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Umbilical, Epigastric, and Spigelian Hernias
David L. Webb, Benjamin S. Powell, Nathaniel F. Stoikes,
and Guy R. Voeller
33
Introduction
Primary ventral hernias are hernias that occur spontaneously
along fascial defects of the anterior abdominal wall. Inguinal
hernias are the most common type of primary ventral hernias
and are discussed separately. This chapter focuses on three
specific types of primary abdominal wall hernias: Spigelian,
epigastric, and umbilical hernias. Though they occur less frequently than their inguinal counterparts, a thorough understanding of the causes and treatment options for these specific
types of hernias is important for any practicing general surgeon. These primary abdominal wall hernias can oftentimes
prove to be a diagnostic challenge, and one must approach
them with a high index of suspicion to prevent a delay in
diagnosis and subsequent surgical intervention. This chapter
will discuss the typical presentation, etiology, and the various treatment options currently available to manage these
specific types of primary ventral hernias.
Embryology
A thorough understanding of the development of the
abdominal wall is necessary to appreciate the nature of the
hernia defects discussed in this chapter. Abdominal wall
and bowel development occur simultaneously during the
third through twelfth weeks of intrauterine life. By the third
week, the embryo has developed cephalic, caudal, and lateral folds (Fig. 33.1). The cephalic fold is anterior and contains the foregut, stomach, and mediastinal contents.
Somatic layer defects in the cephalic fold may result in diaphragmatic, thoracic wall, cardiac, or pericardial defects.
The caudal fold contains the hindgut, bladder, and hypo-
D.L. Webb, MD (*) • B.S. Powell, MD • N.F. Stoikes, MD
G.R. Voeller, MD
Department of Surgery, University of Tennessee Health Science
Center, Memphis, TN, USA
e-mail: david.webb.md@gmail.com
gastric abdominal wall. Defects in the caudal fold may
result in bladder exstrophy. The lateral folds become the
lateral abdominal wall and future umbilical ring. Defects in
the lateral fold may result in a congenital umbilical hernia
or omphalocele depending on the size of the resultant fascial defect. By the sixth week of intrauterine life, rapid
growth of the liver and intestines causes herniation of the
midgut through the umbilical ring. By the tenth week, the
abdominal cavity has enlarged sufficiently to accommodate
the return of the abdominal viscera. The duodenum and
proximal colon undergo a counterclockwise rotation as the
intestines return intra-abdominally. Congenital defects that
result from malformation of the abdominal wall include
both omphalocele and gastroschisis. Omphalocele results
from failure of the intestines to return to the abdomen and
thus remain confined within the umbilical ring. Gastroschisis
is a full-thickness abdominal wall defect that results in the
intestines herniating into the amniotic cavity without a covering membrane.
Anatomy of the Abdominal Wall
Abdominal wall anatomy is complex, and a thorough understanding of the layers of abdominal wall musculature is key
to performing hernia surgery.
The abdominal wall is a hexagonal configuration and is
bordered caudally by the pelvic wall and pubic symphysis,
cranially by the costal margin and xiphoid, and laterally by
the midaxillary line. The rectus abdominis muscle fibers run
vertically from the costal margin to the pubis paralleling the
linea alba at the midline (Fig. 33.2). Each rectus muscle has
its origin on the fifth, sixth, and seventh rib and the xiphoid
process cranially and inserts onto the pubic bone caudally.
The three-layer lateral portion of the abdominal wall is composed of the external oblique, internal oblique, and the transversus abdominis. The fibers of each muscle layer run in
different directions. The fibers of the external oblique run
inferior and anterior, the internal oblique fibers run superior
© Springer International Publishing AG, part of Springer Nature 2018
K.A. LeBlanc et al. (eds.), Management of Abdominal Hernias, https://doi.org/10.1007/978-3-319-63251-3_33
437
438
2
3
Section above arcuate line
Extraperitoneal fascia Transversalis fascia
Fig. 33.1 Formation of ventral abdominal wall. 1. Yolk
sac. 2. Surface endoderm. 3. Amniotic cavity. 4. Neural
tube. 5. Splanchnic mesoderm. 6. Somatic mesoderm
D.L. Webb et al.
