The Abdominal Wall and Peritoneal Cavity

Overview.

The peritoneum is a thin serosal membrane of mesodermal origin that comprises a single layer of mesothelial cells resting on a basement membrane. It is divided into visceral and parietal components, and the space between the two components constitutes the peritoneal cavity. The layer covering the abdominal viscera, omentum, and the mesenteries is designated visceral, whereas the layer covering the abdominal walls, undersurface of the diaphragm, anterior surface of the retroperitoneal viscera, and the pelvis is designated as parietal. The peritoneum is continuous in males, whereas in females it is discontinuous at the ostia of the oviducts to allow communication between the peritoneal cavity and extraperitoneal pelvis.

The layers of peritoneum that invest blood vessels, lymphatics, nerves, adipose tissue, and connective tissue within the abdomen and the pelvis form the various peritoneal ligaments, omentum, and mesenteries. A ligament usually supports a structure within the cavity, whereas a mesentery usually suspends the structure to the retroperitoneum. Omentum is a specialized ligament that connects the stomach to another structure. These ligaments and mesenteries not only serve to suspend and support the visceral organs but also divide the peritoneal cavity into multiple compartments that dictate the location and routes of spread of malignancies and infection.

The mesothelial cells produce a small amount of sterile fluid within the peritoneal cavity that is continuously circulated by the movement of the diaphragm and peristalsis of bowel, and the fluid provides a frictionless surface over which the viscera can move, a site for fluid transport, and local bacterial defense. Peritoneal fluid predominantly flows up the right paracolic gutter into the right supramesocolic compartment, and 90% of the fluid is cleared by the subphrenic lymphatics to the supradiaphragmatic nodes. Areas of relative stasis include (1) the rectouterine pouch or cul-de-sac (pouch of Douglas) in females, (2) the rectovesical region in males, (3) the right lower abdomen at the end of the small bowel mesentery, (4) the left lower abdomen along the sigmoid mesocolon, (5) the right paracolic gutter, and (6) the right subhepatic/subdiaphragmatic space (Morison pouch).

Overview.

The term pneumoperitoneum refers to the presence of air within the peritoneal cavity. Benign postoperative pneumoperitoneum is a separate entity that results from accumulation of free air after abdominal surgery. Usually, free intraperitoneal air clears more rapidly in children than in adults, but the timing can be variable. Timing of clearance usually depends upon the amount of air initially trapped after surgery, which in most cases is related to patient body habitus; obese patients trap less air than thin patients. Several studies have demonstrated clearing of free air in 68% to 90% of children postoperatively by 24 hours, but free air can be seen for as long as 6 to 7 days postoperatively in 2% to 3% of cases.

Etiology.

Free intraperitoneal air is most commonly a consequence of gastrointestinal (GI) tract perforation. In the neonate, this usually results from intestinal obstruction, necrotizing enterocolitis, or spontaneous gastric or bowel perforation, usually at the ileocecal region ( Box 86.1 ). Necrotizing enterocolitis is the most common cause of pneumoperitoneum in the neonatal intensive care unit.

Free intraperitoneal air sometimes results from mediastinal extension in newborns supported by mechanical ventilation. Rarely, nasogastric or nasoduodenal tubes may perforate the bowel. The position of the tube is often a clue to the perforation ( e-Fig. 86.1 ).

In children beyond the neonatal period, perforated peptic ulcers and inflammatory bowel disease (IBD) are other causes of pneumoperitoneum; it should be noted that pneumoperitoneum is rarely found with appendiceal perforation, because the omentum usually seals off the perforation very quickly. Trauma, both accidental and nonaccidental, may also result in pneumoperitoneum.

Clinical Presentation.

Pneumoperitoneum may be suspected clinically because of the history of an underlying condition that predisposes to bowel perforation, detection of acute abdominal distension with increased tympany on physical examination, and clinical deterioration of the patient. Occasionally it is incidentally discovered on imaging of the chest or abdomen.

Imaging.

A single supine abdominal radiograph is usually the most common imaging study requested for patients with suspected abdominal pathology. The cited overall detection rate of free intraperitoneal air on supine imaging ranges from 56% to 59%; detection rates as high as 80% have been quoted on supine abdominal radiographs and 78.7% on supine chest radiographs. It is important to be familiar with the various signs of intraperitoneal free air on supine radiographs, because this may be the only initial study requested by the patient's primary caregiver.

