Anatomy of the anterior abdominal wall

Incision and closure of the abdominal wall is among the most

frequently performed surgical procedures. The abdominal wall is defined
cranially by the xiphoid process of the sternum and the costal margins,
and caudally by the iliac and pubic bones of the pelvis. It extends to the
lumbar spine, which joins the thorax and pelvis and is a point of
attachment for some abdominal wall structures (Flament, 2006).

The abdominal wall is unique in terms of functional anatomy. It is

composed of pairedmuscles and aponeuroses that perform complex
functions. Each muscular and aponeurotic component has a contralateral
component on the other side of the abdominal wall, which functions
synergistically (or antagonistically) to maintain the balance of the torso of
the human body. The abdominal wall also acts as a protective barrier to
contain the viscera. It stabilizes the trunk and the vertebral column, and
allows flexion, extension, and rotation of the trunk. The abdominal wall
works with other organs to maintain the processes of respiration,
micturition, defecation, and childbirth. Because of all of these functional
capabilities, surgeons operating on the abdominal wall require knowledge
of its anatomy, blood supply, and innervation, as well as how each
functional unit functions (Ruotolo et al., 2008).

Generally, the successive layers of the anterior abdominal wall

are : skin - superficial fascia (comprising two layers, outer adipose layer
“Camper's fascia” and inner fibroelastic, membranous layer “Scarpa's
fascia”) - a musculo-aponeurotic ‘plane’ (which is architecturally
complex and composed of several laminae).- transversalis fascia - a
properitoneal adipose layer - parietal peritoneum (Mahadevan, 2012).
Subcutaneous tissue and fascia of the abdominal wall

Subcutaneous tissue is in fact one of the organs of the human body,

the structure of which has only received limited attention by anatomists in
the last century, and regarding which a large gap still persists between
anatomists and surgeons (Lancerotto et al., 2011).

Superficial fascia of the abdomen lies between the skin and

muscles of the anterior abdominal wall and there is no deep fascia in this
region (Kumar et al., 2013).It would render deep breathing or abdominl
distension impossible (Ellis, 2009).Some authers consider the thin layer
of connective tissue covering the muscles as deep fascia (Snell, 2012).

Previous anatomical and radiological studies described two

different fat compartments in the lower abdominal wall, superficial and
deep, separated by a layer of membranous tissue known as Scarpa fascia
(Hunstad & Repta, 2009).

The superficial structures of the abdominal wall from superficial to deep, include the
skin, superficial fat, superficial fascia (Scarpa fascia), deep fat; (Hunstad & Repta,
2009)

The superficial fascia is a soft and movable layer, which

comprises, to a great extent, a single variably fatty superficial layer
known as Camper’s fascia (Arslan, 2005). This fascia is immediately
subjacent to the dermis and similar to superficial fascia elsewhere in the
body (Mahadevan, 2012). The amount of fat in Camper’s fascia varies
depending on the nutritional status of the individual. In the male, it
continues inferiorly with the dartos layer of the scrotum and outer layer of
the penis and spermatic cord, where it becomes thinner, lacking adipose
tissue. In the female, it continues with the superficial fascia covering the
labia majora. Approximation of Camper’s fascia at closure of the
abdominal incision during cesarean delivery appears to prevent
postoperative superficial wound disruption (Del Valle et al., 1992)
(Arslan, 2005).

In the lower wall of the anterior abdomen, a deeper membranous

layer known as Scarpa’s fascia becomes visible. This layer remains
connected, though loosely, to the deep fascia that covers the aponeurosis
of the external abdominal oblique muscle. The strength of the Scarpa’s
fascia can stabilize sutures placed when closing incisions of the
abdominal wall. The space between the deeper fascia that covers the
external oblique and Scarpa’s fascia (superficial inguinal pouch) occupied
by loose connective tissue may serve as a frequent site for retracted
ectopic testis in children (Markman & Barton, 1987). Scarpa's fascia
is more prominent and better defined in the lower half of the anterior
abdominal wall. Also, it is more prominent in children (particularly
infants) than in adults (Forster, 1937).

Superiorly, Scarpa's fascia crosses superficial to the costal margin

and becomes continuous with the retromammary fascia. Laterally it fades
out at the mid-axillary line. Inferiorly, it crosses superficial to the
inguinal ligament and blends with the deep fascia of the thigh about 1 cm
distal to the inguinal ligament. Below the level of the pubic symphysis, in
the male, Scarpa's fascia is prolonged quite distinctly into the scrotum
and around the penile shaft. This prolongation of Scarpa's fascia into the
perineum is known as the superficial perineal fascia or Colles' fascia. A
similar, but less distinct and less readily demonstrable extension of
Scarpa's fascia occurs in the female perineum. As in the male this
extension is known as superficial perineal fascia. (Mahadevan, 2012).

Scarpa’s fascia firmly attaches to the linea alba and symphysis

pubis and forms the fundiform ligament of the penis or the clitoris. In the
upper thigh, it is attached to the fascia lata just below and parallel to the
inguinal ligament. Because of the firm attachment of Scarpa’s fascia to
the fascia lata, inferior spread of fluid is not possible. The space between
the two layers of the superficial fascia allows passage of the cutaneous
vessels, nerves and lymphatics of the superficial inguinal nodes. (Arslan,
2005).

Fig : The two layers of the superficial fascia of the abdominal wall (Arslan, 2005)
 Although the empirical view of abdominal subcutaneous tissue is
that of two layers of fat with differing macroscopic structure of its lobes,
divided by a layer of membranous tissue. Anatomical descriptions range
from that of a single layer of adipose tissue, reported in most common
textbooks and atlases (Moore & Dalley, 2009) (Standring et al., 2005)
to more complex reports by some authors, with varying definitions of
layers and terminology. This situation, however, seems to have ancient
roots, as it was already lamented in the early decades of the nineteenth
century (Darrach, 1830).

