Nontraumatic Abdominal Emergencies

Esophageal Inflammation/Infection

Esophagitis

Esophagitis can arise from a number of causes, including infection, radiation, gastroesophageal reflux, and medications. Infectious esophagitis may have characteristic findings on barium fluoroscopy depending on the causative pathogen. Candida esophagitis manifests with raised mucosal plaques between which barium is trapped. Herpes esophagitis typically presents with multiple small ulcers represented by pooled barium. Larger ulcers are seen with cytomegalovirus and human immunodeficiency virus (HIV) esophagitis. Reflux esophagitis may manifest with strictures, as well as reticular-appearing mucosa distally, indicating Barrett esophagus. In contrast to the detailed mucosal evaluation afforded by barium fluoroscopy, CT findings of infectious esophagitis are nonspecific and insensitive, demonstrating a sensitivity of approximately 55% in one study. Computed tomography findings include long segment thickening of the esophageal wall (greater than 5 mm), as well as a “target" sign caused by mucosal hyperemia and submucosal edema ( Fig. 13-1 ). There is a large overlap in the CT appearance of infectious and noninfectious esophagitis, such as from reflux or radiation. Complications of esophagitis include functional obstruction, aspiration, and perforation.

Esophageal Obstruction

Foreign Bodies

Esophageal foreign bodies are most often ingested by children and patients with cognitive defects. Commonly seen foreign bodies include impacted food boluses, fish and chicken bones, coins, and vinyl gloves. Although most esophageal foreign bodies pass spontaneously, 10% to 20% of cases require endoscopic removal and approximately 1% undergo surgery for treatment. Up to one third of affected adult patients with foreign body impaction have an underlying esophageal stricture contributing to their presentation. Diagnostic workup often starts with radiography, particularly if the ingested item is radiodense (e.g., metallic) or suspected to be lodged in the hypopharynx. Computed tomography is useful in select cases for definitive diagnosis and localization, and identifying suspected complications such as esophageal perforation ( Fig. 13-2 ).

Esophageal Perforation

Mallory-Weiss Tears

The clinical presentation and imaging findings of esophageal perforation depend on the thickness of the esophageal tear. Superficial tears, or Mallory-Weiss tears, commonly result from repeated, forceful retching and may cause “coffee-ground” emesis caused by mucosal bleeding. These tears may have no imaging findings, particularly on CT. On barium studies they may manifest as linear collections of contrast, classically in the distal esophagus, corresponding to mucosal tears identified on endoscopy ( Fig. 13-3 ).

Esophageal Dissection

Intermediate—or intramural—perforation is a rare form of esophageal perforation also referred to as esophageal dissection . This condition can be seen after instrumentation, foreign body impaction, or forceful vomiting. Imaging findings of intramural perforation include a “double-barrel esophagus” caused by an intraluminal flap separating the true and false lumens, which may be accentuated with oral contrast, creating what has been also been termed a mucosal stripe sign . The false lumen of esophageal dissection is often posterior to the true lumen and may be better demonstrated on coronal and sagittal reformatted images. There is considerable overlap between esophageal dissection and an intramural hematoma, which may be distinguished by visualization of contrast in the false lumen with a true dissection ( Fig. 13-4 ).

Transmural Perforation

Similar to esophageal dissection, full-thickness esophageal perforation may be iatrogenic, such as from surgery, stricture dilatation, stenting, or thermal injury. In addition, full-thickness tears may occur from vomiting (Boerhaave syndrome), caused by incomplete cricopharyngeal relaxation and increased intraluminal pressure. On imaging, full-thickness perforation may result in pneumomediastinum, pleural effusions, and leak of oral contrast into the mediastinal and/or pleural spaces ( Fig. 13-5 ). In addition to benign causes, primary or metastatic esophageal tumor may also perforate, particularly following palliative dilatation and/or stenting. Complications of esophageal perforation include mediastinitis, pneumonia (from direct spread of infection or from aspiration), and empyema/abscess formation.

Aortoesophageal Fistulas

Chronically, esophageal perforation may result in fistula formation, including to the trachea, pleural space, and aorta. The majority of aortoesophageal fistulas result from aortic disease fistulizing to the esophagus, such as from rupture of a descending thoracic aortic aneurysm or an infected aortic graft. Primary esophageal disease may result in aortic fistulization as well: esophagitis, foreign body perforation, and advanced esophageal cancer have all been described as underlying causes. Clinically, patients with aortoesophageal fistulas present with the Chiari triad: midthoracic pain or dysphagia, a sentinel episode of hematemesis, and a symptom-free interval that gives way to massive upper GI bleeding. Imaging findings of aortoesophageal fistulas include a focal outpouching of the aorta toward the esophagus, adjacent esophageal wall thickening, and extraluminal gas within or abutting the aortic wall ( Fig. 13-6 ). Oral contrast or angiographic studies may also demonstrate a luminal communication.