Once suspected, the diagnosis can be confirmed on upright or decubitus films. Upright radiographs will show air collecting between the diaphragm and the liver on the right and between the diaphragm and the liver, spleen, stomach, or colon on the left ( Figs. 86.2 and 86.3 ). Young children and those too ill to sit or stand can be examined in the decubitus position. The decubitus view should be obtained with the right side up to allow the liver to fall away from the wall of the peritoneal cavity to allow visualization of free air between the liver and the abdominal wall. Both techniques are considered equally effective.

If decubitus or upright imaging is difficult to obtain, a supine view using a horizontal-beam technique can be utilized. On the horizontal-beam supine radiograph, free peritoneal air may collect between the anterior surface of the liver and the anterior abdominal wall ( Fig. 86.4 ), but small amounts of free air may be more difficult to detect, particularly if located over loops of bowel.

Multiple signs related to pneumoperitoneum are described on plain radiographs ( Table 86.1 ) based on the location and volume of air and its relationship to adjacent structures. The lucency caused by the free air rising to an anterior position in the abdomen is most easily detected when it projects over the liver, thus many right upper quadrant signs of free air are described. The normal density of liver is uniform and typically denser than the heart. Air overlying the liver on a supine radiograph decreases the radiodensity of that portion of the liver.

Small amounts of free air may appear as subtle, localized collections in the right upper quadrant. Linear accumulation of air in the right subhepatic space is known as the hepatic edge sign, whereas triangular collections seen with air in the Morison pouch is known as the Doge cap sign, because it resembles the cap worn by the Venetian Doge. A linear collection of air may also be located in the fissure of the ligamentum teres.

Rigler sign refers to visualization of the bowel wall caused by the presence of air on both sides of the wall ( e-Fig. 86.5 ). The telltale triangle sign is a triangular focus of extraluminal air seen on the cross-table lateral view of the abdomen, created by the external surface walls of adjacent bowel loops and the anterior abdominal wall, as the air collects at the highest point in the peritoneal space.

A sufficiently large amount of free air can be seen as a large, ovoid lucency overlying the abdominal contents ( Fig. 86.6 ). In the supine position, the liver falls away from the anterior peritoneal surface and free air can dissect along both sides of the falciform ligament, which attaches the liver to the anterior abdominal wall. When outlined by free air, the ligament appears as a thin, vertical, opaque line. The distension of the flanks caused by the free intraperitoneal air and the outline of the falciform ligament centrally are the elements of the well-known football sign, so termed because of its similarity to an American football; the falciform ligament represents the central thread in the ball (see Fig. 86.6 ). A less commonly encountered sign of pneumoperitoneum is the inverted V sign, caused by air outlining the medial umbilical folds in the pelvis.

Causes of pneumoperitoneum can sometimes be inferred by certain signs. For example, a ruptured viscus permits both air and fluid to escape into the peritoneal cavity, causing abnormal extraluminal air-fluid levels (compare Figs. 86.3 and 86.4 ). On the other hand, tension pneumomediastinum is an entity in which air dissects along the retroperitoneum and subadventitial layer of the mesenteric vessels and sometimes ruptures into the peritoneal cavity; this will not demonstrate significant extraluminal air-fluid levels unless the patient has underlying ascites from an unrelated cause. The latter is also usually suspected from a history of assisted ventilation and the presence of pneumomediastinum on the chest radiograph.

Apart from plain radiographs, ultrasound (US) can also be used in the detection of pneumoperitoneum by detecting gas over the liver, with a reported sensitivity of 93%, specificity of 64%, and accuracy of 90%. However, US should not be considered definitive in diagnosing or excluding a pneumoperitoneum without extensive expertise and experience, and US findings should be confirmed by appropriate radiographic evaluation.

Although not typically performed for assessment of pneumoperitoneum, computed tomography (CT) is an extremely sensitive method to identify small amounts of intra- or retroperitoneal air, intraperitoneal air-fluid levels, and often the underlying cause of pneumoperitoneum. It can be optimized by reviewing abdominal images using lung-window parameters ( e-Fig. 86.7 and Fig. 86.8 ).

Overview.

A small amount of fluid in the peritoneal cavity is normal. This is more common in females and is often seen incidentally on cross-sectional imaging. Ascites refers to abnormal or pathologic accumulation of fluid within the peritoneal cavity.

Etiology.

Pathologic intraperitoneal fluid collections stem from a variety of causes and most commonly result from sequestration of fluid from the splanchnic vascular bed. Other causes of pathologic intraperitoneal fluid include hemoperitoneum, urinary ascites, bile, pancreatic juices, chylous fluid, and cerebrospinal fluid (CSF). Transudative ascites is most commonly found in patients with hepatobiliary disease, especially cirrhosis; heart failure; hyponatremia; renal failure; peritonitis; and Budd-Chiari syndrome. Exudative ascites can occur secondary to peritoneal infections and peritoneal metastases. Perforation of the GI tract results in the escape of both air and fluid into the peritoneal cavity. In children, the most common causes for ascites are hepatic, renal, and cardiac disease.

