Chapter 35: Abdominal Wall, Omentum, Mesentery, and Retroperitoneum

1. There are important anatomic differences in the rectus sheath structures above and below the arcuate line. The laminae of the internal oblique, which contribute to both the anterior and (along with the transversus abdominis) posterior rectus above the arcuate line, only contribute to the anterior sheath below the arcuate line. There is no aponeurotic posterior covering on the lower portion of the rectus muscles.

2. Rectus diastasis is associated with abdominal wall bulging consequent to separation of the rectus abdominis muscles in the midline. It does not represent a hernia, and surgical interventions for this condition are of questionable, if any, clinical benefit.

3. When resection of abdominal wall desmoid tumors is undertaken, it must be recognized that failure to achieve negative margins is associated with an extremely high risk of local recurrence of the tumor.

4. Primary repair of ventral incisional hernias is associated with unacceptably high failure rates, and repair using other approaches, such as use of prosthetic mesh, is preferred.

5. The addition of the closed videoscopic technique to components separation procedures has been associated with a significant decrease in the incidence of local wound complications.

6. Potential benefits of laparoscopic incisional hernia repairs compared to open repairs with mesh include shorter hospitalization, lower risk of wound complications, and better abdominal wall function. A lower recurrence rate benefit remains controversial.

7. Surgical treatment of sclerosing mesenteritis is most often undertaken to confirm diagnosis and to rule out neoplasm as the cause of a mesenteric mass. Resection possibilities are limited by the extensiveness of the process as well as by the questionable benefit in most cases.

8. Potential surgical interventions in retroperitoneal fibrosis include operative biopsy to rule out neoplasm, ureteral stent placement, open or laparoscopic ureterolysis, and endovascular interventions for iliocaval occlusion.

General Considerations

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. Knowledge of its specific anatomic features is required for management of abdominal wall diseases or during entry into the peritoneal cavity.

Surgical Anatomy

The abdominal wall is an anatomically complex, layered structure with segmentally derived blood supply and innervation (Fig. 35-1). 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 (see Fig. 35-1).

Lateral to the rectus sheath are three muscular layers with oblique fiber orientations relative to one another (Fig. 35-2). 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 (Fig. 35-3). Above the arcuate line, the anterior rectus sheath is formed by the external oblique aponeurosis and the external lamina of the internal oblique aponeurosis, whereas the posterior rectus sheath is formed by the internal lamina of the internal oblique aponeurosis and the transversus abdominis aponeurosis. Below the arcuate line, the anterior rectus sheath is formed by the external oblique aponeurosis, the laminae of the internal oblique aponeurosis, and the transversus abdominis aponeurosis. There is no aponeurotic posterior covering of this lower portion of the rectus muscles, although the endoabdominal, or transversalis, fascia provides contiguous coverage of the posterior aspect of the abdominal above and below the arcuate line.

The blood supply to the muscles of the anterior abdominal wall is derived mainly from the superior and inferior epigastric arteries (Fig. 35-4). 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.

Anterior abdominal wall innervation is segmental. Motor nerves to the rectus, oblique, and transversus abdominis muscles run from the anterior rami of spinal nerves at the T6 to T12 levels. The overlying skin is innervated by afferent branches of the T4 through L1 nerve roots, with T10 nerve roots providing sensation around the umbilicus (Fig. 35-5).

Physiology

The rectus muscles, external obliques, and internal obliques work as a unit to flex the trunk anteriorly or laterally. Trunk rotation is achieved by simultaneous contraction of a unilateral external oblique and the contralateral internal oblique (e.g., rotation to the right is produced by contraction of the left external oblique muscle and the right internal oblique). All of the truncal muscles are involved in raising intra-abdominal pressure. Abdominal musculature contraction that occurs when the diaphragm is relaxed will result in expiration of air from the lungs, or a cough if this contraction is forceful. If the diaphragm is contracted when the abdominal musculature is contracted (Valsalva maneuver), the increased abdominal pressure aids in processes such as micturition, defecation, and childbirth.