The confusion surrounding subcutaneous tissues is closely

connected with that on the so-called superficial fascia. As clearly
described by Wendell-Smith the use of the term ‘‘superficial fascia’’ (or
fascia superficialis) is often improper and inconsistent. Because of this,
the international consensus forum for agreement on official anatomical
definitions abandoned this widely used and widely abused name in the
latest edition of the Termina Anatomica (Wendell-Smith, 1997).

Another terminological problem derives from the custom of calling

some fasciae by the name of the author who first described the anatomical
element in question: Antonio Scarpa described a fascial layer in the
abdominal wall Colles described one in the perineum, Camper is believed
to have described another, to quote only the best-known examples. To
add to the confusion, following a single author’s interpretation, the term
‘‘superficial fascia’’ could or could not be considered synonymous with
fascia of Scarpa, Colles and Camper, etc (Lancerotto et al., 2011).

By the middle of the nineteenth century the existence of a

membranous layer on the deep aspect of the superficial fascia of the
lower abdominal wall was well known.
 Priority for the description of the membranous superficial fascia
(MSF), also known as the deep membranous layer of the superficial
fascia, in the inguinal region is traditionally accorded to Antonio Scarpa
(1752–1832), professor of anatomy and surgery at the University of Pavia
.This layer was first mentioned by Scarpa (1809) in a report on hernia
(Parigi, 2004).

One year later, Abraham Colles, of Dublin, described anatomical

dissections of the MSF in the lower abdomen, perineum, penis and
scrotum (Ullah et al., 2013) (Colles, 1811).

It is interesting to consider the teleological purpose of the MSF.

Scarpa’s assertion that the MSF assists in the prevention of hernias has
been repeated often but it is not consistent with a modern understanding
of hernias (Martin, 1984).

MSF is believed to be designed to bind the skin to the body by two

layers of attachment on each side of the membranous fascia. This
construction supports the skin so that it does not sag with gravity but
allows it to stretch in a way that does not impede movement. Simply put,
the MSF is the scaffold of the skin. As such, its role in reconstructive
surgery is acknowledged and is being investigated in the development of
adipofascial flaps (Worseg et al., 1997).

Thickness of the deepest layer of superficial fascia showed

difference in the upper and lower abdomen. The mean thickness of the
fascia of the lower abdomen was more than the upper abdomen though it
was statistically not significant. Mean thickness of fascia of both the
lower and upper abdomen was higher in males than females. Literature
review reveals that the superficial fascia is the supporting structure for
subcutaneous fat of the abdomen and lower abdominal obesity is more
common in female (Kumar et al., 2011).
Deep structures of the anterior abdominal wall

The abdominal wall can be divided into both midline and

anterolateral groups of muscles comprising four main paired muscle
groups as well as a variably present paired fifth muscle group. The
muscular groups are covered by subcutaneous fat and skin along with
superficial neurovascular structures which overlay the fascia. The rectus
abdominis and the pyramidalis muscles comprise the midline group,
although the presence of the pyramidalis is not consistent among the
population (Van Landuyt et al., 2013) (Lovering & Anderson,
2008). The bilateral anterolateral groups are composed of a trilaminar
structure consisting of the external oblique muscles (EOMs), internal
oblique muscles (IOMs), and transversus abdominis muscles (TAMs)
(Majumder, 2016).

Fig : Fascial component & the perforating vasculature to the adipocutaneous

component of the anterior abdominal wall (Nahabedian, 2017)
Rectus sheath and linea alba
While the muscular components of abdominal wall are of crucial
importance, the restoration of linea alba remains the goal of definitive
abdominal wall reconstruction (Majumder, 2016). Restoration of linea
alba has been shown to improve isokinetic and isometric function of the
abdominal wall and ultimately quality of life (Criss et al., 2014).

The anterior rectus sheath and linea alba are composed of collagen
fibers arranged in lattice configuration. The width and thickness of these
structures fluctuate at various regions of the anterior abdominal wall and
are assessed based on the distance from the umbilicus. The width of the
linea alba ranges from 11 to 21 mm between the xiphoid process and the
umbilicus and decreases from 11 to 2 mm from the umbilicus to the pubic
symphysis. The thickness of the linea alba ranges from 900 to 1200 μm
between the xiphoid and the umbilicus and increases from 1700 to 2400
μm from the umbilicus to the pubic symphysis. The thickness of the
anterior rectus sheath ranges from 370 to 500 μm from the xiphoid to the
umbilicus and increases to 500–700 μm from the umbilicus to the pubic
symphysis. The posterior rectus sheath is slightly thicker than the anterior
rectus sheath above the umbilicus, ranging from 450 to 600 μm and
decreases from 250 to 100 μm from the umbilicus to the arcuate line
(Nahabedian, 2017).

The rectus abdominis arises from the 5th, 6th and 7th costal
cartilages and is inserted into the crest of the pubis. At the tip of the
xiphoid, at the umbilicus and half-way between, are three constant
transverse tendinous intersections; below the umbilicus there is
sometimes a fourth. These intersections are seen only on the anterior
aspect of the muscle and here they adhere to the anterior rectus sheath.
Posteriorly they are not in evidence and, in consequence, the rectus
muscle is completely free behind. At each intersection, vessels from the
superior epigastric artery and vein pierce the rectus (Ellis, 2006).