4
6
5
1
Aponeurosis of external
Aponeurosis of internal
Aponeurosis of transversus
abdominis muscle
Fig. 33.2 The rectus abdominis surrounding the linea alba in the midline where epigastric and umbilical hernias arise
and anterior, and the transversus abdominis fibers run
transversely (Fig. 33.3). Primary ventral hernias rarely form
through the lateral abdominal wall muscle group and typically occur through defects in the linea alba or the semilunar
lines.
The linea alba is formed from the fusion of the aponeuroses of the rectus sheaths and lateral abdominal wall muscles
at the midline and runs from xiphoid process to pubic symphysis. The linea alba is the most common location for both
oblique muscle
oblique muscle
Peritoneum
Anterior layer of rectus sheath
Rectus abdominis muscle
Posterior layer
of rectus sheath
External oblique muscle
Skin
Linea alba
Falciform ligament
Internal oblique muscle
Transversus
abdominis muscle
Subcutaneous
tissue (fatty layer)
primary and incisional hernias on the anterior abdominal
wall. The linea alba is typically wider above the umbilicus
than it is below. In cadaver studies, the average width of the
linea alba above the umbilicus measured approximately
1.7 cm compared to 0.7 cm below. This accounts for the
higher incidence of primary ventral hernias along the linea
alba above the umbilicus.
The semilunar line (Spigelian line) is formed by the mus-
culoaponeurotic junction of the transversus abdominis
Transversus
t
33 Umbilical, Epigastric, and Spigelian Hernias
439
Fig. 33.3 Orientation of the
internal oblique, external
oblique fibers, and the
transversus abdominis of the
abdominal wall
Serratus
anterior
abdominins
Internal oblique
External oblique
Aponeurosis
of the external
oblique
Pectoralis major
Linea alba
Tendinous
intersection
Rectus
abdominis
Inguinal ligamen
(formed by free
interior border of
the external
oblique
aponeurosis)
muscle and runs in a gentle curve from the costal margin to
the groin lateral to the rectus muscle on either side of the
abdomen. The lateral edge of the rectus muscle runs from the
costal margin to pubic symphysis following a similar curve
as the semilunar line. The Spigelian fascia runs between
these two lines and consists of the fused aponeuroses of the
transversus abdominis and internal oblique muscles. The
arcuate line (line of Douglas) runs transversely across the
lower abdomen and marks the inferior margin of the posterior rectus sheath. Below the arcuate line, all three lateral
abdominal wall muscle aponeuroses cross anterior to the rectus muscle. The intersection of the Spigelian line and the
arcuate line is a point of weakness in the abdominal wall and
is often referred to as the Spigelian hernia belt (Fig. 33.4).
The inferior epigastric vessels run in the lateral rectus sheath
at this point in the abdominal wall, and many anatomists propose that this contributes to the relative weakness. A triangle
is formed by the inferior epigastric vessels medially, the
Spigelian line laterally, and the arcuate line superiorly.
Spigelian Hernia
Definition and Epidemiology
Spigelian hernias occur through defects in the Spigelian fascia between the semilunar line laterally and edge of rectus
sheath medially. These hernias typically form below the
4
22
1
6
6 cm
10
Fig. 33.4 Spigelian hernia belt. External and internal obliques are cut
away in this figure. 1. Transversus abdominis. 2. Dorsal lamella of the
rectus sheath. 3. Semicircular line of Douglas. 4. The semilunar line. 5.
Spigelian aponeurosis. 6. Spigelian hernia belt. 7. Hesselbach’s triangle. 8. Inferior epigastric vessels. 9. Anterior superior iliac spine. 10.
Interspinal plane
9
3
1
4
5
8
7
440
D.L. Webb et al.
arcuate line because of the relative weakness that exists due
to the absence of the posterior sheath [1, 2]. The defect typically involves both the transversus abdominis and internal
oblique fasciae, with the external oblique fascia remaining
intact. As a result, Spigelian hernias may be difficult to
appreciate on physical exam and can be missed at the time
of an open operation until the external oblique fascia is
opened [3].