Abdominal Anatomy and Surgical Incisions

Surgeons must deal with the abdominal wall to access pre-, intra-, and retroperitoneal sites. This begs practical questions of where and how to make incisions. Incisions for open surgery are generally located in proximity to the principal operative targets. Laparoscopic port site incisions might be remote from the site of interest and are carefully planned based on the instrument approach angles and working distances both to the operative site and between ports. Orientation of any incision may be determined based on expected quality of exposure, closure considerations including cosmesis, avoidance of previous incision sites, and surgeon preference. In general, 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) (Fig. 35-6). Modifications are numerous and can consist of various extensions to optimize exposure in specific clinical situations. Midline incisions are used for the majority of nonlaparoscopic 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. These incisions are closed in two layers, the more superficial one incorporating the anterior aponeurotic sheath of the rectus medially, transitioning to external oblique muscle and aponeurosis laterally. The posterior, deeper layer consists of internal oblique and transversus abdominis muscle. Similar anatomic considerations are guide closure of transversely oriented muscle-dividing incisions. The Pfannenstiel incision, used commonly for pelvic procedures, is distinguished by transverse skin and anterior rectus sheath incisions, followed by rectus muscle retraction and longitudinal incision of the peritoneum. Irrespective of the incision type, suture apposition of abdominal wall tissues during closure is accomplished without significant tension and with great precision.

Abdominal incisions can lead to short- and long-term complications and patient disability. The question of how large an incision ought to be has no simple answer. In general, it is prudent to make incisions no larger than necessary to safely accomplish the operative goals. Laparoscopic and other minimally invasive surgical methods owe their development in large part to the belief that minimizing surgical injury to the abdominal wall is of significant benefit to the patient. For open surgery, a variety of devices are available to retract the abdominal wall and facilitate peritoneal exposure without subjecting the patient to excessively large incisions or surgical personnel to exhausting retraction tasks (Fig. 35-7). Examples include the Bookwalter™, Omni-Tract¯, and Thompson retractors.

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. Persistence of urachal remnants can result in cysts as well as fistulas to the urinary bladder with drainage of urine from the umbilicus. These are treated by urachal excision and closure of any bladder defect that may be present.

Acquired Abnormalities

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 sometimes mistaken 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 (Fig. 35-8). 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 (Fig. 35-9) 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 in some 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. Mortality in this condition is rare, but has been reported in patients requiring surgical treatment and in the elderly.

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 characteristics that 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. As many as 10% to 15% of FAP patients develop desmoid tumors of the abdominal wall, abdomen, or retroperitoneum, and this condition can account for patient mortality from complications of aggressive local growth. 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. Combined medical treatments and the addition of imatinib have been used with some success in small numbers of patients; radiation therapy has been used in both adjuvant and palliative roles with high response rates.

Other Abdominal Wall Tumors

The abdominal wall may be the site of various benign neoplasms including lipomas and neurofibromas. Surgical treatment is not always mandatory, but local excision is recommended for symptomatic or enlarging lesions. Primary abdominal wall malignancies are exceedingly rare and include subtypes of sarcomas (leiomyosarcoma, malignant fibrous histiocytoma, fibrosarcoma, liposarcoma, and rhabdomyosarcoma), dermatofibrosarcoma protuberans, schwannoma, and melanoma. Magnetic resonance imaging (MRI) or CT is used for tumor staging, and chest CT should be included to rule out pulmonary metastases. These studies define the extent of the tumor and involvement of contiguous structures in anticipation of surgical treatment. Prior to surgery for abdominal wall sarcomas, a core needle biopsy is generally obtained (with image guidance if needed). Once the diagnosis is established, treatment consists of resection with tumor-free margins, applying the same general principles used for extremity sarcoma resection. Meticulous dissection avoiding violation of tumor capsule and maintaining margins greater than 2 cm, if possible, are essential considerations. Extensive resection may leave a considerable abdominal wall defect that will have to be reconstructed. Immediate reconstruction with mesh and/or wound coverage with rotational or free myocutaneous flaps are the best options if primary closure is not feasible. Although these tumors are frequently described as radiation- and chemotherapy-resistant, both modalities have been used in advanced cases in both adjuvant and palliative settings. The very limited experience in these rare conditions makes commentary on the effectiveness of these therapies difficult.

Abdominal wall resection may also be required with contiguous involvement of gastrointestinal or gynecologic malignancies. Primary closure may be feasible, but prosthetic mesh use (even in the setting of bowel resection), absorbable or biologic mesh reinforcement, and myocutaneous flap reconstruction are also options.

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. These may be congenital and due to defective midline fusion of developing lateral abdominal wall elements.

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.