The rectus sheath in composed of anterior and posterior layers

above the level of the arcuate line only, the anterior layer is formed of the
aponeurosis of the external oblique muscle and the anterior division of
the internal oblique aponeurosis, the posterior layer is formed of the
posterior division of the internal oblique aponeurosis and the aponeurosis
of transversus abdominis muscle, while below the arcuate line the rectus
sheath is composed only of one layer anteriorly formed by the
aponeurotic portion of the all three muscles, posterior to rectus muscle
lies the peritoneum (Moore et al., 2006).

Fig : The aponeurotic layers of the anterior abdominal wall include the linea
alba, anterior rectus sheath, posterior rectus sheath, and external oblique fascia
(Nahabedian, 2017)
 The arterial supply of the rectus muscles originates from the
superior and inferior epigastric artery which are embedded in the dorsal
surface of the rectus abdominis muscle. The nerve supply originates from
the ventral rami of Th7 to Th12, frequently completed by additional
branches ofTh6 and LI. The nerves run on the dorsal surface of the
internaioblique muscle, then cross the semilunar line and enter the muscle
from lateral and dorsal (Klinge et al., 2003).

The Following table summarize the anatomy of abdominal wall

muscles: origin, insertion, action and nerve supply

Table : Abdominal wall muscles (Snell, 2012)

Fig : Muscles of the abdominal wall with the anterolateral group comprising the
external and internal oblique along with the transversus abdominis extending medial
to the linea semilunaris. The midline group is comprised of the rectus abdominis and
pyramidalis muscles. Cross sections are illustrated above and below the arcuate line
(Majumder, 2016).
Vascular anatomy of the anterior abdominal wall
Three different sources are responsible for blood supply of the
abdominal wall. (Boyd et al., 1984) they include:

 The "deep superior epigastric" and "deep inferior epigastric" vessel

which form the epigastric network giving origin to "rectus
perforators" these perforators are primary blood supply.
 The "superficial inferior epigastric" and "superficial superior
epigastric" vessels and "superficial circumflex" vessels.
 The lateral "intercostal" and "subcostal" vessels.

It is of great importance to have the proper knowledge of the

vascular supply of the abdominal wall as any abdominal wall
reconstruction procedure is associated with considerable undermining of
the skin and soft tissue which interferes with at least one or more of these
three sources of vascular supply.

Fig : Vascular supply of the abdominal wall. (Hunstad & Repta, 2009)
 The blood supply to the abdominal wall was previously described in a
regional manner by Huger, consisting of three anatomically distinct zones.
Zone I refers to the upper anterior midline of the abdominal wall with the
SEAs and DIEAs as they supply the rectus abdominis and overlying
subcutaneous tissue and skin. Zone II comprises the entirety of the caudal
portion of the anterior abdominal wall. The blood supply in this region arises
from four main arterial conduits with contributions from the femoral and iliac
arteries. The superficial inferior epigastric and superficial external pudendal
arteries originate from the femoral artery to supply the superficial fascia and
skin in this area. The DIEAs and deep circumflex iliac arteries supply the
musculature in this lower area. Zone III is located laterally past linea
semilunaris with lumbar and intercostal arteries which arise from the aortic
system. These arcades supply the lateral abdominal wall and eventually
anastomose with the midline vascular structures (Huger et al., 1979).

Fig : Vascular supply to the abdominal wall with delineated Huger Zones I–III
(Majumder, 2016).
Lymphatic drainage of the anterior abdominal wall

Like divisions of the abdominal wall layers (to superficial and deep
structures) the lymphatics of the abdominal wall can be divided into
superficial lymphatic vessels and deep lymphatic vessels according to
their relation to these layers. Superficial lymphatic vessels are situated
above the deep muscular fascia within the abdominal wall soft tissues,
they are largely affected by abdominoplasty procedures. Deep
lymphatic vessels are situated below the deep muscular fascia within
the abdominal muscle layers themselves, they are not usually affected
by abdominoplasty procedures in spite of myofascial plication which
involves the deep muscular fascia. The abdominal wall lymphatics drains
into the axillary lymph nodes above the level of umbilicus and superficial
inguinal lymph nodes below the level of umbilicus (Moore et al., 2006).
Fig. Lymphatics of the abdominal wall (Hunstad & Repta, 2009).

Nerve Supply of the anterior abdominal wall

The abdominal wall sensory innervation in supplied by

dermatomes from T7 to T12 and L1. From T7 to T11 give origin to
intercostal nerves, T12 gives origin to subcostal nerve and L1 gives 2
branches which originates from the lumber plexus the "iliohypogastric"
and the "ilioinguinal" nerve.
Intercostal and subcostal nerves gives 2 sensory branches which
are the lateral and anterior cutaneous branches, the anterior branches
of these nerves runs in the plain between the "internal oblique" and the
"transversus abdominis" muscles and when they reach the rectus sheath
the pass through the "rectus abdominis" and rectus sheath to give
cutaneous branches (anterior cutaneous branches) which provide
sensory supply to the skin of the midline of the abdomen, while the
lateral branches (lateral cutaneous branches) arise from these nerves
and pass through the "external and internal oblique" muscles near the
mid axillary line and run superficial to the "external oblique" muscle to
provide sensory supply to the majority of skin of the abdominal wall
except skin around the midline. The iliohypogastric and ilioinguinal
nerves follow similar course initially but differ in their termination they
supply the lower part of the abdomen, scrotum or labia majora and the
corresponding inner aspect of the thigh (Richard et al., 2015).

