Abdominal Wall, Umbilicus, Peritoneum, Mesenteries, Omentum and Retroperitoneum

Subcutaneous Tissues

The subcutaneous tissue consists of Camper and Scarpa fasciae. Camper fascia is the more superficial adipose layer that contains the bulk of the subcutaneous fat. Scarpa fascia is a deeper, denser layer of fibrous connective tissue contiguous with the fascia lata of the thigh. Approximation of Scarpa fascia aids in the alignment of the skin after surgical incisions in the lower abdomen.

Muscle and Investing Fasciae

The muscles of the anterolateral abdominal wall include the external and internal oblique and transversus abdominis. These flat muscles enclose much of the circumference of the torso and give rise anteriorly to a broad flat aponeurosis investing the rectus abdominis muscles, termed the rectus sheath. The external oblique muscles are the largest and thickest of the flat abdominal wall muscles. They originate from the lower seven ribs and course in a superolateral to inferomedial direction. The most posterior of the fibers run vertically downward to insert into the anterior half of the iliac crest. At the midclavicular line, the muscle fibers give rise to a flat, strong aponeurosis that passes anteriorly to the rectus sheath to insert medially into the linea alba ( Fig. 44.2 ). The lower portion of the external oblique aponeurosis is rolled posteriorly and superiorly on itself to form a groove on which the spermatic cord lies. This portion of the external oblique aponeurosis extends from the anterior superior iliac spine to the pubic tubercle and is termed the inguinal or Poupart ligament. The inguinal ligament is the lower free edge of the external oblique aponeurosis posterior to which pass the femoral artery, vein, and nerve and the iliacus, psoas major, and pectineus muscles. A femoral hernia passes posterior to the inguinal ligament, whereas an inguinal hernia passes anterior and superior to this ligament. The shelving edge of the inguinal ligament is used in various repairs of inguinal hernia such as the Bassini and the Lichtenstein tension-free repairs (see Chapter 45 ).

The internal oblique muscle originates from the iliopsoas fascia beneath the lateral half of the inguinal ligament, from the anterior two thirds of the iliac crest and lumbodorsal fascia. Its fibers course in a direction opposite to those of the external oblique (i.e., inferolateral to superomedial). The uppermost fibers insert into the lower five ribs and their cartilages ( Figs. 44.2A and 44.3 ). The central fibers form an aponeurosis at the semilunar line, which, above the semicircular line (of Douglas), is divided into anterior and posterior lamellae that envelop the rectus abdominis muscle. Below the semicircular line, the aponeurosis of the internal oblique muscle courses anteriorly to the rectus abdominis muscle as part of the anterior rectus sheath. The lowermost fibers of the internal oblique muscle pursue an inferomedial course, paralleling that of the spermatic cord, to insert between the symphysis pubis and pubic tubercle. Some of the lower muscle fascicles accompany the spermatic cord into the scrotum as the cremasteric muscle.

The transversus abdominis muscle is the smallest of the muscles of the anterolateral abdominal wall. It arises from the lower six costal cartilages, spines of the lumbar vertebrae, iliac crest, and iliopsoas fascia beneath the lateral third of the inguinal ligament. The fibers course transversely to give rise to a flat aponeurotic sheet that passes posterior to the rectus abdominis muscle above the semicircular line and anterior to the muscle below it ( Fig. 44.4A ). The inferiormost fibers of the transversus abdominis originating from the iliopsoas fascia pass inferomedially along with the lower fibers of the internal oblique muscle. These fibers form the aponeurotic arch of the transversus abdominis muscle which lies superior to Hesselbach triangle and is an important anatomic landmark in the repair of inguinal hernias, particularly the Bassini operation and Cooper ligament repairs. Hesselbach triangle is the site of direct inguinal hernias and is bordered by the inguinal ligament inferiorly, lateral margin of the rectus sheath medially, and inferior epigastric vessels laterally. The floor of Hesselbach triangle is the transversalis fascia.

