An internal abdominal herniation is the extension of an abdominal organ through a mesenteric or peritoneal aperture. These rare lesions can be congenital or acquired as a result of trauma or intra-abdominal surgery. There is an association of this lesion with intestinal malrotation. Internal abdominal herniations rarely present during childhood, even when the underlying cause is developmental. The clinical manifestations of internal abdominal herniation are nearly always nonspecific. Patients may report abdominal pain or discomfort that tends to be episodic. The pain is most often localized to the periumbilical region. Nausea may occur. Manifestations of an acute bowel obstruction develop if there is bowel incarceration. CT is the most useful diagnostic imaging study for the evaluation of internal abdominal herniations; contrast studies of the bowel and standard radiographs serve roles as well.^1,2

Six types of intra-abdominal herniations are generally recognized: paraduodenal hernias, hernias through the foramen of Winslow, transmesenteric hernias, pericecal hernias, intersigmoid hernias, and paravesical hernias. Paraduodenal hernias are the most common type in adults; these are further subdivided into left- and right-sided types. Paraduodenal hernias result from a congenital deficiency in mesenteric peritoneal fixation.^3–6

At least three-quarters of paraduodenal hernias occur on the left, with the peritoneal defect located to the left of the distal portion of the duodenum. Small intestine can herniate through this mesenteric defect into the left portion of the transverse mesocolon. Barium examinations show a cluster of slightly dilated loops of small bowel located just lateral to the distal portion of the duodenum and separated from normal small bowel elsewhere in the abdomen. On CT, the herniated small bowel loops are located between the stomach and the tail of the pancreas, posterior to the tail of pancreas, or between the transverse portion of the colon and the left adrenal gland.

Right-sided paraduodenal hernias are also congenital lesions. The pathogenesis involves failure of normal embryonic midgut rotation, resulting in positioning of the proximal aspect of the small bowel to the right of the superior mesenteric artery. With a hernia, this portion of the small bowel projects through a defect in the proximal jejunal mesentery dorsal to the mesenteric artery and directed toward the right-sided mesocolon. Barium studies and CT show the collection of herniated loops of small bowel to be located just lateral and inferior to the second portion of the duodenum. The herniated bowel is usually somewhat dilated.

The foramen of Winslow is a normal peritoneal opening that is located between the portal vein and inferior vena cava, and opens into the lesser sac. Herniations through an enlarged foramen of Winslow may consist of small bowel, colon, or gallbladder. On barium studies, herniated bowel within the lesser sac causes lateral and anterior displacement of the stomach. CT shows extension of bowel and/or mesenteric fat into the portocaval space between the inferior vena cava and portal vein.

Transmesenteric hernias are the most common causes of internal abdominal herniations in children. Most are due to a congenital defect in the small bowel mesentery in the ileocecal region. Affected children may present with clinical manifestations of an acute small bowel obstruction or volvulus. Imaging studies show isolated dilated loops of small bowel in the right lower quadrant.

The other types of internal abdominal herniation are uncommon or rare. The pericecal hernia usually consists of extension of a portion of the ileum through a defect in the cecal mesentery, with the herniated bowel occupying the pericecal fossa. Imaging studies show the cluster of small bowel loops to be located posterior and lateral to the cecum, sometimes extending into the right paracolic gutter. Intersigmoid hernias involve extension of the bowel into a peritoneal pocket that is formed between 2 adjacent portions of the sigmoid colon and the attached mesentery. Paravesical hernias occur into the supravesical fossa between the umbilical segments.

Omental infarction is a rare entity that can cause acute abdominal symptoms. It occurs most commonly in males. The clinical manifestations of omental infarction frequently mimic those of acute appendicitis: acute onset of right lower quadrant pain, nausea, vomiting, dysuria, and fever. Leukocytosis is common. Approximately 15% of omental infarctions occur in children.⁷