Fig : Sensory nerve supply of the abdominal wall (Hunstad & Repta, 2009).
Pathiophysiology of hernia formation

Hernia formation is a multifactorial process involving

endogenous factors including age, gender, anatomic variations, and
inheritance and exogenous factors such as smoking, comorbidity, and
surgical factors (Jansen et al., 2004). However, these factors alone do not
explain why some develop abdominal wall hernias. Already in 1924, the
anatomist Sir Arthur Keith proposed that surgeons should try to perceive
tendons and fascia as living structures in order to understand the hernia
disease properly (Read, 2007).

Fig : Endogenous and exogenous factors involved in hernia formation (Jansen et

al., 2004)

The connective tissue comprises the extracellular matrix (ECM)

and the cells within. The ECM contains proteoglycans and proteins, such
as collagen and elastin, which together form a dense network important
for tissue stability. In healthy tissue, regeneration of ECM involves a
controlled balance between degradation of old and damaged proteins and
synthesis of new ones (Stamenkovic, 2003). In hernia patients, this
balance may be disturbed leading to altered tissue turnover and impaired
tissue quality (Henriksen et al., 2017).

There are 28 genetically different types of human collagen. The

skin and fascia consist mainly of type I collagen with smaller amounts of
type III and V collagen. The same collagen fiber can comprise both type I
and III collagens. The more type III collagen relative to type I collagen,
the thinner and weaker the fiber. Type V collagen is essential during
collagen maturation, as it is involved in the initiation of fibril formation
(Rosch et al., 2003)(Kadler et al., 2007).

Abdominal wall hernias occur due to loss of tissue normal

structure, anatomy and function at the fascial layer, load-bearing muscle
and tendon. So the main factors of occurrence of hernia are either primary
fascial pathology or surgical wound failure. In both cases, the pathology
occurs at the level of cellular and extra-cellular molecular matrix (Franz,
2009).

Abnormal collagen metabolism was an early biological mechanism

proposed for the development of primary and incisional hernias
(Peacock, 1984).Immature collagen isoforms were measured in patients
with inguinal and incisional hernias (Junge et al., 2004).

Medicine provides many clues for the role of the extra-cellular

matrix during hernia formation. Some acquired disorders of the
connective tissue can predispose to hernia formation due to a laxity in
fascial planes. Ehlers-Danlos syndrome is a collection of collagen isoform
disorders, also predisposing to hernia formation. There is growing
evidence that patients with large vessel aneurysmal disease express
pathological extra-cellular matrix metabolism, predisposing to dilated
aortas and hernias. Some studies found disordered collagen fibers and
impaired hydroxylation of the collagen can predispose to hernia
formation (Read, 2006) (Thomas et al., 2008). Further, patients with
direct inguinal, bilateral inguinal, or recurrent inguinal hernia are at
higher risk of ventral hernia formation suggesting a systemic
predisposition to hernia formation (Henriksen et al., 2013).

The wound healing process is complex and involves important

steps in ECM turnover, which are important in the understanding of
secondary hernia formation, that are incisional or recurrent hernias. First
step of the wound healing process includes vasoconstriction and clot
formation secondary to activation of both platelets and the coagulation
cascade. The following inflammatory phase initiates the immune
response in order to eliminate bacteria from the wound. A wound
colonized with bacteria at a high tissue concentration will not heal
properly as illustrated by the fact that surgical site infection is a well-
known risk factor for incisional hernia formation (Jensen et al., 2016).
During the inflammatory response, several growth factors are involved,
which among others activate fibroblasts leading to the proliferative phase
of wound healing beginning on day 3. This involves fibroblast and
myofibroblast proliferation, followed by migration, leading to wound
contraction. The fibroblasts produce type I and III procollagens and
deposit ECM. In unwounded dermis, there is 80 % type I collagen and 20
% type III collagen, whereas there is 40 % type III collagen in wounded
dermis, resulting in thinner collagen fibers with less strength. Lastly, the
remodeling phase takes place and may last up to 2 years. During this
phase, the immature type III collagen is replaced by the mature and
stronger type I collagen (Velnar et al., 2009). Any imbalance in this
process may lead to hernia formation. Interestingly, the type I to III
collagen ratio is even more decreased in patients with secondary hernias
as compared with patients with primary hernias, suggesting that hernia
recurrence is also associated with collagen imbalance (Peeters et al.,
2014).

The final strength of the wound depends on the respective

anatomic region, and the duration and quality of the wound healing
process. However, surgically traumatized fascial or aponeurotic tissues
never regain their original strength, indicating that a midline aponeurotic
scar is relatively weak despite uncomplicated healing conditions. It has
been demonstrated that minor mechanical stress impacts positively on
wound healing in various tissues. Sutured wounds of aponeurosis benefit
from mechanical stress in terms of organization and alignment of
collagen fibrils as well as enhanced maturation of collagen cross-linking
(Oryan, 1995).

Biological Components of incisional hernia

Acute wound healing fails when there is a deficient quantity or

quality of tissue repair. Ultimately, it is the time required for the recovery
of wound breaking strength that determines the risk of acute wound
failure. Inadequate hemostasis due to platelet dysfunction or poor
technique can result in hematoma formation with ensuing mechanical
disruption of a provisional wound matrix. A delayed or deficient
inflammatory response can result in wound contamination or infection
with abnormal signalling for progression into the fibro-proliferative phase
of acute tissue repair (Robson et al., 2001). A prolonged inflammatory
response due to the presence of a foreign material, like a mesh implant, or
wound infection will delay the progression of acute wound healing into
the fibroproliferative phase where rapid gains in breaking strength should
occur (Robson et al.,1970). Delayed fibroblast responses in turn impede
the synthesis of a provisional wound matrix, prolonging the period of
time a surgical wound is subjected to increasing mechanical loads and
dependent entirely on suture material and technique for strength (franz,
2009).