Spigelian hernias can occur anywhere along the length of the Spigelian line or zone—an aponeurotic band of variable width at the lateral border of the rectus abdominis. However, the most frequent location of these rare hernias is at or slightly above the level of the arcuate line. These are not always clinically evident as a bulge and may come to medical attention because of pain or incarceration. The largest review of surgical management of these hernias suggests that the risk of incarceration is as high as 17% at the time of diagnosis. This has been cited as a justification for mandatory repair of Spigelian hernias after they have been diagnosed. Repair may be accomplished with either open or laparoscopic procedures.

Incisional Hernias

As many as 10% to 20% of patients may eventually develop hernias at incision sites following open abdominal surgery. The etiology of any given case of incisional hernia can be difficult to determine. Obesity, primary wound healing defects, multiple prior procedures, prior incisional hernias, and technical errors during repair may all be contributory. Repair of incisional hernias can be technically challenging, and a myriad of methods have been described. The most important distinctions in surgical management of incisional hernias are primary versus mesh repair and open versus laparoscopic repair.

Primary repairs of incisional hernia include both simple suture closure and components separation. Primary repair by simple suture approximation, even for small hernias (defects <3 cm), is associated with high reported hernia recurrence rates. In a randomized prospective study of open primary and open mesh incisional hernia repairs in 200 patients, investigators from the Netherlands found that after 3 years, recurrence rates were 43% and 24%, respectively. Risk factors for recurrence were primary suture repair, postoperative wound infection, prostate problems, and surgery for abdominal aortic aneurysm.

In an effort to decrease suture line tension associated with primary repair, Ramirez described the components separation technique in 1990. This procedure entailed creation of large subcutaneous flaps lateral to the fascial defect followed by bilateral incision of the external oblique aponeuroses and, if necessary, incision of the posterior rectus sheaths bilaterally. The net effect is up to 10 cm of medial mobilization of the rectus muscles allowing for primary apposition of the fascia. Early reports of components separation demonstrated a high wound infection rate (20%) and an 18.2% hernia recurrence rate at 1 year. However, as the technique evolved, an improved understanding of key operative elements, including maximal preservation of the rectus perforator vessels and minimal dissection of the subcutaneous tissues, has led to fewer postoperative wound complications. In recent years, further modifications have included the endoscopic components separation technique as well as the addition of mesh reinforcement to primary fascial edge closure. Using the former closed technique with videoscopic control, effective external oblique division is achieved without creation of extensive subcutaneous flaps. This has been shown to dramatically decrease wound complications associated with the open procedure. The use of either permanent implant or biologic materials with components separation may lead to a hernia recurrence rate as low as 4% at 1 year of follow-up.

Mesh repair has become the standard in the elective management of most incisional hernias. Mesh can be placed as an underlay deep to the fascial defect (intra- or preperitoneal), an interlay either bridging the gap between the defect edges or within the abdominal wall musculoaponeurotic layers (intraparietal), or an onlay (superficial to the fascial defect). Laparoscopic repairs use an underlay technique. Each mesh material type has specific density, porosity, and strength characteristics. Some of the commercially available meshes for incisional hernia repair are listed in Table 35-1. Permanent mesh implants are made of prosthetic materials that do not degrade over time. Their principal advantages are ease of use, relatively low cost, and durability. Absorbable meshes are degraded and eliminated from tissues, gradually losing the structural integrity needed for tissue support. They can be useful for temporary abdominal wall closure in contaminated or infected fields but will eventually leave patients with an incisional hernia. Biologic meshes are prepared from collagen-rich porcine, bovine, or human tissues from which all antigenic cellular materials have been removed. These can also be chemically treated to crosslink collagen molecules, increasing strength and durability at the cost of some impairment in host cellular ingrowth. Over time, biologic mesh-derived collagen is incorporated into the host tissue, remodeled, and eventually replaced by host collagen. These characteristics may be useful in the setting of contaminated or infected fields. However, when used to bridge ventral hernia defects, biologic meshes are associated with excessively high hernia recurrence rates and ought to be reserved for tissue reinforcement rather than replacement. Newer prosthetic absorbable mesh materials are now available that share some of the characteristics of biologics (e.g., host tissue ingrowth and replacement with collagen) and can also be used for reinforcement of primary closure at a considerably lower cost.