Omental infarction can occur with or without torsion. Idiopathic omental infarction (i.e., occurring without torsion) is sometimes associated with an identified predisposing factor, such as venous kinking or compression related to a prolonged unusual patient position or vascular congestion after a large meal. In some individuals, anomalous venous drainage renders a portion of the omentum prone to vascular congestion and infarction. Omental torsion causes compromised venous and arterial blood flow; this usually occurs as a gradual process. Torsion (primary torsion) sometimes occurs as a volvulus of the free edge of the omentum; potential predisposing factors include obesity and developmental variations of the omentum (e.g., bifid or elongated). A more common mechanism (secondary torsion) involves an acquired attachment of part of the omentum to another structure, such as a neoplasm, surgical adhesion, hernia, or cyst. A developmental defect in the omental attachment to the cecum or ascending colon occasionally is associated with omental torsion.^8,9

At surgery and gross pathology, omental infarction due to torsion appears as an edematous, reddish-blue or black portion of the greater omentum that connects to the normal omentum by an elongated, twisted, narrow segment. With idiopathic infarction, there is an omental mass that contains areas of hemorrhagic infarction. Progression to an abscess can occur.

CT of the patient with omental infarction usually shows a mass in the omental fat. Classically, this appears as an ovoid or cake-like lesion adherent to the peritoneum and located in the umbilical region or anterolateral to the right half of the colon. There is infiltration of adjacent fat. Free intraperitoneal fluid is typically present.¹⁰

With sonography, idiopathic omental infarction may appear as a hyperechoic mass that contains poorly defined nodular or linear hypoechoic areas (i.e., hemorrhagic infarction). There is a paucity of vessels within the mass; peripheral hyperemia is sometimes present on Doppler examinations. Omental torsion appears sonographically as a hyperechoic mass that is hyperemic, but contains an avascular, hypoechoic, blind-ending tubular structure that represents the actual twisted and infarcted omental tissue. This pattern frequently mimics the findings of appendicitis.^11,12

Epiploic appendagitis results from torsion or thrombosis of 1 of the fatty appendages that project from the colonic serosa. The usual clinical presentation is acute abdominal pain, most often in the left lower quadrant. Patients with involvement of the right colon often have symptoms that mimic those of acute appendicitis. Epiploic appendagitis is a self-limited condition for most patients.

The normal appendages are generally indistinguishable from the adjacent intra-abdominal fat on CT. When surrounded by intraperitoneal fluid, normal appendages appear as fat-containing pedunculated structures arising from the serosal surface of the colon. An inflamed epiploic appendage appears on CT as an oval or pedunculated hypoattenuating lesion in contact with the colon. There is usually hazy increased attenuation of the ovoid appendage, as well as associated thickening of the visceral peritoneal lining of the appendage (hyperattenuating rim) and stranding in the surrounding fat (Figure 38-1). Occasionally, there is a central high attenuation focus within the lesion due to venous thrombosis. Sonography shows a hyperechoic mass at the point of maximum pain, adjacent to the anterior peritoneal wall and fixed during deep breathing. There is no flow in the lesion on color Doppler examination. The imaging findings are usually sufficient for a confident diagnosis, obviating the need for laparotomy despite the presence of acute abdominal symptoms.^13–16

Mesenteric adenitis is an inflammatory process of mesenteric lymph nodes. Viral infection is the most common pathogenesis; other potential pathogens include Yersinia, Shigella, Salmonella, and Helicobacter jejuni. Mesenteric adenitis usually is a self-limited condition; those patients with clinical manifesations of a bacterial process respond to antibiotic therapy. Progression to suppuration is a rare complication. Patients with mesenteric adenitis may have high fever, abdominal pain, and tenderness and guarding to palpation. The clinical findings, therefore, can closely resemble those of appendicitis. In addition, the pain in these patients often is localized to the right lower quadrant.

Abdominal radiographs provide little useful information for the differentiation between mesenteric adenitis and acute appendicitis, unless an appendicolith is present. Some patients with mesenteric adenitis have findings suggestive of enteritis, with mild mucosal thickening in slightly prominent loops of small intestine. With sonography and CT, the appendix is shown to be normal in patients with mesenteric adenitis. Rao et al proposed an imaging diagnosis based on the demonstration of 3 or more mesenteric nodes with short-axis diameters of at least 5 mm (Figure 38-2). The enlarged mesenteric lymph nodes are often in a group. Thickening of the ilial and/or cecal wall is sometimes present.^17,18