The mechanism by which the collagen-rich early laparotomy

wound matrix attaches to uninjured tissue at the wound border is also
poorly understood. This mechanism is important since acute laparotomy
wounds most often fail at the scar to normal tissue interface (Viidik &
Gottrup, 1986).

 Different tissue also heals at different rates. Native tissues with

collagen bundles organized in a parallel orientation, like fascia, ligament
or tendon, re-gain breaking strength faster than tissue with a more
complex, three dimensional fiber network, such as in the dermis. The
time required to achieve 50% wound breaking strength is greater in tissue
with high collagen content, again, as in the case of dermis. Conversely,
more “simply” arranged soft tissues like abdominal wall fascia, with
lower tissue collagen content, but organized in a purely parallel manner
along lines of tension, should achieve uninjured breaking strength faster
(franz, 2009).
Fig. : Incisional hernias occur when suture fails, suture lines are too loose, or suture
pulls through the tissue adjacent to the wound. This develops before the laparotomy
wound scar is mechanically capable of withstanding the distractive forces. The
provisional matrix (PM) is comprised of immature and weak matrix glycoproteins and
collagen isoforms. In addition, the scar to wound interface is not developed.

It is not known whether delays in the appearance of

fibroproliferative growth factors contribute to the development of
incisional hernias. Surgical wound therapy with proliferative growth
factors is known to stimulate the appearance of fibroblasts and collagen
into the wound thereby accelerating the gain in wound breaking strength
(Mustoe et al., 1987).

Inadequate nutrition also impairs the immune response limiting

opsonization of bacterial and sterilization of wounds. Several vitamin and
mineral deficiencies also have been described that predispose to altered
wound repair. Vitamins C, A, and B6 each are required for collagen
synthesis and cross-linking. Deficiencies in Vitamins B1 and B2 as well
as zinc and copper cause syndromes associated with poor wound repair.
Finally, essential fatty acids are required for cell synthesis, particularly in
areas of high cell turnover such as healing wounds (Williams & Barbul,
2003).
 Perioperative shock is a well recognized risk factor for incisional
hernia formation (Mudge & Hughes, 1985). Besides systemic
hypotension, a too tight continuous suture line closure may exacerbate
laparotomy wound ischemia. Emergency operations may also be
associated with wound contamination and altered surgical technique.
Laparotomies following gunshot wounds to the abdomen or for
perforated viscous may leave devitalized tissue and high levels of bacteria
in the surgical wound. High wound bacterial counts are known to lead to
wound failure, and in this case, incisional hernia formation (Robson,
1979).
Most studies designed to improve laparotomy and hernia wound
outcomes have focused on surgical technique and the mechanical
properties of suture material and mesh. Surgical wound failure is most
often due to suture pulling through adjacent tissue and not suture fracture
or knot slippage (Carlson, 1997).

Abdominal wall tendons and fascia are connective tissues placed

under intrinsic and extrinsic loads that are likely dependant upon
mechanical signals to regulate fibroblast homeostasis. Mechanical signals
are transmitted to the structural cell via integrin receptors. In brief, a load
imparted on a soft-tissue or bone is transmitted to structural cells through
the extra-cellular matrix via transmembrane integrin receptors located on
the cell surface. In one proliferative pathway, subsequent activation of the
focal adhesion kinase (FAK) complex, leads to cytoskeletal changes, and
the further activation of downstream signalling tyrosine kinases like c-src
and the MAP kinase proliferation pathway (Schmidt et al., 1998).

The varying mechanical forces exerted across anatomically

different celiotomy incisions such as midline vs. transverse therefore may
affect repair fibroblast activation, provisional matrix assembly and
collagen deposition and ultimately the temporal recovery of laparotomy
wound tensile strength. Surgical experience has long held that transverse
abdominal wall incisions oriented parallel to the predominant myofascial
fibers regain unwounded tissue strength faster, but a clear benefit on
wound outcomes has never been proven (Carlson, 1997).

To summarize, the fundamental mechanism of abdominal wall

hernia formation is the loss of structural integrity at the musculo-
tendinous layer. This results in the inability to contain abdominal organs,
support upright posture and maintain increased intra-peritoneal pressure
during Valsalva. Primary abdominal wall hernias have been associated
with extra-cellular matrix diseases. Incisional hernias and recurrent
inguinal hernias more often involve a combination of technical and
biological limitations. Defects in wound healing and extra-cellular matrix
synthesis contribute to the high incidence of incisional hernia formation
following laparotomy (franz, 2009).

Pathogenesis of the epigastric hernia

The anterior rectus sheath forms the major and most conspicuous
part of the anterior abdominal wall. This sheath contains three strata: the
superficial stratum, the middle stratum and the deep stratum. The
superficial stratum has tendinous fibres that run downward and laterally
and, when followed, will come from the external oblique aponeurosis of
the other side. In the middle stratum, the tendinous fibres run downward
and medially at right angles to those of the superficial stratum; these are
the tendinous fibres of the external oblique muscle of the same side. In
the deep stratum, the tendinous fibres run upwards and medially, and
these fibres originate from the anterior lamina of the internal oblique
aponeurosis. Due to these anatomical structures, a triple criss-cross layer
pattern is formed. The tendinous fibres in these three strata are bound
together by loose tissue that facilitates their movement. In the posterior
rectus sheath, a similar triple-layer pattern is seen.The triple-layer criss-
cross pattern offers firmness to then texture of the aponeurosis in both the
anterior and the posterior rectus sheaths and therefore makes them less
liable for herniation. (Askar, 1978) (Askar, 1984).