The transversalis fascia covers the deep surface of the transversus abdominis muscle and with its various extensions forms a complete fascial envelope around the abdominal cavity ( Fig. 44.5 ; see Fig. 44.4B ). This fascial layer is regionally named for the muscles that it covers (e.g., iliopsoas fascia, obturator fascia, and inferior fascia of the respiratory diaphragm). The transversalis fascia binds together the muscle and aponeurotic fascicles into a continuous layer and reinforces weak areas where the aponeurotic fibers are sparse. This layer is responsible for the structural integrity of the abdominal wall, and by definition, a hernia results from a defect in the transversalis fascia.

The rectus abdominis muscles are paired muscles that appear as long, flat, triangular ribbons wider at their origin on the anterior surfaces of the fifth, sixth, and seventh costal cartilages and the xiphoid process than at their insertion on the pubic crest and pubic symphysis. Each muscle is composed of long parallel fascicles interrupted by three to five tendinous inscriptions ( Fig. 44.5 ), which attach the rectus abdominis muscle to the anterior rectus sheath. There is no similar attachment to the posterior rectus sheath. These muscles lie adjacent to each other, separated only by the linea alba. In addition to supporting the abdominal wall and protecting its contents, contraction of these powerful muscles flexes the vertebral column.

The rectus abdominis muscles are contained within the rectus sheath, which is derived from the aponeuroses of the three flat abdominal muscles. Superior to the semicircular line, this fascial sheath completely envelops the rectus abdominis muscle with the external oblique and anterior lamella of the internal oblique aponeuroses passing anterior to the rectus abdominis and the aponeuroses from the posterior lamella of the internal oblique muscle, transversus abdominis muscle, and transversalis fascia passing posterior to the rectus muscle. Below the semicircular line, all these fascial layers pass anterior to the rectus abdominis muscle except the transversalis fascia. In this location, the posterior aspect of the rectus abdominis muscle is covered only by transversalis fascia, preperitoneal areolar tissue, and peritoneum.

The rectus abdominis muscles are held closely in apposition near the anterior midline by the linea alba. The linea alba consists of a band of dense, crisscrossed fibers of the aponeuroses of the broad abdominal muscles that extends from the xiphoid to the pubic symphysis. It is much wider above the umbilicus than below, thus facilitating the placement of surgical incisions in the midline without entering the right or left rectus sheath.

Preperitoneal Space and Peritoneum

The preperitoneal space lies between the transversalis fascia and parietal peritoneum and contains adipose and areolar tissue. Coursing through the preperitoneal space are the following:

• Inferior epigastric artery and vein

• Medial umbilical ligaments, which are the vestiges of the fetal umbilical arteries

• Median umbilical ligament, which is a midline fibrous remnant of the fetal allantoic stalk or urachus

• Falciform ligament of the liver, extending from the umbilicus to the liver

The round ligament, or ligamentum teres, is contained within the free margin of the falciform ligament and represents the obliterated umbilical vein coursing from the umbilicus to the left branch of the portal vein ( Fig. 44.6 ). The parietal peritoneum is the innermost layer of the abdominal wall. It consists of a thin layer of dense, irregular connective tissue covered on its inner surface by a single layer of squamous mesothelium. The anatomy and physiology of the peritoneum are covered in greater depth later in this chapter.

Vascular Supply

The anterolateral abdominal wall receives its arterial supply from the last six intercostal and four lumbar arteries, superior and inferior epigastric arteries, and deep circumflex iliac arteries ( Fig. 44.7 ). The trunks of the intercostal and lumbar arteries, together with the intercostal, iliohypogastric, and ilioinguinal nerves, course between the transversus abdominis and internal oblique muscles. The distal-most extensions of these vessels pierce the lateral margins of the rectus sheath at various levels and communicate with branches of the superior and inferior epigastric arteries. The superior epigastric artery, one of the terminal branches of the internal mammary artery, reaches the posterior surface of the rectus abdominis muscle through the costoxiphoid space in the diaphragm. It descends within the rectus sheath to anastomose with branches of the inferior epigastric artery. The inferior epigastric artery, derived from the external iliac artery just proximal to the inguinal ligament, courses through the preperitoneal areolar tissue to enter the lateral rectus sheath at the semilunar line of Douglas. The deep circumflex iliac artery, arising from the lateral aspect of the external iliac artery near the origin of the inferior epigastric artery, gives rise to an ascending branch that penetrates the abdominal wall musculature just above the iliac crest, near the anterior superior iliac spine.