Gastric Emergencies

Gastric Inflammation and Infection

Gastritis

Gastritis has many potential underlying causes, including Helicobacter pylori infection, nonsteroidal antiinflammatory medications, and alcohol. Inflammation of the stomach is most commonly diffuse, but it can also be focal process. H. Pylori gastritis may be isolated to the antrum or greater curvature. On fluoroscopy, gastritis manifests with thickened rugal folds, erosions, and foci of ulceration, identified by persistent pooling of oral contrast. On CT, gastric inflammation appears as low-attenuation submucosal edema and mucosal hyperemia, which result in mural stratification. As previously discussed, attention to the degree of gastric distention helps discern true gastric wall thickening from artificial thickening resulting from collapsed lumen.

A subset of patients with gastritis can develop the emphysematous variant, an uncommon form with a high mortality rate. The underlying pathologic process in emphysematous gastritis is mucosal disruption and invasion of the gastric wall by a gas-producing organism, particularly Escherichia coli . On CT this condition presents with signs of gastritis (e.g., mural stratification), accompanied by gas bubbles in the stomach wall and potentially portal venous gas. Differentiation between emphysematous gastritis and more benign gastric emphysema may be difficult, but the latter is much more common, is typically seen in relatively asymptomatic patients, and appears with more linear intramural gas with no wall thickening to suggest gastritis ( Fig. 13-7 ).

Peptic Ulcer Disease

Although the incidence of peptic ulcers has decreased since the advent of H. pylori treatment and proton pump inhibitors, they remain a potential cause for presentation to the ED. Whereas superficial ulcers can be seen only with endoscopy or with barium fluoroscopy, deeply penetrating ulcers may be identified on CT as a focal mucosal outpouching, submucosal edema, perigastric fat stranding, and in the case of perforation, extraluminal gas ( Fig. 13-8 ). In patients who have undergone gastric surgery, particularly Billroth and Roux-en-Y gastric bypass procedures, marginal gastric ulcers may appear at the gastrojejunal anastomosis. These ulcers can be deeply penetrating, usually begin at the jejunal side of the anastomosis, and typically develop 2 to 4 years following surgery.

Gastric Obstruction

Gastric Volvulus

An uncommon cause of gastric obstruction, gastric volvulus presents clinically with Borchardt triad: sudden epigastric pain, intractable retching, and inability to pass a nasogastric tube. The two subsets of gastric volvulus are organoaxial and mesenteroaxial, although many are seen as a combination of these. Organoaxial gastric volvulus is the most common type and results from rotation about the long axis (line connecting the pylorus to the cardia) of the stomach with the antrum anterosuperiorly and the fundus posteroinferiorly ( Fig. 13-9 ). This type of gastric volvulus is more commonly associated with diaphragmatic defects and vascular compromise. Mesenteroaxial gastric volvulus is less common and results from rotation of the stomach about its short axis, resulting in the antrum being positioned above the gastroesophageal junction ( Fig. 13-10 ). These are more commonly chronic and less likely to be associated with diaphragmatic hernias.

On imaging, gastric volvulus presents with a distended stomach, nonpassage of oral contrast, and an abnormal lie to the stomach. Gastric volvulus requires at least 180 degrees of rotation and gastric outlet obstruction. Asymptomatic patients with large hiatal hernias may present with an abnormal lie, that is, organoaxial positioning of the stomach without volvulus. These patients are predisposed to both gastric volvulus and hiatal hernia incarceration, particularly when the fundus “redescends” into the abdomen, obstructing the mouth of the hernia sac.

Bezoars

Ingested foreign bodies may be a cause of gastric or small bowel obstruction and often fall into two major categories: trichobezoars and phytobezoars. Trichobezoars are composed of hair and are most common in women and psychiatric patients, often those with long hair. When the hair extends from the stomach into the small and/or large bowel this has been termed Rapunzel syndrome ( Fig. 13-11 ). Phytobezoars are composed of fruit or vegetable matter, commonly oranges and persimmons. Patients with decreased gastric motility, such as those who have undergone gastric surgery, are predisposed to formation of phytobezoars, which may also pass into the small bowel and cause obstruction more distally as well. Patients who have undergone organ transplantation also have an increased risk for developing bezoars, which is hypothesized to be secondary to decreased gastric motility, either due to vagus nerve injury or a side effect of cyclosporine.

Gastric Perforation

Peptic Ulcer Disease

Perforation complicates peptic ulcer disease in approximately 2% to 10% of affected patients. The imaging findings of perforation can vary depending upon the location of the perforated ulcer. Ulcers on the anterior wall and greater curvature perforate freely into the peritoneal space, whereas more posterior ulcers may have a relatively contained perforation into the lesser sac. Perforation of peptic ulcers within the duodenal bulb and stomach remains one of the most common causes of GI perforation, warranting close examination of the stomach and proximal duodenum for ulcers when free intraperitoneal gas is identified on CT ( Fig. 13-12 ).