Fig . Different patterns of decussation at the linea alba abdominalis described by

Askar (Ponten et al., 2012).

Pathological anatomy responsible for epigastric herniation, a

theory by Askar (part I)

Askar suggested in 1978 that in 30–40 % of the general population,

the fibres decussate once with the fibres of the opposite side in the
abdominal wall. In the other 60–70 %, the fibres decussate two or three
times. Askar assumes that epigastric herniation is found exclusively in
patients with a single anterior and single posterior crossing pattern. This
is probably a congenital factor predisposing to developing an epigastric
hernia (Fitzgibbons & Greenburg, 2002). Bur, both biopsy studies and
postmortem (or cadaver) studies do not confirm the first part of Askar’s
theory (Ponten et al., 2012).

Pathological anatomy responsible for epigastric herniation, a theory

by Askar (part II)

Askar suggested that another mechanism is responsible for the

acquirement of an epigastric herniation. Originating from the sternocostal
portion of the diaphragm, there are fine tendinous fibres. These fine fibres
are viewed as the posterior aspect of the upper part of the midline
aponeurosis. Normally, the function of these tendinous slips, coming from
the diaphragm, is to synchronize the movements of the diaphragm with
those of the respiratory zone in the upper part of the anterior wall. They
appear to be responsible for the occurrence of an actual epigastric hernia
due to powerful contractions of the diaphragm, as occurs in a severe
spasm caused by coughing or straining. The fact that all epigastric hernias
occur in the midline and that the hernial orifice is transversely placed,
either rhomboid or oval, strongly supports this suggestion (Askar, 1984).
However, the statement that the acquired herniation is due to a
single strenuous event seems rather unlikely. Pathak and Poston show that
it is more likely that the herniation is due to repeated strenuous exertion
(Pathak & Poston, 2006).
Pathological anatomy responsible for epigastric herniation, a theory
by Moschowitz

Moschowitz suggests that epigastric herniation is linked to the role

of vascular lacunae at the linea alba of the anterior abdominal wall. These
vascular lacunae are formed when small blood vessels, which run
between the transversalis fascia and the peritoneum, perforate the linea
alba. As they pierce the transversalis fascia, a layer of fascial fibres is
being pushed upwards and a space is created between the peritoneum and
the fascia. During the periods of increased abdominal tension, parts of the
pre-peritoneal fat derived from the falciform ligament are forced into the
space along the blood vessels and pierce the aponeurosis. Over a period
of chronic and acute intermittent straining, the fascial defect enlarges and
an epigastric hernia is formed (Lang et al., 2002).

Fig : a Linea alba, b falciform ligament, c peritoneum, d perforating vessel, e (true)

epigastric hernia (Ponten et al., 2012).

Recent microscopic anatomical studies show that not only the

macroscopic anatomy of the linea alba is important in epigastric hernia
pathology, but that the microscopic aspects should also be considered.
Degeneration of collagen is associated with the requirement of several
ventral hernias (Fachinelli & Trindade, 2007). In the abdominal wall,
damaged collagen fibres are continuously repaired in the progress of
proliferation and remodelling. The normal turnover of collagen is very
slow, and it may take many years before the collagen is degraded and
replaced (Sorensen, 2006). showed that patients with ventral hernias
have a significant less amount of total collagen in the abdominal wall
compared to controls without ventral hernias. Especially the amount of
type I collagen was about 20 % less than the amount of collagen in the
controls (Fachinelli & Trindade, 2007).
Fachinelli et al. reported that a significant higher amount of elastin
is found in the abdominal wall in patients with ventral hernias. These
findings suggest that not only anatomical diversity but also microscopic
and histological factors plays a role in the acquirement of epigastric
hernias (Fachinelli et al., 2011).
 Fascial layers of the abdomen and their
importance

Subcutaneous tissue has recently been a subject of increasing

interest. New surgical approaches have been developed in which
subcutaneous tissue is the primary object, such as flaps in Plastic
Reconstructive surgery, and fat removal techniques in Aesthetic surgery
procedures (Matarasso, 2010).

Subcutaneous tissue is in fact one of the organs of the human body,

the structure of which has only received limited attention by anatomists in
the last century, and regarding which a large gap still persists between
anatomists and surgeons (Lancerotto et al., 2010).

 Functionally, the membranous superficial fascia may play a role in

the integrity of the skin and support for subcutaneous structures
particularly large veins, by ensuring their patency. Understanding the
topographic anatomy of this fascial layer may help explain subcutaneous
tissue deformities and provide the anatomic basis for surgical correction.
Abdominal surgeons rely on the superior strength of the fascial layer of
the abdominal wall to secure celiotomy wound closures (Abu–Hijleh et
al., 2012). Scarpa's fascia is the structure that allows surgical closure in
abdominoplasty procedures to be performed under remarkably high
tension without vascular compromise to the skin. The strength of the
Scarpa’s fascia can stabilize sutures placed when closing incisions of the
abdominal wall. (Lockwood, 1991).
 The superficial fascia is easy to identify. It divides the
subcutaneous tissue into two sublayers: the superficial adipose tissue
(SAT) and the deep adipose tissue (DAT), and each has its characteristic
features. The superficial fascia is a fibroelastic layer mainly composed of
collagen and elastic fibres; however, small fat lobules are often observed
between the fibres. While macroscopically this fascia appears to be, and
can be isolated as, a well-defined membrane (Stecco, 2015).