The incidence of Spigelian hernias in the pediatric population is low. It has been theorized that the hernia may result
from a congenital defect in fusion of the mesenchymal layers
and is often associated with cryptorchidism [4]. Spigelian
hernias in the adult population are typically acquired. It has
been theorized that these hernias may be related to the
stretching of the abdominal wall caused by previous surgery,
collagen disorders, obesity, COPD, or pregnancy. For whatever cause, the acquired weakness in the Spigelian fascia
allows interdigitation of fat that acts as a lead point for the
hernia. The male to female ratio is 1:1.8, and some authors
estimate that it comprises about 0.12% of all abdominal wall
hernias. Ultrasound and CT scan are useful aids in diagnosis,
but as shown by the Mayo study below, there are false negatives with these tests.
History
Adriaan van den Spieghel first described the Spigelian or
semilunar line in the seventeenth century as the medial concave line that is the boundary between the muscle and the
anterior aponeurosis of the transversus abdominis. Klinkosch
first described the Spigelian hernia in 1764. In the early nineteenth century, Sir Astley Cooper published a series of 23
hernias that occurred along the Spigelian line [5, 6].
Current Literature
Literature specific to repair of Spigelian hernias tends to be
limited to small case series and date back as far as the 1930s.
Louis River published one of the first case series in which he
described his management of five patients with Spigelian
hernias. He reviewed the anatomic defects present in each of
his patients and described his method of primary tissue
repair. Watson, Read, and Weiss followed by publishing their
personal experiences in managing Spigelian hernias. These
publications all predated the routine use of synthetic mesh
reinforcement for hernia repair and, therefore, all advocated
for a primary tissue repair.
The current literature specific to this type of primary ventral hernia is still limited to small cases series but now
includes discussion regarding the ideal method of repair for
these types of hernias. Some authors still favor a primary tissue repair, despite the growing majority advocating a meshbased repair performed via either an open or laparoscopic
approach. Hsieh published a case series of 11 patients with
Spigelian hernias. Seven patients received an open primary
tissue repair with the remaining four patients receiving an
open preperitoneal repair with mesh [7]. Mean follow-up
was 8.5 years for the primary repair group versus 6.7 years
for the mesh repair group. They found no recurrences in
either group with similar complication rates. The paper
unfortunately illustrates the low number of these hernias
repaired by any one group, making it difficult to judge one
method of repair being superior to another.
Larson et al. published the largest case series to date from
their experience at the Mayo Clinic. They described a total of
81 hernia repairs over a 20-year time period. Mass, pain, or
bowel obstruction were the most common symptoms on presentation. Preoperative imaging was done in 21 patients and
was positive in 15. Open primary tissue repair was performed
in 75 patients, open mesh repair in 5 patients, and laparoscopic mesh onlay repair in 1. Mean follow-up for 76 patients
was 8 years with 3 reported hernia recurrences, all in the primary suture repair group [8].
In 2006, Malazgirt published a prospective multicenter
study consisting of 34 patients with Spigelian hernias [9].
Twenty-three patients underwent an open intraperitoneal
mesh repair, six patients received an open preperitoneal
mesh repair, three received a laparoscopic intraperitoneal
onlay mesh repair, and two patients received an open primary tissue repair. Mean follow-up was 30 months, and
overall postoperative complication and recurrence rates were
low. The authors concluded the type of repair is surgeon
dependent but that preperitoneal repairs, either open or laparoscopic, yield shorter hospital stays and better patient
compliance.
Spigelian hernia does lend itself to a laparoscopic extraperitoneal hernia repair as published by Koksal et al. [10].
They described an approach in which the trocar setup is virtually identical to a traditional TEP inguinal hernia repair.
The preperitoneal space is dissected and used to allow space
for mesh placement. The mesh is placed a little more cephalad than when done for an inguinal hernia. The authors of
this chapter have performed a similar type of laparoscopic
preperitoneal mesh repair on 24 patients with Spigelian hernias diagnosed incidentally during TEP inguinal hernia
repairs with no known recurrences to date.
Moreno-Egea et al. showed that laparoscopic repair might
be more beneficial to patients in regard to morbidity and hospital length of stay [11]. Twenty-two patients in their study
underwent elective repair of Spigelian hernia; eleven had
open preperitoneal repair, while the other 11 had laparoscopic repair. In the laparoscopic group, eight were per-
33 Umbilical, Epigastric, and Spigelian Hernias
441
formed via the TEP method, while the other three underwent
a laparoscopic intraperitoneal onlay mesh placement.
Average length of stay in the open group was 5 days, while
the laparoscopic approach was 1 day, with a p value <0.001.