The venous drainage of the anterior abdominal wall follows a relatively simple pattern in which the superficial veins above the umbilicus empty into the superior vena cava by way of the internal mammary, intercostal, and long thoracic veins. The veins inferior to the umbilicus, the superficial epigastric, circumflex iliac, and pudendal veins, converge toward the saphenous opening in the groin to enter the saphenous vein and become a tributary to the inferior vena cava ( Fig. 44.8 ). The numerous anastomoses between the infraumbilical and supraumbilical venous systems provide collateral pathways whereby venous return to the heart may bypass an obstruction of the superior or inferior vena cava. The paraumbilical vein, which passes from the left branch of the portal vein along the ligamentum teres to the umbilicus, provides important communication between the veins of the superficial abdominal wall and portal system in patients with portal venous obstruction. In this setting, portal blood flow is diverted away from the higher pressure portal system through the paraumbilical veins to the lower pressure veins of the anterior abdominal wall. In this setting, dilated superficial paraumbilical veins are termed caput medusae.

The lymphatic supply of the abdominal wall follows a pattern similar to the venous drainage. Those lymphatic vessels arising from the supraumbilical region drain into the axillary lymph nodes, whereas those arising from the infraumbilical region drain toward the superficial inguinal lymph nodes. The lymphatic vessels from the liver course along the ligamentum teres to the umbilicus to communicate with the lymphatics of the anterior abdominal wall. It is from this pathway that carcinoma in the liver may spread to involve the anterior abdominal wall at the umbilicus (Sister Mary Joseph node or nodule).

Innervation

The anterior rami of the thoracic nerves follow a curvilinear course forward in the intercostal spaces toward the midline of the body (see Fig. 44.7 ). The upper six thoracic nerves end near the sternum as anterior cutaneous sensory branches. Thoracic nerves 7 to 12 pass behind the costal cartilages and lower ribs to enter a plane between the internal oblique muscle and the transversus abdominis. The seventh and eighth nerves course slightly upward or horizontally to reach the epigastrium, whereas the lower nerves have an increasingly caudal trajectory. As these nerves course medially, they provide motor branches to the abdominal wall musculature. Medially, they perforate the rectus sheath to provide sensory innervation to the anterior abdominal wall. The anterior ramus of the tenth thoracic nerve reaches the skin at the level of the umbilicus, and the twelfth thoracic nerve innervates the skin of the hypogastrium.

The ilioinguinal and iliohypogastric nerves often arise in common from the anterior rami of the twelfth thoracic and first lumbar nerves to provide sensory innervation to the hypogastrium and lower abdominal wall. The iliohypogastric nerve runs parallel to the twelfth thoracic nerve to pierce the transversus abdominis muscle near the iliac crest. After coursing between the transversus abdominis muscle and internal oblique for a short distance, the nerve pierces the internal oblique to travel under the external oblique fascia toward the external inguinal ring. It emerges through the superior crus of the external inguinal ring to provide sensory innervation to the anterior abdominal wall in the hypogastrium. The ilioinguinal nerve courses parallel to the iliohypogastric nerve but closer to the inguinal ligament than the iliohypogastric nerve. Unlike the iliohypogastric nerve, the ilioinguinal nerve courses with the spermatic cord to emerge from the external inguinal ring with its terminal branches providing sensory innervation to the skin of the inguinal region and scrotum or labium. The ilioinguinal nerve, iliohypogastric nerve, and genital branch of the genitofemoral nerve are commonly encountered during the performance of inguinal herniorrhaphy.