The superficial fascia does not have a uniform thickness. It is a

well-defined, white layer in the lower abdomen where it is called
Scarpa’s fascia. It thickens towards the inguinal ligament where a
multilayered structure of collagen bundles, extending in different
directions. In upper abdomen, the superficial fascia is much thinner,
appearing as a translucid collagen layer through which adipose tissue can
be seen (Markman & Barton, 1987). According to Sterzi, there are
fibrous thickenings inside the superficial fascia of the trunk. These
collagen fibrous bundles originate in the back and extend in an oblique
direction to the anterior region of the trunk and in a craniocaudal
direction. The distribution of these reinforcements of the superficial
fascia corresponds to the lines in the dermis described by Langer in 1862.
This structure has high-structural stability, mechanical resilience and
elastic properties (Stecco, 2015).

The point of maximal attachment between these layers is variable.

It is loose in the lower abdomen, where subcutaneous tissues can be
dissected off the rectus sheath and the external oblique with relative ease.
As one proceeds toward the xiphoid, the attachments become firmer and
render dissection more difficult. At the iliac crest and inguinal ligament,
the fibrous framework of the subcutaneous layer becomes more dense
again and adheres firmly to the underlying structures. These attachments
are especially firm at the inguinal area. These attachments prevent
infections or oedema passing from one region to the other (Carriquiry,
1996).

The transversalis fascia is a part of the continuous layer of

endoabdominal fascia enclosing the abdominal cavity. Transversalis
fascia covers the internal surface of the transversus abdominis muscle and
aponeurosis, separating them from the underlying preperitoneal fat and
peritoneum. The structure of the transversalis fascia in the lower portion
of the groin, that part between the transversus abdominis arch superiorly
and the iliopubic tract and Cooper's ligament inferiorly, is of anatomic
importance to the surgeon, since this is the "weak area" in which inguinal
hernias occur (Condon, 1971).
 Incisional hernias and recurrent hernias in
anterior abdominal wall

“Ventral hernia” is defined as a protrusion of loops of intestine,

fat, or fibrous tissue through a defect orweakened region of the anterior
abdominal wall. The protrusion may involve, for example, preperitoneal
fat, intestinal contents, or omentum. Ventral hernia may be congenital or
acquired (Faylona, 2017).

Ventral hernias occur in the anterior abdominal wall and include

epigastric, umbilical, spigelian, parastomal, and most incisional hernias.
Epigastric and umbilical are primary ventral hernias. Incisional hernias
can develop anywhere an incision has been made but most commonly
occur at the midline, given that midline incisions are most commonly
used during laparotomies (Muysoms et al.,2009).

The exact global incidence of incisional hernia is unknown.

Presumably, the wide variation in abdominal approaches, comorbidities
among patients and techniques for surgical closure of the abdominal wall
leads to a broad range of incidence rates (Dietz et al., 2018). A certain
percentage of patients are not aware of their hernia (asymptomatic).
Patients with incisional hernia usually report rather unspecific symptoms
and occasionally experience pain and gastrointestinal problems, such as a
postprandial feeling of fullness. Bulges or discomfort can be experienced
by patients at the operative site. Larger hernias may be associated with
lesions of the skin overlying the hernia sac or with chronic spinal
complaints. If the hernia sac is large, a portion of the small intestine may
protrude through the abdominal wall, significantly complicating surgical
repair. It is not uncommon that patients with incisional hernia experience
social exclusion and are limited in their ability to work. In addition, self-
care may be substantially impaired.

Ultrasound evaluation via dynamic abdominal sonography for

hernia (DASH) has been prospectively shown to be superior to both
computed tomography and physical examination for detection of
incisional hernia (Beck et al., 2013).

Acquired ventral hernia is usually due to a previous laparotomy

and is also synonymous with incisional hernia. Patients have a 2%–20%
risk of developing an incisional hernia after laparotomy. Several factors
have been identified that may contribute to the development of an
incisional hernia. These factors may be divided into surgeon factors and
patient factors. Patient factors include advanced age, high BMI, smoking
history,steroids, history of malignancy, and medical comorbidities such
as diabetes, pulmonary diseases, and connective tissue disorders (Chevrel
& Rath, 2000) ,( Clark, 2001), (Hoer et al., 2002). Surgeon factors
pertain to the laparotomy closure technique, the choice of suture material,
and the surgeon’s experience. Also the site of incision is important.Some
of these factors can be controlled and some cannot (Faylona, 2017).

The following conditions predispose to a failure of incisional

hernia repair: infection after the initial procedure, prior recurrences, large
hernias, postoperative complications such as infection and hematoma,
overweight, previous multiple procedures, old age, chronic obstructive
airway disease, and prolonged postoperative abdominal distention.
Recurrence rates were reported to be between 30 and 50% after primary
closure without the use of prosthetic materials. Creation of a tension-free
repair with a prosthetic material has generally lowered the recurrence
rate. Laparoscopic repair of ventral incisional hernias has demonstrated
an acceptable complication rate and an excellent recurrence rate when
compared directly and historically with results obtained by open repair.
Recurrence rates after incisional hernia repair have frequently been found
to be directly proportional to the size of the defect (Clark, 2001).

As the most common complication after laparotomy, incisional

hernias are typically the inciting factor in the development of these
complex defects (Heller et al., 2012). Most experts agree that loss of
domain and hernia volumes greater than 30% of abdominal contents are
mandatory characteristics for defining large, complex abdominal wall
defects. However, the true complexity of such defects cannot be
measured solely by a standard definition. The difficulty seen in repairing
these defects ultimately depends on a multitude of factors. These include
the location, size, depth, and condition of the surrounding tissue
associated with the defect (Lowe et al., 2003).