In recent years, the trend toward use of minimally invasive surgical methods has exerted a great influence on incisional hernia management. However, open repairs continue to be performed extensively, mostly using a mesh underlay technique, often with extensive dissection of a preperitoneal space to accommodate a large sheet of polypropylene or woven polyester mesh. This method isolates mesh from the peritoneal contents. Although the implications of direct mesh contact with peritoneal structures is somewhat controversial, dense adhesions to intestine may complicate reoperation, and at least anecdotally may predispose to erosion and fistulization even without a concomitant bowel resection. Meshes with adhesion barrier coatings of fish oil, oxidized cellulose, or hyaluronic acid have been offered as solutions for this concern. Expanded polytetrafluoroethylene (ePTFE) prostheses are also used if contact with peritoneal structures is unavoidable because this material tends not to be associated with development of dense adhesions.

Laparoscopic incisional hernia repair was first described by LeBlanc and Booth in 1993. Since that time, numerous studies have examined early and late results compared to open repair. In 2000, data from 407 patients undergoing laparoscopic incisional hernia as part of a multicenter trial revealed a recurrence rate of only 3.4%, with a mean follow-up of more than 2 years. Of the recurrences noted, the vast majority were felt to be secondary to technical errors committed early in the surgeons’ experience that were avoided during the later cases. Studies using pooled multicenter data or meta-analyses of published reports have tended to strongly favor laparoscopic incisional hernia repairs based on fewer wound complications, fewer overall complications, and lower recurrence rates when compared to the open technique. Authors speculate that these benefits are achieved by eliminating repeated abdominal incisions and improving detection of unsuspected secondary defects that might not otherwise be appreciated during open repair. However, a recent Cochrane database review of studies totaling 880 cases and including the results from 10 randomized controlled trials concluded that short-term recurrence rates did not differ significantly and laparoscopic repairs were associated with higher in-hospital costs despite generally shorter lengths of stay. The major benefit for laparoscopic repairs compared to open repairs was a consistently lower risk of wound infections. In a recent multicenter randomized trial, in addition to lower infection rates, superior early physical function was also demonstrated very early after laparoscopic repairs compared to open repair.

The technique of laparoscopic incisional hernia repair generally involves laterally placed ports for midline defects and contralaterally placed ports for lateral defects. All adhesions to the anterior abdominal wall are divided, taking great care not to injure the intestine either directly or with thermal or electrical energy. The contents of the hernia sac are completely reduced, but in contrast to open repairs, the sac itself is left in situ. Once the area encompassing all fascial defects is defined, a mesh is fashioned to allow for sufficient overlap (at least 4 cm) under the healthy abdominal wall. After insertion into the abdomen, the mesh is fixed into position with transfascial sutures, placed circumferentially around the mesh, and spiral tacks are placed according to surgeon preference (Fig. 35-10). It has been proposed that transfascial sutures contribute to excessive postoperative pain, and some surgeons have eliminated them from the aforementioned technique, relying solely on spiral tacks for the strength of the repair. LeBlanc reviewed the utility of transfascial sutures and recommended a minimum 5-cm overlap of mesh from defect edge if transfascial sutures are not used.

Surgical Anatomy

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.

The blood supply to the greater omentum is derived from the right and left gastroepiploic arteries. The venous drainage parallels the arterial supply to a great extent, with the left and right gastroepiploic veins ultimately draining into the portal system.

Physiology

In the early twentieth century, the British surgeon Rutherford Morison noted that the omentum tended to wall off areas of infection and limit the spread of intraperitoneal contamination. He termed the omentum the “abdominal policeman.” Shortly after his description was published, several reports suggested intrinsic hemostatic characteristics of the omentum. In 1996, researchers from the Netherlands demonstrated that the concentration of tissue factor in omentum is over twice the amount per gram of that found in muscle. This facilitates activation of coagulation at sites of inflammation, ischemia, infection, or trauma within the peritoneal cavity. The consequent local production of fibrin contributes to the ability of the omentum to adhere to areas of injury or inflammation.

Omental Infarction

Interruption of the blood supply to the omentum is a rare cause of an acute abdomen that may be secondary to torsion of the omentum around its vascular pedicle, thrombosis or vasculitis of the omental vessels, or omental venous outflow obstruction. Fewer than 100 cases have been reported, and the diagnosis is most likely to be made in male adults. Depending on the location of the infarcted omental tissue, this disease process may mimic appendicitis, cholecystitis, diverticulitis, perforated peptic ulcer, or ruptured ovarian cyst, with abdominal pain and tenderness typical at locations typical for these conditions. Abdominal examination may reveal a tender, palpable mass. The diagnosis is generally inferred from abdominal CT or ultrasonography, which shows a localized inflammatory mass of fat density. In patients with convincing imaging who are clinically stable without signs of worsening peritonitis, supportive care is sufficient. However, some cases may be indistinguishable from more worrisome surgical conditions. In these instances, laparoscopic exploration can establish an accurate diagnosis and permit resection of the infarcted tissue, which should result in rapid resolution of symptoms.