Congenital Abnormalities

Abnormalities resulting from persistence of the omphalomesenteric duct

During fetal development, the midgut communicates widely with the yolk sac through the vitelline or omphalomesenteric duct. As the abdominal wall components approximate one another, the omphalomesenteric duct narrows and comes to lie within the umbilical cord. Over time, communication between the yolk sac and intestine becomes obliterated, and the intestine resides free within the peritoneal cavity. Persistence of part or all of the omphalomesenteric duct results in a variety of abnormalities related to the intestine and abdominal wall ( Fig. 44.9 ).

Persistence of the intestinal end of the omphalomesenteric duct results in Meckel diverticulum. These true diverticula arise from the antimesenteric border of the small intestine, most often the ileum. A rule of 2s may be applicable to these lesions in that they are found in approximately 2% of the population, are within 2 feet of the ileocecal valve, are often 2 inches in length, and contain two types of ectopic mucosa (gastric and pancreatic). Meckel diverticula may be complicated by inflammation, perforation, hemorrhage, or obstruction. GI bleeding is caused by peptic ulceration of adjacent intestinal mucosa from hydrochloric acid secreted by ectopic parietal cells located within the diverticulum. Intestinal obstruction associated with Meckel diverticulum is usually caused by intussusception or volvulus around an abnormal fibrous connection between the diverticulum and posterior aspect of the umbilicus. These lesions are discussed in Chapter 50 .

The omphalomesenteric duct may remain patent throughout its course, producing an enterocutaneous fistula between the distal small intestine and umbilicus. This condition is manifested with the passage of meconium and mucus from the umbilicus in the first few days of life. Because of the risk for mesenteric volvulus around a persistent omphalomesenteric duct, these lesions are promptly treated with laparotomy and excision of the fistulous tract. Persistence of the distal end of the omphalomesenteric duct results in an umbilical polyp, which is a small excrescence of omphalomesenteric ductal mucosa at the umbilicus. Such polyps resemble umbilical granulomas except that they do not disappear after silver nitrate cauterization. Their presence suggests that a persistent omphalomesenteric duct or umbilical sinus may be present, and hence they are most appropriately treated by excision of the mucosal remnant and underlying omphalomesenteric duct or umbilical sinus, if present. Umbilical sinuses result from the persistence of the distal omphalomesenteric duct. The morphology of the sinus tract can be delineated by a sinogram. Treatment involves excision of the sinus. Finally, the accumulation of mucus in a portion of a persistent omphalomesenteric duct may result in the formation of a cyst, which may be associated with the intestine or umbilicus by a fibrous band. Treatment consists of excision of the cyst and associated persistent omphalomesenteric duct.

Acquired Abnormalities

Desmoid Tumor

Desmoid tumors, also known as fibromatosis , aggressive fibromatosis , or desmoid-type fibromatosis , are uncommon mesenchymal neoplasms that are locally aggressive but lack metastatic potential. They are rare tumors and have an incidence in the general population of 2 to 4 cases per million population per year. These tumors occur in young or middle-age adults and are uncommon in children or elderly patients. In sporadic cases, there is a female predominance of two to one. Ten to 15% of cases occur in patients with familial adenomatous polyposis (FAP), Gardner syndrome (FAP, desmoid tumor, and osteomas of the skull and mandible, sebaceous cysts, and cutaneous and subcutaneous fibromas), or Turcot syndrome (FAP and brain tumor). Males are affected as commonly as females in these instances.

Desmoid tumors encompass at least two distinct clinicopathological entities based on their underlying molecular biology. Sporadic desmoid tumors are most commonly associated with somatic mutations of the CTNNB1 gene, causing an abnormal stabilization of β-catenin, accumulation of β-catenin within the nucleus, and activation of the Wnt signaling pathway. This results in dysregulated gene transcription, the activation of oncogenes, and tumor production. Desmoid tumors associated with FAP are caused by germline mutations of the adenomatous polyposis coli (APC) gene. ^, Normally APC regulates cellular β-catenin levels by participating in the phosphorylation, ubiquitination, and degradation of β-catenin in the proteasome. Patients with FAP possess a truncated, inactive form of the APC protein, causing the accumulation of nuclear β-catenin and the overexpression of target oncogenes.