Generally, the term complex abdominal wall has a number of

interpretations but generally refers to a patient’s abdomen that contains a
ventral or an incisional hernia or defect plus one or more of the following
characteristics: (a) Any additional condition that would be classified as a
clean contaminated or a contaminated field (including but not limited to
stomas) (b) An enterocutaneous fistula (c) A history of, or an ongoing,
mesh or wound infection (d) A large-sized defect (often de fi ned as >10
cm in diameter) (e) Loss of domain (f) One or more recurrences (Ott &
Diaz, 2013).
Table : Conditions contributing to the complex abdominal wall hernia (Ott & Diaz,
2013)
 Procedures for ventral hernia repair

Despite numerous advances in surgical techniques over the last

century, successful long-term treatment of ventral hernias remains a
challenge for general surgeons. These hernias range from small, isolated
fascial defects to large, complex recurrent hernias with visceral
involvement. In the last three decades, several randomized controlled
trials (RCTs) helped to compare surgical techniques and support
standardized approaches to treating patients with incisional hernias.

For centuries, manual reduction or “taxis” was the only treatment

for incarcerated ventral hernias. In the late 1800s and early 1900s,
surgeons began to warn against the risk of returning compromised bowel
to the abdomen especially in cases of complicated hernias (Sur & Katz,
2013).

Primary sutures repair, in which the fascial edges are dissected out
and reapproximated with interrupted sutures was adopted by many
surgeons for small defects less than 2 cm, without a long-term increase in
recurrence risk compared to a mesh repair (Gunter & Greenberg, 2016).

Then, the technique relaxing aponeurotic incisions was an

important step toward reducing tension in primary suture repairs, which is
well known as “component separation”. Despite these advances in
surgical technique, primary ventral hernia repairs continue to be
associated with high recurrence rates (Ramirez et al., 1990)(Clark,
2001) (Sur & Katz, 2013).
 Among different suturing techniques, the Mayo technique (since
1895) is one of the most common approaches to the repair of incisional,
umbilical, and epigastric hernias (Mittermair et al., 2002).

Mesh-based repair was also considered in the treatment of ventral

hernias. In a concise summary, Shankaran et al. described this ideal
prosthesis as noncarcinogenic; capable of being sterilized; chemically
inert; unlikely to produce a signi fi cant host immune response; resistant
to mechanical forces, infection, and visceral adhesions; and amenable to
mass fabrication in an affordable manner (Shankaran et al., 2011).

Mesh-based repair, whether laparoscopic or open, was associated

with a significantly reduced risk of recurrence compared to suture repairs,
and so surgeons were encouraged to “abandon” primary suture repair of
incisional hernias, even for small defects (Burger et al., 2004).

The synthetic nondegradable meshes, sometimes referred to as

‘classical’ or ‘traditional’ meshes, are generally the least expensive. The
earlier materials used for these meshes – perlon and nylon – were later
abandoned because perlon caused intense inflammatory responses and
nylon was shown to degrade in the long-term (Sanders & Kingsnorth,
2012). Currently, nearly all synthetic nondegradable meshes are made
from one of three basic materials: polypropylene, polyethylene
terephthalate polyester or expanded polytetrafluoroethylene (ePTFE)
(Herrero et al., 2013).

Biological meshes were used for hernia repair because they were believed
to promote regeneration, rather than scarring, and because they could also
be used in contaminated or infected fields (Bellows et al., 2006).
Although biological meshes are routinely used in infected fields, their
high costs remain a barrier to widespread use (Peppas et al., 2010).

Mesh-based repair is associated with many complications. The

most common complication following use of a surgical mesh is hernia
recurrence (Ahonen-Siirtola et al., 2015). Fundamentally, recurrence is
caused by early degradation of the mesh, early removal of the mesh (as
necessary following infections) or mesh failure (Lowham et al., 1997)
(Bellows et al., 2006). The rate of infection for open ventral incisional
hernia repair is reported to be 6% to 10% (Sanchez et al., 2011).

For bridging meshes or when meshes are placed within the

abdomen, viscera-mesh adhesion is a concern. Several studies have
shown that biface (Aubé et al., 2004) and barrier-coated
(Schreinemacher et al., 2013) composite meshes are effective at
reducing adhesion formation.

Postoperative pain is also a common complication of incisional

hernia repair (Berger, 2014). While acute and early postoperative pain
may be related to the type of mesh used, it is equally likely attributable to
nerve damage from the operation (Brown & Finch, 2010). On the other
hand, late-onset chronic postoperative pain is generally considered to be a
complication of the mesh itself, and is most commonly associated with
foreign body reaction and the resulting stiffness and shrinkage (Sajid et
al., 2013).

Seroma formation is one of the most common events following

ventral hernia repair. The use of mesh increases the risk of seroma (Klink
et al., 2010).Seroma formation in relation to the mesh is an annoying
complication. While the majority of seromas do not require any
intervention, some require aspiration if they become painful or infected.
Infected mesh often needs to be operatively removed, thus resulting in
increased morbidity for the patient (Scott et al., 2005). It has been
demonstrated that seroma is not merely an accumulation of serum, but
exudate resulting from an acute in fl ammatory reaction (Bullocks et al.,
2006).

Seroma formation can be seen as a consequence of the inflamatory

foreign body reaction with monocytes and macrophages involved at the
interface of connective tissue and implant. These cells produce a variety
of cytokines, which regulate the local immune response, wound healing,
and scar formation .

A seroma is usually manifested as a localized and well-

circumscribed swelling, pressure or discomfort, and occasional drainage
of clear liquid from the immature surgical wound (Bernatchez et al.,
1996).