Abdominal wall and retroperitoneum

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Abdominal wall and
retroperitoneum
ABDOMINAL WALL
The abdominal wall provides structure,protection, and support for
abdominal and retroperitoneal structures and is defined
superiorly by the costal margins, inferiorly by the pelvic
ring,and posteriorly by the vertebral column.
The abdominal wall is an anatomically complex, layered structure
with segmentally derived blood supply and innervation.
It is mesodermal in origin and develops as bilateral migrating
sheets, which originate in the paravertebral region and envelop
the future abdominal area. The leading edges of these
structures develop into the rectus abdominis muscles, which
eventually meet in the anterior midline.
The rectus abdominis is longitudinally oriented and encased
within an aponeurotic sheath, the layers of which are fused
in the midline at the linea alba. The rectus insertions are on
the pubic bones inferiorly and on the fifth and sixth ribs, as
well as the seventh costal cartilages and the xiphoid process
. superiorly.
The lateral border of the rectus muscles has a curved shape
identifiable as the surface landmark, the linea semilunaris.
Three tendinous intersections cross the rectus muscles at
the level of the xiphoid process, umbilicus, and about
halfway between the xiphoid process and
the umbilicus.
Lateral to the rectus sheath are three muscular layers with oblique
fiber orientations relative to one another . These layers are
derived from laterally migrating mesodermal tissues during the
sixth to seventh week of fetal development. The external oblique
muscle runs inferiorly and medially, arising from the margins of
the lowest eight ribs and costal cartilages. The external oblique
muscles originate on the latissimus dorsi and serratus anterior
muscles, as well as on the iliac crest.
Medially, the external obliques form a tendinous aponeurosis,
which is contiguous with the anterior rectus sheath. The inguinal
ligament is the inferior-most edge of the external oblique
aponeurosis, reflected posteriorly in the area between the anterior
superior iliac spine and pubic tubercle.
The internal oblique muscle lies deep to the external oblique and
arises from the lateral aspect of the inguinal ligament, the iliac
crest, and the thoracolumbar fascia. Its fibers course superiorly and
medially and form a tendinous aponeurosis that contributes
components to both the anterior and posterior rectus sheath. The
lower medial and inferior-most fibers of the internal oblique may
fuse with the lower fibers of the transversus abdominis muscle (the
conjoined area).
The inferior-most fibers of the internal oblique muscle are
contiguous with the cremasteric muscle in the inguinal canal. These
relationships are of critical significance in the management of
inguinal hernias. The transversus abdominis muscle is the deepest
of the three lateral muscles and runs transversely from the lowest
six ribs, the lumbosacral fascia, and the iliac crest, to the lateral
border of the rectus abdominis. The arcuate line (semicircular line
of Douglas) lies roughly at the level of the anterior superior iliac
spines.
The blood supply to the muscles of the anterior abdominal wall is
derived mainly from the superior and inferior epigastric
arteries.The superior epigastric artery arises from the internal
thoracic artery, while the inferior epigastric artery arises from the
external iliac artery. A collateral network of branches of the
subcostal and lumbar arteries also contributes the abdominal wall
blood supply. The lymphatic drainage of the abdominal wall is
predominantly to the major nodal basins in the superficial inguinal
and axillary areas.
Abdominal Anatomy and Surgical
Incisions
incisions for open peritoneal access can be longitudinal (in or off
the midline), transverse(lateral to or crossing midline), or oblique
(directed either upward or downward toward the flank)
procedures on the gastrointestinal tract. Incising the fused midline
aponeurotic tissue of the linea alba is simple and does not injure
skeletal muscle.
Paramedian incisions through the rectus abdominis sheath
structures have largely been abandoned in favor of midline or
nonlongitudinal incisions. Incisions lateral to the midline made
with transverse or oblique orientations can either divide the
successive muscular layers or bluntly separate the fibers.
This latter muscle-splitting approach, exemplified by the
classic McBurney incision for appendectomy, may be less
destructive to tissue but offers more limited exposure.
Subcostal incisions on the right (Kocher incision for
cholecystectomy) or left (for splenectomy) are archetypal
muscle-dividing incisions that result in transection of
intervening musculoaponeurotic tissues, including a portion
of the rectus abdominis.
Congenital abnormalities
The abdominal wall layers begin to form within in first
weeks following conception. In early embryonic
development, there is a large central defect through which
pass the vitelline (omphalomesenteric) duct and allantois.
The vitelline duct connects the embryonic and fetal midgut
to the yolk sac. During the sixth week of development, the
abdominal contents grow too large for the abdominal wall
to completely contain them, and the embryonic midgut
herniates into the umbilical cord. While outside the
developing abdomen, it undergoes a 270-degree
counterclockwise rotation on the developing mesentery.