There were no postoperative complications in the laparoscopic approach, but the conventional method had four
patients with hematomas.
An approach the authors of this chapter have also used is
a hybrid laparoscopic and open approach. We first perform a
diagnostic laparoscopy, placing a 5 mm laparoscope intraabdominally to evaluate the exact location of the Spigelian
hernia. After proper identification of the hernia defect, we
then make a small incision over the hernia and repair the
defect with a Ventralex ST-type patch via an open anterior
approach. This allows complete excision of the hernia sac
and closure of the fascia over the patch. This approach is
excellent for managing larger hernia sacs that may lead to
seromas and skin bulging if not excised.
Epigastric Hernia
Definition and Epidemiology
to their relative size of the hernia defect, and patients often
present with pain with physical activity, upper abdominal
discomfort, or an enlarging bulge in the upper abdomen. In
cases of diagnostic uncertainty, patients require a complete
physical examination and work-up to rule out other causes of
abdominal pain as epigastric hernias can mimic other intraabdominal pathology such as symptomatic cholelithiasis and
peptic ulcer disease.
History
Arnaud de Villeneuve of France first described epigastric
hernias in 1285. In 1742, Rene’ de Garengeot more clearly
defined this type of hernia and attributed its symptoms
pathology of the underlying intra-abdominal organs. Maunior
described with the first repair of an epigastric hernia in 1802,
but the procedure quickly fell out of favor because of complications probably due to the iatrogenic injury of intraabdominal viscera at the time of repair. In 1885, Terrier
published his account of a successful epigastric hernia repair
and helped bring renewed attention to treatment of these
types of hernias.
An epigastric hernia is primary abdominal wall hernia that
forms through a defect in the linea alba between the xiphoid
process and umbilicus [12]. The exact incidence of epigastric hernias is largely unknown owning to a variety of different factors. They are diagnosed infrequently in the children
and are typically found in the adult population with a male to
female ratio of approximately 3:1.
Several theories regarding the etiology of epigastric hernias have been put forward since the early 1900s. In 1914,
Moschcowitz described the vascular lacunae hypothesis. He
theorized that vascular lacunae formed when small blood
vessels penetrated the linea alba [13]. These points of penetration were felt to result in a small space through which preperitoneal fat from the falciform ligament could begin to
herniate through and enlarge over time. Alternatively, Askar
proposed the decussation theory for the formation of epigastric hernias in 1978. Askar dissected a large number of
cadavers and emphasized the importance that fibers crossing
the midline play in reinforcing the linea alba. He found individuals who did not have triple lines of fiber decussation
reinforcing the linea alba were more likely to form epigastric
hernias [14]. Most likely, the etiology of epigastric hernias is
multifactorial and results from a combination of these anatomic hypotheses coupled with inherited collagen disorders
and environmental factors including increased intraabdominal pressure.
The presentation of epigastric hernias is widely variable
and patient dependent. Symptoms may be out of proportion
Literature
There is a relative paucity of randomized controlled trials
devoted solely to the repair of epigastric hernia. Despite
this, a number of case series detailing repair methods for
epigastric hernias have been published over the years.
Ponten recently published the largest case series report to
date devoted solely to epigastric hernias. His series
included 235 epigastric hernia repairs over a 5-year period;
68 patients received a mesh-based repair versus 167
patients with a primary suture repair. Hernia recurrence
rate was lower in the mesh-based repair group compared to
the primary repair group (10.9% vs. 14.9%). Incidence of
chronic pain was equivalent in both groups [15]. Similarly,
Stabilini published a retrospective series comparing suture
repair versus open preperitoneal mesh placement with
polypropylene mesh [16]. The mean hernia defect size was
2.5 cm (range of 0.5–10 cm). Recurrence rate was 14.7%
in the suture repair group vs. 3.1% in the mesh group.
There were more local wound complications with the mesh
group; however, this does not seem to offset the recurrence
risk in the suture group. Unfortunately, most other data on
epigastric hernias in the last 20 years is isolated to smaller
case reports [17, 18]. Most studies on the topic combine
epigastric hernias into the broader category of primary
ventral hernias, and these will be discussed later in this
chapter [19].
442
D.L. Webb et al.