The lesser sac, Morison pouch, paracolic gutters, pelvis, and recesses formed by many of the peritoneal ligaments are all sites where fluid can collect ( Fig. 86.9 ). Typically, small amounts of ascites collect in the pelvis when the patient is supine. As the amount of fluid increases, it moves cephalad along the paracolic gutters into the subhepatic spaces and Morison pouch, and it can sometimes be identified in the fossa of the ligamentum teres ( e-Fig. 86.10 ). Ascites eventually spreads through the peritoneal cavity and into the mesenteric recesses ( e-Fig. 86.11 ); in cases of inflammation, loculations may occur. Encysted collections of CSF may be seen adjacent to the tip of a ventriculoperitoneal shunt tube (“CSF pseudocyst”), usually as a result of an inflammatory response around the shunt tube tip entrapping fluid ( Fig. 86.12 ).

Clinical Presentation.

The clinical hallmark of ascites is abdominal distension, which in itself is a nonspecific sign. The clinical findings are in part governed by the underlying etiology. Early satiety and dyspnea can be seen with increasing accumulation of fluid within the abdominal cavity.

Abdominal compartment syndrome is an uncommon sequela of acute accumulation of large-volume ascites or other material that leads to intraabdominal hypertension. Increased pressure in a confined space leads to progressive organ failure with significant associated mortality. It is most commonly described after trauma but can also be seen in the setting of surgery and other entities, such as pancreatitis. The diagnosis is usually made at the bedside with measurement of intravesical pressure. The criteria for diagnosis of abdominal compartment syndrome include elevation of intraabdominal pressure to 20 mm Hg or higher, coupled with impaired function of at least one organ; typically, it affects respiratory or renal function.

Imaging.

Diagnosis of ascites is usually made based on clinical history, physical examination, and aspirated fluid analysis. Imaging is usually performed to confirm clinical ascites; estimate its volume; identify loculations, septations, or internal echoes; or to assist in sampling or draining of ascitic fluid.

Abdominal radiographs are only sensitive to large amounts of intraperitoneal fluid. In such cases, the gas-filled bowel loops will appear centrally located within the abdomen ( Fig. 86.13 ). Separation of bowel loops may also occur as a result of ascites, but this appearance can be simulated by large amounts of intraluminal fluid or thick-walled bowel loops ( e-Fig. 86.14 ).

US is an extremely sensitive imaging modality for ascites. Simple ascites appears as anechoic fluid and can be seen in the various peritoneal recesses. Septations, loculations, and internal echoes usually suggest complex fluid, which can be seen in the setting of blood, chyle, inflammatory cells, or peritoneal metastases (see e-Fig. 86.14 ). Ascites occasionally will pass through the esophageal hiatus or patent pleuroperitoneal canals to present as intrathoracic fluid.

CT is equally sensitive to detect ascites, although it does not visualize internal septations, which are easily seen on US. Because of radiation exposure, CT is not the first-line modality in the evaluation of ascites.

Abdominal compartment syndrome is suggested on CT by a ratio of anteroposterior to transverse diameters of the abdomen exceeding 0.81 ( e-Fig. 86.15 ). However, abdominal measurements on a single CT scan may be nonspecific, because an increased anteroposterior abdominal dimension may be seen with chronic ascites. Other telling findings include an elevated diaphragm, the presence of hemoperitoneum, increasing girth on serial examinations, attenuated inferior vena cava or renal veins, and shock bowel. Although not specific, a combination of these findings in the appropriate clinical setting or worsening on sequential imaging studies should raise the possibility of abdominal compartment syndrome.

Treatment.

The course, prognosis, and treatment of ascites depend entirely on the cause. Drainage of the ascitic fluid can usually provide symptomatic relief; however, in most cases treatment is aimed at the underlying disorder. The treatment for abdominal compartment syndrome includes emergent drainage or decompressive laparotomy. The mortality rate in abdominal compartment syndrome remains high, at approximately 60% to 70%.

Overview.

Peritonitis is a generalized or localized inflammatory process that affects the peritoneum. Acute generalized peritonitis is usually of infectious etiology and can be further subclassified as primary and secondary. Primary peritonitis, also called spontaneous bacterial peritonitis, is a primary infection of the peritoneal cavity that does not result from spread from the visceral organs. Secondary peritonitis results from secondary infection of the peritoneum, usually from urogenital or GI sources, particularly perforation. Abscesses may develop locally and at sites where fluid is likely to accumulate. The subhepatic and subphrenic spaces are common distant sites for abscess formation.