At the end of the twelfth week, it returns to the
abdominal cavity.
Defects in abdominal wall closure may lead to
omphalocele or gastroschisis.In omphalocele,
viscera protrude through an open umbilical ring and
are covered by a sac derived from the amnion. In
gastroschisis, the viscera protrude through a defect
lateral to the umbilicus and no sac is present.
During the third trimester, the vitelline duct
regresses. Persistence of a vitelline duct remnant on
the ileal border results in a Meckel’s diverticulum
. Complete
failure of the vitelline duct to regress results in a
vitelline duct fistula, which is associated with drainage of small
intestinal contents from the umbilicus.If both the intestinal and
umbilical ends of the vitelline duct regress into fibrous cords, a
central vitelline duct (omphalomesenteric) cyst may occur.
Persistent vitelline duct remnants between the gastrointestinal tract
and the anterior abdominal wall may be associated with small
intestinal volvulus in neonates.When diagnosed, vitelline duct
fistulas and cysts should be excised along with any accompanying
fibrous cord.The urachus is a fibromuscular tubular extension of the
allantois that develops with the descent of the bladder to its pelvic
position.persistance of urachal remnants result drainage of urine
from the umbilicus.these are treated by urachal excision and
closure of bladder defect
Rectus Abdominis Diastasis. Rectus abdominis diastasis
(or diastasis recti) results from a separation of the two rectus
abdominis muscle pillars. This results in the characteristic
bulging of the abdominal wall in the epigastrium that is
sometimesmistaken for a ventral hernia despite the fact that the
midline aponeurosis is intact and no hernia defect is present.
Diastasis may be congenital, as a result of a more lateral
insertion of the rectus muscles to the ribs and costochondral
junctions, but is more typically an acquired condition with
advancing age, obesity,or following pregnancy. In the
postpartum setting, rectus diastasis tends to occur in women of
advanced maternal age,after multiple or twin pregnancies, or
in women who deliver high-birth-weight infants.
Diastasis is usually easily identified on physical examination
Computed tomography (CT) scanning can provide an accurate
measure of the distance between the rectus pillars and will
differentiate rectus diastasis from a true ventral hernia if
clarification is required. Surgical correction of rectus diastasis
by plication of the broad midline aponeurosis has been
described for cosmetic indications and for disability of
abdominal wall muscular function. However, these approaches
introduce the risk of an actual ventral hernia and are of
questionable value in addressing any actual pathology
Rectus Sheath Hematoma
Hemorrhage from the network of collateralizing vessels within
the rectus sheath and muscles can result in a rectus sheath
hematoma. Although a history of trauma might be elicited,
other less obvious events including sudden contraction of the
rectus muscles with coughing, sneezing, or any vigorous
physical activity may also cause this condition.
Spontaneous rectus sheath hematomas occur most frequently in
the elderly and in those on anticoagulation therapy. Patients
frequently describe the sudden onset of unilateral abdominal
pain that may be confused with lateralized peritoneal disorders
such as appendicitis.
History and physical examination alone may be diagnostic. Pain
typically increases with contraction of the rectus muscles,and a
tender mass may be palpated. The ability to appreciate an
intra-abdominal mass is ordinarily degraded with contraction
of the rectus muscles. Fothergill’s sign is a palpable abdominal
mass that remains unchanged with contraction of the rectus
muscles and is classically associated with rectus hematoma.
A hemoglobin/hematocrit level and coagulation studies should be
obtained. Both ultrasonography and CT.can provide
confirmatory imaging information and exclude other disorders.
Specific treatment depends on the severity of the
hemorrhage.Small, unilateral, and stable hematomas may be
observed without hospitalization. Bilateral or large hematomas
will likely require hospitalization, as well as potential
resuscitation.
Transfusion or coagulation factor replacement may be indicated
insome situations. Angiographic embolization is required
infrequently,but may be necessary if hematoma enlargement,
free bleeding, or clinical deterioration occurs.
Surgical therapy is used in the rare situations of failed
angiographic treatment or hemodynamic instability that
precludes any other options. The operative goals are
evacuation of the hematoma and ligation of any bleeding
vessel identified.
Desmoid Tumors
Desmoid tumors of the abdominal wall are fibrous
neoplasms originating from the musculoaponeurotic
structures of the anterior abdomen. They are also referred
to collectively as aggressive fibrosis, a term that describes
their aggressive and infiltrative local behavior. They do
not have metastatic potential, and although there is
marked cellularity in biopsy specimens, there are no
specific histologic characteristicsthat suggest malignancy,
per se.