Typically, desmoid tumors present as a firm, nonpainful, nontender mass in the abdominal wall, shoulder, hip, limbs, mesentery, or pelvis. About 10% to 15% of patients with FAP will develop a desmoid tumor, most of which are located within the mesentery or abdominal wall. Desmoids infiltrate surrounding structures and spread along tissue planes and muscles. They have been associated with trauma, pregnancy, and oral contraceptive use. Surgical history is a particularly important risk factor for the occurrence of a desmoid tumor. A metaanalysis of five European FAP registries of 2260 patients identified prior surgery as an independent risk factor for the development of a desmoid tumor.

Magnetic resonance imaging (MRI) is the preferred imaging modality for diagnosis, local staging, and follow-up of patients with desmoid tumors. On T1-weighted MRI images, these tumors appear as a homogeneous mass, isointense compared with muscle. T2-weighted images show a hyperintense lesion with greater heterogeneity and a signal that is slightly less intense than fat ( Fig. 44.10 ).

The diagnosis is usually established by core needle biopsy. Histologically, desmoids are characterized by well-differentiated bundles of spindle cells with abundant collagenous matrix. The nuclear overexpression of β-catenin may be a useful diagnostic feature, although some nondesmoid soft tissue neoplasms may also exhibit this staining pattern.

Traditionally, resection of the tumor with a wide margin of normal tissue was the standard of care. The locally aggressive, infiltrative nature of these tumors often required large soft tissue resections with complex reconstructive techniques to achieve tumor-free surgical margins. Local recurrence is common despite this aggressive treatment. A number of retrospective studies have shown progression-free survival rates of 50% at 5 years for patients managed with a “watchful waiting” approach. Spontaneous regression occurs in as many as 30% of cases. These observations made “watchful waiting” the preferred strategy for managing most patients with desmoid tumors that are not causing severe symptoms or close to critical structures. This approach requires close observation with physical examination and MRI to identify tumor progression as early as possible. Patients with progression of the tumor or the appearance of tumor-related complications are treated with complete resection.

Radiation therapy has been used principally as adjuvant therapy after surgical resection with positive or close resection margins. It has also been used to treat patients who develop recurrent disease following resection. The applicability of radiation therapy to treat young patients with abdominal wall desmoid tumors is limited by the long-term potential for radiation-induced secondary malignancies, most notably sarcoma.

Systemic treatment options for patients with desmoid tumors include antihormonal therapies, nonsteroidal antiinflammatory drugs (NSAIDs), low-dose chemotherapy, tyrosine kinase inhibitors, and full-dose chemotherapy. Antihormonal agents, such as tamoxifen, have been used either alone or in combination with NSAIDs as first-line medical therapy. Advantages to their use include limited toxicity, rare adverse events, and low cost. Observational studies have demonstrated the arrest of tumor progression with combination therapy. Cytotoxic chemotherapy has also been used to treat patients with aggressively growing, symptomatic, or life-threatening desmoid tumors who are not surgical candidates and have failed treatment with antihormonal therapies and NSAIDs. Recommended regimens have included “low-dose” methotrexate with or without vinblastine/vinorelbine or conventional dose chemotherapy with anthracycline-based regimes, such as doxorubicin. Lastly, phase II studies have shown that tyrosine kinase inhibitors such as imatinib and sorafenib may produce 1-year progression-free survival rates of 66%. Unfortunately, the absence of internal controls or randomization of patients in these studies of systemic therapy makes it difficult to attribute observed slowing of tumor progression to the real activity of systemic treatment versus the natural history of the disease.