Umbilical Hernia
Definition and Epidemiology
An umbilical hernia is a primary ventral hernia located at or
near the umbilicus and is seen frequently in surgical practice.
Congenital umbilical hernias result from failure of the umbilical ring to close properly during embryological development. The formation of the umbilicus occurs early in gestation
as a result of the fusion of the body stalk containing the
umbilical vessels and allantois with the extracoelomic yolk
stalk containing the vitelline duct and vessels. As described
previously, the fetal midgut typically returns to the abdominal
cavity by the twelfth week gestation, and the abdominal wall
closes as the celomic sac obliterates. Failure of this process
can result in formation of an umbilical hernia.
Umbilical hernias in infants are quite common, and the
vast majority will close spontaneously by the age of 2 years.
Hernias that persist after the age of 5 years will typically
require surgical repair. Umbilical hernias in the adult population are most commonly acquired defects. They occur more
frequently in women and in patients with conditions that
result in increased intra-abdominal pressure, such as pregnancy, obesity, ascites or abdominal distention, and chronic
pulmonary disease.
Small asymptomatic umbilical hernias barely detectable
on physical exam may be managed with observation. Patients
presenting with symptoms (typically periumbilical pain with
physical activity), an enlarging hernia defect, incarceration,
thinning of the overlying skin, or recurrent ascites should
undergo prompt surgical repair.
ascites, a significantly higher incidence rate compared to
the general population [21]. As depicted in Fig. 33.5, hernias in this setting also tend to enlarge quickly and become
symptomatic. The etiology of umbilical hernia in cirrhotics
is multifactorial. Increased intra-abdominal pressure secondary to ascites, abdominal wall muscle weakness secondary to hypoalbuminemia, and recanalization and varices
formation of the umbilical vein at the umbilicus secondary
to portal hypertension all play a role in umbilical hernia
formation in this patient population [21]. Further, tense
ascites may also cause pressure necrosis and perforation of
the overlying umbilical skin that may lead to evisceration,
ascites drainage, and bacterial peritonitis [22–26].
The treatment of cirrhotic patients with umbilical hernia
remains somewhat controversial. Historically, cirrhotics
were treated nonoperatively secondary to the exceedingly
high rate of perioperative complications and hernia recurrences [27–29]. Expectant management, however, often
leads to progression of disease and subjected patients to
History
The first reported umbilical hernia repair in the United States
was performed by Stoser in 1894. A few years later in 1898,
Mayo proposed his “vest-over-pants” repair that quickly
gained wide acceptance in the surgical community [20]. This
technique employed the imbrication of the superior and inferior fascial edges during the repair and was seen as a technical breakthrough since it significantly reduced the morbidity
over earlier approaches. Now, small hernia defects (<2 cm)
in low-risk patients are typically repaired with primary fascial reapproximation. Larger umbilical hernia defects are
typically repaired with prosthetic mesh reinforcement.
Umbilical Hernia and Cirrhosis
Umbilical hernia in the setting of cirrhosis and recurrent
ascites bears special mention. Umbilical hernia occurs in
up to 20% of patients with liver cirrhosis complicated by
Fig. 33.5 Umbilical hernia in a cirrhotic patient with ascites
33 Umbilical, Epigastric, and Spigelian Hernias
443
complications associated with the hernia. Operating in this
setting further increases the risks associated with a potential
surgical repair. As medical care for cirrhotic patients has
improved over the years, a number of studies have shown a
significant decrease in perioperative complications in regard
to umbilical hernia repair in this patient population.
Marsman et al. reported their experience of cirrhotic
patients with an umbilical hernia and ascites who underwent
elective hernia repair (n = 17) versus expectant management
(n = 13) [30]. They found expectant management was associated with a higher rate of both morbidity and mortality. Ten
of thirteen patients (77%) required hospitalization for incarceration with six patients requiring emergent operations.
Two patients died from hernia-related complications. In the
treatment group, complication rate was low, and only 4
recurrences were encountered in the 17 patients who underwent elective hernia repair.
A number of other studies have also reported favorable
outcomes and have suggested elective umbilical hernia repair
in cirrhotic patients in order to avoid complications associated with expectant management [24, 31–33].