Desmoid tumors of the abdominal wall have a slight female
predominance and occur either sporadically or in the
setting of familial adenomatous polyposis (FAP), with the
greatest risk incurred in Gardner’s syndrome.
In non-FAP settings, abdominal wall desmoids occur most
frequently in postpartum women or in surgical scars.
Radical resection with frozen section margins and
immediate mesh reconstruction of any consequent
abdominal wall defect is the most commonly
recommended treatment.
Involvement of margins is associated with recurrence rates
as high as 80%. Extensive infiltration and involvement of
peritoneal structures frequently makes desmoid resection
technically unfeasible. Medical treatment with an
antineoplastic agent such as doxorubicin, dacarbazine, or
carboplatin can produce remission for variable periods in
up to 50% of patients, although the prognosis of advanced
desmoids, particularly in FAP, is poor, with a 5-year
mortality rate as high as 50% reported.
Abdominal Wall Hernias
Hernias of the anterior abdominal wall, or ventral hernias,
represent defects in the parietal abdominal wall fascia and
muscle through which intra-abdominal or preperitoneal
contents can protrude. Ventral hernias may be congenital
or acquired.
Acquired hernias may develop via slow architectural
deterioration of the musculoaponeurotic tissues, or they
may develop from failed healing of an anterior abdominal
wall incision (incisional hernia). The most common finding
is a mass or bulge, which may increase in size with
Valsalva. Ventral hernias may be asymptomatic or cause a
considerable degree of discomfort and will generally enlarge
over time. Physical examination reveals a bulge on the
anterior abdominal wall that may reduce spontaneously,
with recumbency, or with manual pressure. A hernia that
cannot be reduced is described as incarcerated and generally
requires surgical correction. Incarceration of an intestinal
segment may be accompanied by nausea, vomiting, and
significant pain, and is a true surgical emergency. If the
blood supply to the incarcerated bowel is compromised, the
hernia is described as strangulated, and the localized
ischemia may lead to infarction and perforation.
Primary ventral hernias (nonincisional) are generally
named according to their anatomic location. Epigastric
hernias are located in the midline between the xiphoid
process and the umbilicus. They are generally small and
may be multiple, and at elective repair, they are usually
found to contain omentum or a portion of the falciform
ligament.
Umbilical hernias occur at the umbilical ring and may be
present at birth or develop later in life. Umbilical hernias are
present in approximately 10% of all newborns and are more
common in premature infants. Most congenital umbilical
hernias close spontaneously by 5 years. If closure does not
occur, elective surgical repair is usually advised. Adults with
small, asymptomatic umbilical hernias should be followed
clinically.
Surgical treatment is offered if a hernia is observed to enlarge
or is associated with symptoms, or if incarceration occurs.
Surgical treatment can consist of primary sutured repair or
placement of prosthetic mesh for larger defects (>2 cm) using
open or laparoscopic methods.
Patients with advanced liver disease, ascites, and umbilical
hernia require special consideration. Enlargement of the
umbilical ring usually occurs in this clinical situation as a result
of increased intra-abdominal pressure from uncontrolled
ascites.
First line of therapy is aggressive medical correction of
the ascites and paracentesis for tense ascites with respiratory
compromise. These hernias are usually filled with ascitic fluid,
but omentum or bowel may enter the defect after large-volume
paracentesis. Uncontrolled ascites may lead to skin breakdown
on the protuberant hernia and eventual ascitic leak, which can
predispose the patient to bacterial peritonitis. Patients with
refractory ascites may be candidates for transjugular
intrahepatic portocaval shunt (TIPS) or eventual liver
transplantation.Umbilical hernia repair should be deferred until
after the ascites is controlled.
OMENTUM
The greater omentum and lesser omentum are fibrofatty
aprons that provide support, coverage, and protection of
peritoneal contents.These structures begin to develop
during the fourth week of gestation.
The greater omentum develops from the dorsal
mesogastrium,which begins as a double-layered structure.
The spleen develops in between the two layers, and later
in development, the two layers fuse, giving rise to the
intraperitoneal spleen and the gastrosplenic ligament. The
fused layers then hang from the greater curvature of the
stomach and drape over the transverse colon, to which its
posterior surface becomes fixed
The gastrocolic ligament and the gastrosplenic ligament are
those segments of the greater omental apron that connect the
named structures. In the adult, the greater omentum lies in
between the anterior abdominal wall and the hollow viscera
and usually extends into the pelvis.