Abdominal Wall Sarcoma

Soft tissue sarcomas are a diverse group of mesenchymal malignancies that account for less than 1% of malignancies. The classification of sarcomas is based on the cell type they resemble histologically and immunohistochemically. The most common subtypes of sarcoma are liposarcoma, myxofibrosarcoma, leiomyosarcoma, rhabdomyosarcoma, and undifferentiated pleomorphic sarcomas. Less than 5% of soft tissue sarcomas affect the abdominal wall.

Patients present most commonly with a firm, painless, poorly circumscribed soft tissue mass that is fixed to the surrounding skeletal muscle and fascia. Radiation exposure and genetic syndromes (i.e., neurofibromatosis and Li-Fraumeni syndrome) are important predisposing factors. Cross-sectional imaging with CT or MRI will characterize the morphology of the tumor and define its anatomic site of origin and its relationship to surrounding structures. MRI provides better definition of the soft tissues. CT of the chest can document the presence of pulmonary metastases. The diagnosis is best established by core needle biopsy. Deep lesions can be biopsied using CT guidance. Open biopsy of the tumor should be avoided because of the risk of compromising the curative resection by inappropriate orientation of the incision and promoting local extension of the tumor by raising tissue flaps or the development of a postoperative hematoma. If an open biopsy is required, it should be performed by the surgeon who will perform the definitive resection.

Standard treatment of localized disease is resection of the tumor with margins that are free of microscopic disease. Most surgeons attempt to obtain at least a 2-cm margin of normal tissue around the tumor. Less than 5% of sarcomas metastasize to lymph nodes; therefore, lymphadenectomy is not performed unless there is evidence of lymphatic spread. Resection of these tumors often results in a large soft tissue defect that requires reconstruction with a myocutaneous flap or synthetic mesh prosthesis. Radiation therapy has been used in patients with large, high-grade sarcomas either before or after resection. Much of the evidence for this approach has come from clinical trials enrolling patients with extremity sarcomas.

The prognosis of these tumors depends upon the grade and stage of the tumor and the adequacy of resection. The grade of the tumor is based on tumor differentiation, mitotic count, and the presence or absence of necrosis. The American Joint Committee on Cancer staging system combines the size of the tumor, the involvement of lymph nodes, the presence of metastases, the type and grade of the sarcoma. There are no large series that address the outcomes after resection of sarcomas located in the abdominal wall exclusively. In studies that include other anatomic sites, local recurrence rates after resection with negative margins average 10% to 15%. Depth, size, positive margin status, and high tumor grade are associated with increased risk of recurrence. Soft tissue sarcomas are discussed in greater detail in Chapter 32 .

Metastatic Disease

Metastases from advanced malignancies may also present as soft tissue masses of the abdominal wall. These tumors may result from hematogenous spread of a malignancy or by implantation of tumor during biopsy or resection of an intraabdominal malignancy. Almost always, abdominal wall metastases occur in the setting of advanced malignancy. Malignancies most commonly associated with hematogenous metastasis to the abdominal wall include lung, colon, renal carcinoma, as well as melanoma. The incidence of tumor implantation after laparoscopic colon resection for colorectal adenocarcinoma is about 1%, similar to the risk of tumor recurrence in the wound after open colectomy. This occurs most frequently in the setting of peritoneal carcinomatosis.

Similar to desmoid tumors and sarcomas, these patients present with a firm abdominal wall mass that may or may not be associated with pain or tenderness. Cross-sectional imaging will characterize the mass and distinguish it from an incarcerated abdominal wall hernia. The diagnosis is established by core needle biopsy. Immunohistochemistry staining of the tumor may allow identification of the type of primary tumor and facilitate differentiation from primary sarcomas of the abdominal wall.

The treatment of abdominal wall metastases is dictated by the biology or natural history of the primary tumor, by symptoms, and by the presence of other sites of disease. The vast majority of patients will have disseminated disease, and treatment should be either palliative systemic therapy or directed toward symptom relief. Asymptomatic patients with multiple sites of disease will not need a change to this approach. Patients with symptomatic tumors not responsive to systemic therapy can benefit from selective use of radiation therapy for palliative purposes or resection if it does not cause excessive morbidity.