Omental Cysts

Cystic lesions of the omentum and mesentery are related disorders, likely resulting from either peritoneal inclusions or degeneration of lymphatic structures. 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 intra-abdominal 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 c-kit 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.

Surgical Anatomy

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. During fetal development, after the herniated and 270-degree rotated midgut returns to its intraperitoneal location, the reduced mesentery achieves its final fixation state. The duodenum and lateral colon segments become fixed to the retroperitoneum, whereas the small intestinal mesentery, transverse colon mesentery, and sigmoid colon mesentery remain mobile (Fig. 35-11). Defects in these normal developmental steps starting with midgut rotation result in the spectrum of disorders associated with midgut malrotation. The related anatomic anomalies of the mesentery include paraduodenal or mesocolic hernias (Fig. 35-12), which can present as chronic or acute intestinal obstruction in children or adults.

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 rise to the various terms used to describe this condition. It is not clear if these variations represent stages in a sequential process or differences in basic pathobiology. Abdominal pain is the most frequent presenting symptom, followed by the presence of 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 (Fig. 35-13). 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 (Fig. 35-14) 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. The extent and location of mesenteric involvement define and, in some cases, limit the options for surgical intervention. In addition to simple biopsy, bowel and mesenteric resection can be considered, particularly in cases where this is technically feasible based on mass size and the ability to avoid injury to small intestinal blood supply. Often, however, the involvement of the vascular structures at the mesenteric root makes resection unfeasible. Rarely, an ostomy of some type for fecal diversion in the face of obstruction can be considered. Positron emission tomography with CT scanning has proven effective in ruling out neoplasia for focal mesenteric masses, leaving the sclerosing mesenteritis diagnosis as one of exclusion.

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

Cysts of the mesentery are benign lesions with an incidence of less than 1 in 100,000. The etiology of such cysts remains unknown, but several theories regarding their development exist, including degeneration of the mesenteric lymphatics or peritoneal inclusions arising as congenital anomalies.

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. Tillaux was the first to record this physical finding and, in 1850, the first to successfully remove a mesenteric cyst.

CT (Fig. 35-15), ultrasound, and MRI all have been used to evaluate patients with mesenteric cysts. Cysts generally appear unilocular without solid component on imaging. Less frequently, they may be multiple or multilocular or difficult to distinguish from solid mesenteric tumors with cystic components such as a cystic stromal tumor or mesothelioma. Mesenteric cystic lymphangioma may present as numerous, often large cysts in the setting of abdominal pain. These can be difficult to treat and almost invariably recur after excision.

When symptomatic, simple mesenteric cysts are surgically excised either openly or laparoscopically. Cyst unroofing or marsupialization is not recommended because mesenteric cysts have a high propensity to recur after drainage alone. On rare occasion, adjacent mesentery or bowel may be densely adherent to the cyst, or mesenteric vessels must be sacrificed in order to achieve complete excision. In this case, segmental bowel resection inclusive of the adjacent mesentery is performed.

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.

Surgical Anatomy

The retroperitoneum is defined as the space between the posterior envelopment of the peritoneum and the posterior body wall (Fig. 35-16). 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 tissue stranding (Fig. 35-17).

Management of retroperitoneal infections includes identification and treatment of the underlying condition, intravenous antibiotics, and drainage of all well-defined collections. Image-guided 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 retroperitoneal fibrosis, also known as Ormond’s disease, or a secondary reaction to an inciting inflammatory process, malignancy, or medication. Idiopathic retroperitoneal fibrosis is a rare disorder, usually affecting 0.5 per 100,000 patients annually. Men are twice as likely to be affected as women, with no predilection for any particular ethnic group. The disease primarily affects individuals in the fourth to the sixth decades of life.