Most studies indicate that preoperative medical management of ascites is essential in cirrhotic patients undergoing
elective umbilical hernia repair in order to prevent postoperative complications and hernia recurrences. The treatment of
ascites usually combines sodium restriction, diuretics, and
paracentesis [34, 35]. If ascites can be adequately medically
managed preoperatively, elective umbilical hernia repair in
cirrhotic patients is now usually indicated. The method of
repair, open primary repair, open mesh repair, and laparoscopic repair with intraperitoneal onlay mesh, is still debated
in the literature, with each approach offering its own potential benefits and risks [35]. No high-quality randomized control trials have been performed to date to advocate one repair
over the others. For patients scheduled for liver transplantation, umbilical herniorrhaphy should be done during
transplantation.
Current Literature
Repair options for umbilical hernia include open primary
suture repairs and mesh-based repairs. Mesh repairs can be
performed via either an open approach or with laparoscopic
assistance. Most of the data currently available indicate
lower recurrence rates with mesh-based repairs when compared to primary suture repairs. This has to be balanced with
the potential complications of mesh placement.
Asolati published a retrospective review analyzing predictors of recurrence in patients undergoing elective umbilical
hernia repair in single-center VA hospital over a 6-year span
[36]. Two hundred and twenty-nine patients were included in
the study with 97 patients receiving a primary suture repair
(43%) versus 132 patients receiving a mesh repair (57%).
Seven recurrences in the suture repair group were identified
vs. four in the mesh repair group (7.7% vs. 3%). In their
patient population, African-American gender, diabetes, and
hyperlipidemia were found to be the factors that were significant for recurrence. Smoking, obesity, and type of hernia nor
size was found to be insignificant in their study.
Eryilmaz looked at their experience of repairing umbilical
hernias with either mesh or suture repair [37]. Over a 5-year
span, they performed suture repair on any hernia less than
3 cm and polypropylene mesh repair on any hernia larger
than 3 cm. Primary repair was performed in 63 patients, with
mesh repair in 48 patients. The recurrence rate in the suture
repair group was 14% vs. 2% in the mesh group. They concluded that mesh should be used in all umbilical hernia
repairs. Arroyo in 2001 and Sanjay in 2005 [38, 39] both
showed lower recurrence rates with the use of mesh for
repair of umbilical hernia. Sanjay had a follow-up of
4.5 years. Schumacher [39] in 2003 found that in patients
with a BMI >30, the recurrence rate of umbilical hernia was
32% vs. only 8% in those with a BMI < 30. He also found
that the larger the hernia, the higher chance of recurrence if
the repair was done without mesh.
More recently, Christoffersen et al. published their findings from a prospective cohort study based on patients from
the Danish Ventral Hernia Database [40]. They compared
outcomes of patients undergoing elective open mesh and
sutured repair for small (<2 cm) umbilical and epigastric hernias. Over a 4-year period, 4786 patients met inclusion criteria and included 3438 patients receiving primary suture
repair vs. 1348 patients receiving a mesh repair with a mean
follow-up of 21 months. Reoperation rates for hernia recurrence were significantly lower for the mesh repair group
compared to the primary suture repair group (2.2% vs.
5.6%). They concluded that even small (<2 cm) primary
umbilical and epigastric hernias should be repaired with
mesh reinforcement.
In 2008, the authors of this chapter published our initial
experience with use of the Bard Davol Ventralex hernia patch
in primary umbilical and epigastric hernia repairs [41]. The
retrospective review included 88 patients with average BMI
of 32. Average OR time was 52 min, and postoperative follow- up ranged from 8 days to 3 years. No hernia recurrences
were found in follow-up. Two patients developed mesh
infection requiring subsequent mesh explantation. From our
experience with this composite patch, we concluded it has a
valuable role in primary umbilical and epigastric hernia
repairs. In addition, we performed a cost comparison of
umbilical hernias being repaired via an open approach with
the Ventralex patch compared to a laparoscopic approach.
The laparoscopic group had no recurrences and no mesh
infections but at a significantly higher cost. The laparoscopic
repair was on average $1200 more expensive per case
444
Other Mesh Patches
D.L. Webb et al.
compared to the open approach using the Ventralex hernia
patch. Since Davol introduced the Ventralex patch for repair
of small ventral hernias, other companies have followed suit
and introduced similar mesh products for the same indication. They work in a similar fashion to the Ventralex patch
(Fig. 33.6).