Etiology.

Primary peritonitis may occur spontaneously in patients without underlying pathology, and it is usually seen in association with postnecrotic cirrhosis and nephrotic syndrome. Access of organisms to the peritoneal cavity through the fallopian tubes is another putative cause of this condition, supported by the increased occurrence in patients with intrauterine contraceptive devices.

Secondary peritonitis in children is most commonly caused by a perforated appendix. Other causes of bowel perforation that could potentially result in secondary peritonitis include IBD, incarcerated hernias, complications of Meckel diverticulum, midgut volvulus, intussusception, hemolytic uremic syndrome, necrotizing enterocolitis, typhlitis, and traumatic perforation. Peritoneal dialysis is another cause of peritonitis in children and is the most common cause of dialysis failure.

Granulomatous peritonitis is usually associated with infectious etiologies such as tuberculosis, histoplasmosis, or pneumocystosis, most often in immunocompromised hosts. Involvement of the peritoneum occurs in approximately 4% of patients with tuberculosis but is reported to occur in 10% of children aged less than 10 years. Noninfectious causes for granulomatous peritonitis include foreign material, such as talc and barium, meconium, bowel contents, bile, or gallstones. Meconium peritonitis is a sterile peritonitis that results from prenatal perforation of the bowel; this is discussed in Chapter 102 .

Clinical Presentation.

Patients usually come to medical attention with fever (≥39.5°C), diffuse abdominal pain, nausea, and vomiting. Signs of peritoneal inflammation on physical examination include rebound tenderness, abdominal wall rigidity, and decreased or absent bowel sounds from a paralytic ileus. Patients with infectious granulomatous peritonitis secondary to histoplasmosis or pneumocystosis are nearly always immunocompromised.

Imaging.

Abdominal radiographs in patients with peritonitis often show a nonspecific, adynamic ileus pattern with dilated bowel, multiple intraluminal air-fluid levels, and evidence of ascites; in addition, the properitoneal fat plane may be obliterated ( e-Fig. 86.16 ). US may demonstrate intraperitoneal fluid with internal echoes and septations, and abscesses are identified as focal collections of mixed echogenicity.

CT demonstrates enhancement of the peritoneal lining with associated dense ascites ( Fig. 86.17 ). Abscesses appear as focal fluid collections with relatively high attenuation values and densely enhancing walls ( Fig. 86.18 ). On magnetic resonance imaging (MRI), abscesses in the peritoneum show similar findings as elsewhere, with high internal T2 signal and dense peripheral enhancement. Both gallium citrate- and indium-labeled white blood cells have been used as scintigraphic agents in the diagnosis of abscesses, although these are rarely used.

Granulomatous peritonitis is secondary to a spectrum of lesions, as previously discussed. Peritoneal tuberculosis has been subdivided into three overlapping subtypes—a wet type; a fibrotic type; and a dry, plastic type—with decreasing ascites and increasing soft tissue components along the spectrum. The wet type is the most common and is characterized by ascites, which on CT is often (but not always) of high density with free or localized fluid collections ( Fig. 86.19 ). Dry plastic or fibrotic fixed patterns are characterized by a relative lack of ascites and a variable amount of peritoneal and omental nodules and masses, peritoneal adhesions, and fibrotic fixation of the small bowel and mesentery as the predominant features. Omental involvement is usually seen as diffuse, infiltrating, ill-defined enhancing lesions that produce a “smudged” appearance of the omentum (see Fig. 86.19 ). The findings in tuberculosis are indistinguishable from those in histoplasmosis. Although no single CT feature is diagnostic of peritoneal tuberculosis, additional imaging features that help in diagnosis include concomitant central, low-attenuation lymph node enlargement, miliary microabscesses in the liver or spleen, splenic or lymph node calcification, and inflammation that involves the terminal ileum and cecum.

Treatment.

The treatment of peritonitis includes correction of the underlying etiology and supportive therapy. General supportive measures include vigorous intravenous rehydration, correction of electrolyte disturbances, and infection control. Early control of the infection can be achieved medically, operatively, and through image-guided percutaneous interventions.

Overview.

Abdominal wall calcification is uncommon in infants and children. The etiology depends upon the location of the calcification (skin, muscles, soft tissue, or peritoneum) and on the age of the patient. Most causes of intraabdominal calcification are related to specific organs, and these are discussed in the appropriate chapters.

Etiology.