Although allergic or autoimmune mechanisms have been postulated, the pathogenesis of this condition remains uncertain. In the closely related condition of chronic perioaortitis, an association with the HLA-DRB1*03 allele, which has been linked to autoimmune diseases such as systemic lupus erythematosus, type 1 diabetes mellitus, and myasthenia gravis, is of particular interest in defining an autoimmune cause of retroperitoneal fibrosis. Circulating antibodies to ceroid, a lipoproteinaceous by-product of vascular atheromatous plaque oxidation, are present in more than 90% of patients with retroperitoneal fibrosis. The relationship of these finding to the occurrence of fibrosis remains uncertain. The early inflammatory reaction is predominated by T-helper cells, plasma cells, and macrophages, but is subsequently replaced by collagen-synthesizing fibroblasts. Microscopically, the infiltrate is indistinguishable from the periadventitial involvement of aortic aneurysmal disease, Reidel’s thyroiditis, sclerosing cholangitis, and Peyronie’s disease. 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.

Retroperitoneal fibrosis may also appear secondarily with a variety of inflammatory conditions including abdominal aortic aneurysm, pancreatitis, histoplasmosis, tuberculosis, or actinomycosis. It also is associated with a variety of malignancies, including prostate, pancreas, and gastric cancer, as well as non-Hodgkin’s lymphoma, stromal tumors, and carcinoid tumors. Retroperitoneal fibrosis has been described in association with autoimmune disorders including ankylosing spondylitis, systemic lupus erythematosus, Wegener’s granulomatosis, and polyarteritis nodosa.

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. Other medications that have been linked to retroperitoneal fibrosis include β-blockers, hydralazine, α-methyldopa, and entacapone, which inhibits catechol-O-methyltransferase and is used as an adjunct with levodopa in the treatment of Parkinson’s disease. The retroperitoneal fibrosis regresses upon discontinuation of these medications.

Presenting symptoms depend on the structure or structures affected by the fibrotic process. Initially, patients complain of the insidious onset of dull, poorly localized abdominal pain. Sudden-onset or severe abdominal pain may signify acute mesenteric ischemia. Other symptoms of retroperitoneal fibrosis may include unilateral leg swelling, intermittent claudication, oliguria, hematuria, or dysuria.

As with the patient’s symptomatology, findings on physical examination vary with the retroperitoneal structure involved. Consequently, findings may include hypertension, the palpation of an abdominal or flank mass, lower-extremity edema (unilateral or bilateral), or diminished lower-extremity pulses (unilateral or bilateral). Laboratory evaluation may reveal elevated blood urea nitrogen and/or creatinine levels. As with many autoimmune inflammatory processes, the erythrocyte sedimentation rate almost always is elevated in patients with retroperitoneal fibrosis.

Many imaging modalities have been used with various sensitivities to diagnose retroperitoneal fibrosis. Abdominal/lower-extremity ultrasonography is the least invasive imaging procedure but is technician dependent. It may be useful if iliocaval compressive or renal symptoms predominate. A lower-extremity ultrasound may show deep venous thrombosis, whereas abdominal ultrasonography may identify a mass lesion or hydronephrosis. Once the diagnostic procedure of choice, intravenous pyelography (IVP) is less commonly used today. If the ureters are involved, IVP findings include ureteral compression, ureteral deviation toward the midline, and hydronephrosis.

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. If there is diminished renal function, avoidance of the use of intravenous contrast will reduce the ability to characterize retroperitoneal tissue planes. In this case, MRI may be used, since the signal intensity of the fibrotic process is discrete from muscle or fat. Additionally, magnetic resonance angiography will generally provide a good assessment of the degree of iliocaval involvement. Once a mass lesion is identified, the mass should be biopsied to rule out a retroperitoneal malignancy. The specimen may be retrieved using image-guided techniques or surgical retroperitoneal biopsy, which may be performed laparoscopically or during open laparotomy.

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. Laparoscopic ureterolysis has been shown to be as efficacious as open the open procedure. Patients with iliocaval thrombosis require anticoagulation, although appropriate duration of therapy is uncertain. Endovascular interventions for iliocaval occlusion have also been shown to be effective in small numbers of patients. Prednisone is initially administered at a relatively high dose (60 mg every other day for 2 months), and then gradually tapered over the next 2 months. Therapeutic efficacy is assessed based on patient symptoms and interval imaging studies. Cyclosporin, tamoxifen, and azathioprine have also been used to treat patients who respond poorly to corticosteroids.

The overall prognosis in idiopathic retroperitoneal fibrosis is good, with 5-year survival rates of 90% to 100%. Because long-term recurrences have been described, lifelong follow-up is warranted.

Entries highlighted in bold are key references.

General References

Abdominal Wall

Omentum

Mesentery

Retroperitoneum