Since publication of our initial experience with the original Ventralex hernia patch, the patch itself has undergone
significant refinement by the manufacturer. The initial version of the Ventralex hernia patch was a composite mesh
patch composed of both polypropylene and ePTFE. Some
concern existed regarding the use of composite mesh products for implantation during hernia repair because the two
synthetic materials may contract at different rates following
placement. This could result in “taco-ing” or “cupping” of
the patch and potentially expose the abdominal viscera to the
polypropylene component of the patch and possibly result in
clinical morbidity. To address this concern, Bard Davol
introduced a newer version of the patch, the Ventralex ST
hernia patch. The Ventralex ST patch is composed entirely of
polypropylene mesh with its visceral side coated with a proprietary hydrogel coating to allow for safe intraperitoneal
placement. The hydrogel layer (Sepramesh) swells after
placement to minimize tissue attachment to the visceral side
of the mesh acting as an adhesion barrier to minimize potential visceral adhesion formation during mesh incorporation
and re-peritonealization of the mesh patch.
We converted to the newer version of the mesh patch
immediately after it was commercially available and are currently analyzing our results in over 200 placements. In addi-
tion, we have been active participants in the American Hernia
Society Quality Collaborative (AHSQC) since its inception
in 2013. The AHSQC is a quality improvement database
designed to track patient outcomes following hernia repair.
To date, we have over 140 patients who have undergone primary umbilical and epigastric hernia repairs with the
Ventralex ST patch being followed longitudinally in the
AHSQC database. Preliminary analysis shows excellent
results with very low complications and recurrence rates.
Presentation and Diagnosis of Anterior Abdominal Wall Hernias
Patients can present with a variety of different symptoms
when they have primary anterior abdominal wall hernias
depending on hernia location and hernia contents. Umbilical
hernias tend to be the most common anterior abdominal wall
hernias and often are easier to diagnose than their Spigelian
and epigastric hernia counterparts. Typically they present
with a reducible bulge at the umbilicus that can at times be
tender. If patients have an acute incarceration/strangulation
of omentum, they can present with pain and erythema, but
more frequently it is a chronic incarceration without signs of
strangulation. Incarcerated small intestine can present as a
bowel obstruction or perforation. If the hernia is very large,
it can contain multiple viscera with a variety of related
symptoms.
Epigastric hernias can at times be difficult. Often a thor-
ough history is the best clue with patients complaining of a
Fig. 33.6 Other
commercially available mesh
patches for use in repair of
small ventral hernias
33 Umbilical, Epigastric, and Spigelian Hernias
445
bulge and/or pain in the epigastrium. Physical exam is helpful if the defect is large enough to palpate and confirms the
diagnosis. If there is still concern about the true etiology of
the pain, an abdominal ultrasound or CT scan can be helpful
in the diagnosis [1, 42, 43]. Most epigastric hernias are small
in nature and often only have preperitoneal fat in the hernia.
However, the size of the hernia can vary widely and contain
a variety of tissues including preperitoneal fat, omentum,
stomach [44], liver [45], colon, or small intestine. There have
even been reported epigastric hernias causing pancreatitis
[46]. Due to this fact, a variety of symptoms can be present.
Spigelian hernias are often difficult to diagnose due to
their relative rarity and low clinical suspicion, especially in
obese patients. Presentation is often similar to the abovementioned hernias except they are found along the Spigelian
line and not in the midline. Patients’ presentations will be
different depending on hernia sac contents as well. Once
again ultrasound and CT scan have aided in the diagnosis,
but there are false negatives with these methods, and diagnostic laparoscopy is an excellent diagnostic tool in the
patient with pain in this area and a negative work-up.
Preoperative Planning
Most primary anterior abdominal wall hernias can be
repaired in a similar fashion regardless of defect location.
The method of repair, open vs. laparoscopic, is mostly
dependent on surgeon preference, but one should tailor the
surgical approach to the individual patient. Hernia defect
size along with patient factors such as body habitus, tobacco
use, and diabetes mellitus may influence the approach that is
best suited in each individual case. As with most hernias, a
tension-free repair is ideal so mesh is usually used unless
there is a clear contraindication to doing so. We tend to recommend open repair in most primary anterior abdominal
wall defects due to our success using the Ventralex ST-type
patch with most of these hernias. The patients have similar or
less pain than their laparoscopic counterparts; it is less
expensive, and it is an easy repair to perform. These patches
allow a sublay repair through a small incision with minimal
morbidity. For larger hernias and in patients at increased risk
for wound complications, we typically favor the laparoscopic
approach to allow for wider overlap of the hernia defect and
decreased wound infection and mesh infection rates.
