but subsequently four
chromosomal loci have been identified when comparing
15,000 cases and 150,000 controls [108]. These loci appear to
be associated with both direct and indirect inguinal hernias.
Their proteins are expressed in mouse connective tissue, and
two of them (WT1 and EFEMP1) are thought to play roles in
connective tissue maintenance through their action on extracellular matrix enzymes including metalloproteinases that are
known to degrade both collagen and elastin.
Intra-abdominal Diseases Causing Hernias
Ascites due to liver and 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
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 justified. Indeed the chance of unexpected “pathology” in an
otherwise normal hernial sac has been estimated (!) to be
0.00098% [109]. Routine histology is certainly unnecessary
and obviously uneconomical.
Interestingly the histological examination of sacs obtained
from children with hernia, hydrocele, 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 [110].
Thickening of a hernial sac per se is not necessarily due to
significant pathology; peritoneum is an 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
70
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 is reactive and certainly not neoplastic [111].
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. [112] 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 [112]. While this may
not now always be necessary, these patients clearly need medical optimization before surgery [113]. There is now little doubt
that elective surgery has significantly [114, 115] improved the
quality of life of these patients with mesh repairs well tolerated and outcomes similar to patients without cirrhosis [116].
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,
5 right femoral, 3 left inguinal, 1 epigastric, and 1 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 [117]. 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 right-sided
hernias [118]. 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 one’s suspicions
allowing a tailored minimally invasive staged approach when
appropriate [119, 120]. A tender inguinal mass may not represent a hernia as demonstrated in Fig. 3.11!
Inguinal Hernia and Appendectomy
Over a hundred years ago, Hoguet first reported the development of inguinal hernia in patients who had undergone previous appendicectomy [121]. 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 [122–124].
B.M. Stephenson
Fig. 3.10 Residual collection in a large long-standing hernia after
emergency surgery for gastric perforation
Fig. 3.11 A diverticular abscess presenting as a hernia. Fortunately a
colocutaneous fistula did not develop in this frail 78-year-old lady
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 conflicting results. While some investigators [124] have shown that denervation of the transversus
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
investigators have failed to detect any significant denervation
of the musculature in and around the right groin [125].
3 Epidemiology and Etiology of Primary Groin Hernias
71
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 flank muscles are opened by splitting in their fiber 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% [126].
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. Only when laparoscopic appendectomy is fully embraced as a standard
approach (with reasons for and with durable follow-up of
converted cases) will we know if this technique also contributes to a later lower incidence of subsequent inguinal herniation. The debate regarding open or laparoscopic appendectomy
will no doubt continue before this becomes universal surgical
practice even in the developed world [127, 128].
Inguinal Hernia and Prostatic Surgery
It is not really surprising that men being investigated and/or
treated for prostate cancer are found to have an inguinal hernia given the incidence of this disease with increasing age.
The majority of these are asymptomatic or at most minimally
symptomatic. However it is of interest to note that patients
undergoing treatment for prostate cancer (retropubic prostatectomy, minimally invasive approaches, or radiotherapy
alone) in Sweden had an almost fourfold increase in later
groin hernia repair as compared to over 100,000 controls
[129]. The findings of this nationwide, population-based
study are not particularly new but illustrate the frequency of
the problem and the dilemma facing surgeons.
Clearly prostatic surgery, whichever operative approach is
used, leads to a further weakening of the anatomy of this
area. Symptomatic inguinal hernias are justifiably repaired,
but what of those found incidentally at preoperative workups? Are there any identifiable risk factors that might be useful in predicting which patients would benefit from
prophylactic surgery? The answer seems to be yes. The presence of a processus vaginalis, either patent or not, on dissecting the preperitoneal space is an important risk factor for the
later development of an inguinal hernia [130].
Now that we may have identified those at later risk, how
should these be managed? Is there just a theoretical risk or are
concerns about prosthetic mesh infection, close to a neobladder- urethral anastomosis, valid? Certainly there are a
number of reports suggesting that repairs can be safely
accomplished with and without mesh [130–133], but should
incidental hernias be repaired with prosthetics? In view of the
concerns about infection, absorbable meshes have been used,
but the results have been poor. Another approach that seems
worthy of consideration is a concerted dissection, isolation,
and transection of any identified processus vaginalis off the
vas deferens and spermatic vessels [134, 135]. When the processus was formally transected, less than 1% of patients
developed herniation at a median follow-up of 42 months.
Although to date there are no randomized trials comparing
these different approaches, we will have to wait to see if
exploiting anatomy is indeed better than augmenting it.
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 [136].
Ryan, from the Shouldice Clinic, reported only five hernias
related to pelvic fractures in 8000 hernia repairs [137].
Figure 3.12 illustrates an unusual case of a patient whose
hernia was related to a pelvic fracture: a 40-year-old man
Fig. 3.12 Herniography on a 40-year-old man who had sustained a fracture
of both pubic rami. The patient developed a “pantaloon” inguinal hernia