The lesser omentum, otherwise known as the hepatoduodenal
and hepatogastric ligaments, develops from the mesoderm
of the septum transversum, which connects the embryonic
liver to the foregut.
The common bile duct, portal vein, and hepatic artery are
located in the inferolateral margin of the lesser omentum,
which also forms the anterior border of the foramen of
Winslow.
Omental Cysts
Omental cysts are far less common than mesenteric cysts.
Omental cysts may present as an asymptomatic
abdominal mass or may cause abdominal pain with or
without appreciable mass or distention.
Physical examination may reveal a freely mobile intraabdominal mass. Both CT and abdominal ultrasound
reveal a well-circumscribed, cystic-mass lesion arising
from the greater omentum. Treatment involves resection
of all symptomatic omental cysts. Resection of these
benign lesions is readily accomplished using laparoscopic
techniques.
Omental Neoplasms
Primary tumors of the omentum are rare. Benign tumors of the
omentum include lipomas, myxomas, and desmoid tumors.
Primary malignant tumors of the omentum are usually
mesodermally derived and may share immunohistochemical
characteristics of gastrointestinal stromal tumors including ckit immunopositivity. Metastatic tumors of the omentum are
common, with metastatic ovarian cancer having the highest
preponderance of omental involvement. Cancers of any
portion of the gastrointestinal tract, as well as melanoma,
uterus, and kidney cancer, may also metastasize to the
omentum.
MESENTERY
The small and large intestinal mesenteries serve as the major
pathways for arterial, venous, lymphatic, and neural
structures to course to and from the bowel. Mesenteric
tissues develop from embryonic dorsal mesentery that
attaches the foregut, midgut, and hindgut to the posterior
abdominal wall.
The dorsal mesentery becomes the greater omentum
proximally, the small intestinal mesentery in the region of
the jejunum and ileum, and the mesocolon in the region of
the colon.
Sclerosing Mesenteritis
Sclerosing mesenteritis, also referred to as retractile mesenteritis,
mesenteric panniculitis, or mesenteric lipodystrophy, is an
inflammatory and fibrotic process involving the intestinal
mesentery. There is no gender or race predominance, but the
condition is most commonly diagnosed in individuals older
than 50 years of age.
The etiology of this process is unknown, but its cardinal feature is
increased tissue density within the mesentery. This can be
localized and associated with a discrete nonneoplastic
mesenteric mass, or it can be more diffuse, sometimes
involving large swaths of mesentery without well-defined
borders.
There may be varying relative degrees of fat tissue degeneration,
inflammation, and fibrosis on histologic examination, giving a mass
or, much more rarely, intestinal obstruction. However, many cases
are discovered incidentally when imaging studies, most frequently
CT scan, are performed for unrelated reasons.
CT of the abdomen shows a mass lesion or an area of the mesentery
with a higher density than normal mesenteric tissue.
Vascular structures are seen coursing through the affected areas,
which sometimes involve in the mesenteric root. Although CT
cannot definitively distinguish sclerosing mesenteritis from a
mesenteric tumor, identification of a “fat ring sign” or hypodense
zone around the mass area has been suggested as a means of
distinguishing sclerosing mesenteritis from lymphoma.
The presence of a hyperattenuating stripe has also been suggested as
radiologic finding that would favor the mesenteritis diagnosis.
Operative findings range from a discrete mesenteric mass to broad
areas of mesenteric nodularity and thickening. Surgical biopsy has
frequently been used to confirm the diagnosis and to rule out a
neoplastic process.
In most cases of sclerosing mesenteritis, the process appears to be
self-limited and may even demonstrate regression if followed with
interval imaging studies. Clinical symptoms are very likely to
improve without intervention, and therefore,aggressive surgical
treatments are generally not indicated. In clinically problematic
cases that are not amenable to resection because of widespread
mesenteric involvement or unfavorable location, medical treatment
has been given to alleviate severe symptoms. Among the agents that
have been used are corticosteroids, colchicine, tamoxifen, and
cyclophosphamide.
Mesenteric Cysts
Mesenteric cysts may be asymptomatic or cause acute or chronic
symptoms of a mass lesion. Acute pain is generally caused by
rupture or torsion of the cyst or from acute hemorrhage into
the cyst cavity.
Mesenteric cysts may also cause intermittent abdominal pain
secondary to compression of adjacent structures or reversible
torsion of the cyst. Mesenteric cysts can also be the cause of
nonspecific symptoms such as anorexia, nausea, vomiting,
fatigue, and weight loss.
Physical examination may reveal a mass lesion that is mobile
only from the patient’s right to left or left to right (Tillaux’s
sign), in contrast to the findings with omental cysts, which should
be freely mobile in all directions.