Open Repair of Primary Anterior Abdominal Wall Hernias
Open hernia repair has long been the mainstay of treatment for
anterior abdominal wall hernias. The method of repair, either
a sutured primary fascial closure or a mesh-based repair,
should be tailored to the individual patient and take into
account hernia defect size and patient factors such as body
habitus, smoking status, and other medical comorbidities that
may influence the risk of hernia recurrence. For smaller defects
less than 2 centimeters in low-risk patients, a sutured repair
may be ideal. Because of the increased risk of hernia recurrence associated with a sutured primary fascial closure, most
authors now advocate a mesh-based repair for hernia defects
larger than 2 centimeters. Some feel all primary ventral hernia
defects should be repaired with mesh reinforcement.
Patient Positioning and Theater Setup
Patients undergoing open ventral hernia repair are typically
positioned in the supine position. Arms may be tucked
depending on surgeon preference. All patients undergoing an
open anterior ventral hernia repair should receive appropriate prophylactic antibiotic coverage prior to skin incision.
We also advocate the use of a barrier dressing, such as an
Ioban incise drape, to help minimize potential contamination
from skin flora.
Incision and Access
A vertical midline incision is typically used for epigastric
hernias directly overlying the hernia defect. A curved, infraumbilical incision is used when repairing primary umbilical
hernias.
Operative Steps
Dissection is continued down through the subcutaneous tissues until the hernia sac is identified. The redundant hernia
sac is dissected away from the subcutaneous tissues and
transected at the level of the fascia. The subcutaneous fat is
then elevated off circumferentially from the underlying fascia for 2–3 cm to get back into good, healthy non-attenuated
fascia (Fig. 33.7). The appropriate-sized mesh prosthetic is
then selected to provide adequate overlap of the hernia
defect. The mesh prosthetic is then placed through the hernia defect intraperitoneally in the sublay position. Care must
be taken to ensure the mesh prosthetic lays flush against the
anterior abdominal wall circumferentially without interposition of any abdominal viscera or omentum between the
mesh prosthetic and the visceral surface of the abdominal
wall. We fixate the mesh patch to the abdominal wall fascia
using permanent suture. The total number of points of fixation is dependent on mesh size, and the sutures include purchase of both the polypropylene skirt of the Ventralex ST
patch and overlying fascia (Fig. 33.8). For a medium-sized
446
D.L. Webb et al.
Fig. 33.7 Placement of the Ventralex patch into the hernia defect
Fig. 33.8 After the Ventralex patch has been placed with four Prolene
U-stitches securing it in place
Ventralex ST patch (6.4 cm circle), we typically place four
2.0 Prolene U-stitches at the 12, 3, 6, and 9 o’clock positions.
For the small patch (4 cm circle), we fixate at the 12 and 6
o’clock positions only. The fascia is then closed over the
mesh to add another barrier of protection from possible
wound infections (Fig. 33.9). If there is evidence of isch-
Fig. 33.9 Fascial closure over the mesh to reinforce repair and separate mesh from subcutaneous fluid collection
emic bowel at any point of the procedure, synthetic mesh
should be used with caution given the risk of possible mesh
infection.
Closure
We typically tack the umbilical stalk down to the fascial
closure when repairing umbilical hernias to achieve a satisfactory cosmetic appearance of the umbilicus postoperatively. The skin is closed in layers with buried
absorbable suture, and the incision is typically dressed
with skin glue.
Laparoscopic Repair of Primary Anterior Abdominal Wall Hernias
Patient Positioning and Theater Setup
Laparoscopic repair of epigastric and umbilical hernias is
performed in the same fashion as the laparoscopic intraperitoneal onlay mesh (IPOM) ventral hernia repair discussed in
previous chapters. Patients are typically positioned in the
supine position with bilateral arms tucked, and laparoscopic
towers are positioned on both sides of the bed. All patients
should receive appropriate prophylactic antibiotics prior to
skin incision.