Fat necrosis is one of the causes of abdominal wall calcification in neonates and infants. Although there are many causes of fat necrosis, the majority are associated with neonatal asphyxia, sepsis, gestational diabetes, and hypothermia. Older children with hypothermia, hepatic failure, and renal failure may also experience subcutaneous fat necrosis.

Abdominal wall calcification may be seen in fibrodysplasia ossificans progressiva and in myositis ossificans, but are more common in the thoracic wall. Calcifications secondary to dermatomyositis are more likely to be in the extremities than in the trunk, but calcifications can be found in the abdominal wall. Subcutaneous hemangiomas may contain phleboliths. Abdominal wall calcification in infants has also been described after subcutaneous emphysema and in prune-belly syndrome.

The most common cause of peritoneal calcification in the neonate is meconium peritonitis, discussed in Chapter 102 . Peritoneal calcification in older children is rare. Intestinal perforation with subsequent peritonitis may cause calcification. Other causes include granulomatous peritonitis, peritoneal dialysis ( Fig. 86.20 ), calcification along surgical scars, hyperparathyroidism, and peritoneal malignancies such as ovarian adenocarcinoma.

Clinical Presentation.

Clinical presentation is strongly dependent on the underlying cause. Subcutaneous fat necrosis appears clinically as firm, erythematous plaques. Patients may develop hypercalcemia, particularly when involvement is extensive.

Imaging.

Most abdominal wall and peritoneal calcifications are detected incidentally on plain radiographs and/or CT scans obtained for other clinical indications. Shape of calcifications, location, and correlation with any predisposing condition may help identify the underlying etiology. Peritoneal calcification associated with calcified lymph nodes is significantly more likely to be associated with malignancy, whereas a sheetlike appearance of peritoneal calcification is associated more frequently with benign disease (see Fig. 86.20 ).

Overview.

Anterior abdominal wall defects encompass a variety of conditions, most commonly omphalocele and gastroschisis. Omphalocele refers to a midline defect larger than 4 cm that typically contains both gut and the liver and may or may not include other abdominal organs. It has a covering bilayer membrane consisting of the peritoneum as the inner layer and the amnion as the outer layer, with Wharton jelly in between ( Fig. 86.21A ). It is differentiated from the less common umbilical cord hernia in that the latter is less than 4 cm, does not contain liver, has a normal abdominal wall, and has few associated anomalies. Gastroschisis is a defect located lateral to the umbilical cord insertion, most commonly to the right, with no covering membrane ( Fig. 86.21B ), and typically containing gut without abdominal organs although a gonad may occasionally protrude. Unlike all of the previously mentioned defects, an umbilical hernia is not associated with gut malrotation, is covered by skin, and usually becomes apparent several weeks after birth.

Overview.

Omphaloceles are the second most common anterior abdominal wall defect (gastroschisis is the first), with a prevalence of approximately 1 to 5 in 10,000 live births. It is more common in boys.

Etiology.

An omphalocele forms when fusion fails in the lateral folds of the body wall, the rectus muscles fail to meet in the midline, and the herniated bowel fails to return into the peritoneal cavity, with the umbilical cord inserting into the covering membrane (see Figs. 86.21 and 86.22 ). Involvement of the cephalic folds results in the spectrum of pentalogy of Cantrell: midline supraumbilical abdominal wall defect, defect in the diaphragmatic pericardium, deficiency of the anterior diaphragm resulting in herniation of the heart, congenital intracardiac abnormalities, and sternal clefts ( e-Fig. 86.23 ). Failure of caudal fold development results in cloacal exstrophy.

Clinical Presentation.

Associated anomalies are present in 50% to 70% of cases. Chromosomal anomalies, primarily trisomies, occur in 40% to 60%. Smaller defects, absence of liver in the sac, and abnormal amounts of amniotic fluid are associated with an increased incidence of other anomalies, and 50% of these patients have congenital heart disease. Omphaloceles are also associated with Beckwith-Wiedemann syndrome and omphalocele–bladder exstrophy–imperforate anus–spinal defect complex. Intrauterine growth retardation and prematurity commonly coexist.

Imaging.

Diagnosis is usually made on antenatal US. Antenatal evaluation includes assessment of umbilical cord insertion, presence or absence of a covering membrane, contents of the omphalocele, and coexisting anomalies. Multiple associated anomalies indicate a poorer prognosis, as do oligohydramnios and polyhydramnios.

Treatment.

Definitive treatment is surgical and may consist of primary closure or a staged procedure. If primary closure is not possible, the sac may be covered with nonadherent dressings to prevent trauma to the sac and exposure of the underlying bowel until delayed closure is possible.