CT ,ultrasound, and MRI all have been used to evaluate patients
with mesenteric cysts.
When symptomatic, simple mesenteric cysts are surgically
excised either openly or laparoscopically.
Mesenteric Tumors
Primary tumors of the mesentery are rare. Benign tumors of the
mesentery include lipoma, cystic lymphangioma, and desmoid
tumors. Primary malignant tumors of the mesentery are similar
to those described for omentum. Liposarcomas,leiomyosarcomas,
malignant
fibrous
histiocytomas,
lipoblastomas,
and
lymphangiosarcomas have all been described.
Metastatic small intestinal carcinoid in mesenteric lymph nodes
may exceed the bulk of primary disease and compromise blood
supply to the bowel. Treatment of mesenteric malignancies
involves wide resection of the mass. Because of the proximity to
the blood supply to the intestine, such resections may be
technically unfeasible or involve loss of substantial lengths of
bowel
RETROPERITONEUM
The retroperitoneum is defined as the space between the posterior
envelopment of the peritoneum and the posterior body wall.The
retroperitoneal space is bounded superiorly by the diaphragm,
posteriorly by the spinal column and iliopsoas muscles, and
inferiorly by the levator ani muscles. Although technically
bounded anteriorly by the posterior reflection of the
peritoneum, the anterior border of the retroperitoneum is quite
convoluted, extending into the spaces in between the mesenteries
of the small and large intestine.
Because of the rigidity of the superior, posterior, and inferior
boundaries, and the compliance of the anterior margin,
retroperitoneal tumors tend to expand anteriorly toward the
peritoneal cavity.
Retroperitoneal Infections
The posterior reflection of the peritoneum limits the spread of most
intra-abdominal infections into the peritoneum.Accordingly, the
source of retroperitoneal infections is usually an organ contained
within or abutting the retroperitoneum. Retrocecal appendicitis,
contained perforation of duodenal ulcers, iatrogenic perforation
with esophagogastroduodenoscopy or endoscopic retrograde
cholangiopancreatography, and complicated pancreatitis may all
lead to retroperitoneal infection with or without abscess
formation. The substantial space and rather nondiscrete
boundaries of the retroperitoneum allow some retroperitoneal
abscesses to become quite large prior to diagnosis.
Patients with a retroperitoneal abscess usually present with pain
and fever, but more worrisome signs of sepsis may also be present
depending on clinical severity. The site of pain may be variable
and can include the back, pelvis, or thighs. Erythema may be
observed around the umbilicus or flank.
The diagnosis is best established by CT, which may demonstrate a
unilocular or multilocular collection along with retroperitoneal soft
tissueStranding.
Management of retroperitoneal infections includes identification
and treatment of the underlying condition, intravenous antibiotics,
and drainage of all well-defined collections. Imageguided
percutaneous drainage is strongly favored, but operative drainage
may sometimes be needed for adequate drainage of complex or
multiple collections. The mortality rate of retroperitoneal abscess
has been reported to be as high as 25%, and even higher in rare
cases of necrotizing fasciitis of the retroperitoneum.
Retroperitoneal Fibrosis
Retroperitoneal fibrosis is a class of disorders characterized by
hyperproliferation of fibrous tissue in the retroperitoneum. This
may be a primary disorder as in idiopathic nretroperitoneal
fibrosis, also known as Ormond’s disease, or a secondary reaction
to an inciting inflammatory process, malignancy, or medication.
Although allergic or autoimmune mechanisms have been postulated,
the pathogenesis of this condition remains uncertain.
The fibrotic process begins in the retroperitoneum just below the
level of the renal arteries. Fibrosis gradually expands, encasing
the ureters, inferior vena cava, aorta, mesenteric vessels, or
sympathetic nerves. Bilateral involvement is noted in 67% of
cases.
There is strong evidence that methysergide, a semisynthetic ergot
alkaloid used in the treatment of migraine headaches, plays a causal
role in some cases of retroperitoneal fibrosis.
Presenting symptoms depend on the structure or structures affected
by the fibrotic process.
Abdominopelvic CT with oral and intravenous contrast is the
imaging procedure of choice and will generally allow the extent of
the fibrotic process to be determined.
Once malignancy, drug-induced, and infectious etiologies are ruled
out, treatment of the retroperitoneal fibrotic process is instituted.
Corticosteroids, with or without surgery, are the mainstay of
medical therapy. Surgical treatment consists primarily of
ureterolysis or ureteral stenting and is required in patients who
present with significant hydronephrosis.
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