Malignancy

Gastric adenocarcinoma is complicated by perforation in 0.4% to 6.0% of cases and is more common in patients older than 65 years of age. Although typically found in locally advanced gastric cancer, a focal ulcerated malignancy may perforate if the ulcer crater is deeply penetrating. Perforation of GI lymphoma is most commonly seen in the small bowel, but gastric lymphoma may also perforate; perforation is seen in a higher percentage of T-cell lymphoma involving the GI tract than with B-cell lymphoma ( Fig. 13-13 ). Clues to an underlying malignancy as a cause of gastric perforation include focal gastric wall thickening with soft tissue attenuation in the submucosa, as well as evidence of tumor outside of the stomach such as lymphadenopathy or metastases.

Gastric Banding

Perforation related to gastric banding can be seen acutely in 0.1% to 0.8% of patients and may have a varied clinical presentation. Computed tomography may demonstrate free or loculated extraluminal gas or abscess formation. Chronic perforation of the stomach complicates 1% to 3% of patients with gastric bands and results from erosion of the band into the stomach lumen. On fluoroscopy, demonstration of contrast outlining the band can confirm erosion, which may also manifest on CT with gas surrounding the band. In addition, CT may show inflammation or fluid tracking along the connector tubing and/or port; when seen, this should prompt evaluation of the band as the site of erosion or infection ( Fig. 13-14 ).

Duodenal Emergencies

Duodenal Inflammation and Infection

Zollinger-Ellison Syndrome

A subset of patients with duodenal ulcers will have Zollinger-Ellison syndrome, typically caused by a gastrin-secreting tumor in the gastrinoma triangle, an anatomic space defined by the junctions of the cystic and common bile ducts, the neck and body of the pancreas, and the second and third portions of the duodenum. The increased serum gastrin levels stimulate peptic acid secretion and lead to duodenal mucosal ulceration. Computed tomography findings of Zollinger-Ellison syndrome include reflux esophagitis, gastritis, and multiple duodenal ulcers, including distal to the duodenal bulb ( Fig. 13-15 ). This conglomerate of findings should prompt a search for an adjacent hyperenhancing nodule representing a gastrinoma, although these may be difficult to identify on routine portal venous phase CT and may require multiphase phase CT, endoscopic ultrasonography (EUS), or octreotide scan to aid in detection.

Diverticulitis

Duodenal diverticula are very common, occurring in approximately 23% of patients, most common in the second portion and typically arising medially. Although a relative minority of duodenal diverticula cause symptoms, up to 1% of patients will have a complication from a duodenal diverticulum that requires treatment, including diverticulitis, perforation, and obstruction in the case of intraluminal diverticula. Computed tomography findings of duodenal diverticulitis resemble those seen in inflamed diverticula elsewhere in the GI tract: a focal, round outpouching from the duodenal lumen with wall thickening and adjacent fat stranding and fluid ( Fig. 13-16 ). Treatment of duodenal diverticulitis may be operative or nonoperative (i.e., antibiotics), depending on the clinical condition and stability of the patient.

Groove Pancreatitis

A rare form of chronic pancreatitis, groove pancreatitis occurs because of inflammation in the pancreaticoduodenal groove, including the pancreatic head and pancreatic rests in the duodenal wall. Clinically patients may present with normal serum amylase and lipase levels. The focal inflammation in the duodenal wall may result in benign-appearing common bile duct strictures and duodenal obstruction. The imaging appearance of groove pancreatitis may overlap with pancreatic adenocarcinoma considerably, but groove pancreatitis classically manifests with low-attenuation cystic areas (“cystic degeneration”) in the descending duodenal wall and soft tissue in the pancreaticoduodenal groove resulting from fibrosis. This disease can be particularly well characterized on magnetic resonance cholangiopancreatography (MRCP), which can demonstrate both the well-marginated T2-hyperintense cystic areas and biliary strictures without underlying mass lesion. These findings, along with a lack of vascular invasion, help differentiate between groove pancreatitis and adenocarcinoma of the pancreaticoduodenal groove ( Fig. 13-17 ). Associated fibrosis, which can result from chronic inflammation, may demonstrate delayed contrast enhancement on CT and magnetic resonance imaging (MRI).

Duodenal Obstruction

Malrotation and Volvulus

Although malrotation is rare in adulthood—80% of patients will present in the first month of life and 90% within the first year—some cases remain quiescent for years and present later in life. Affected patients may present clinically with symptoms of proximal bowel obstruction, namely, severe abdominal pain and bilious vomiting. On imaging studies the findings of malrotation are the same as those seen in childhood: a duodenum that does not cross the spine, reversal of the relationship between superior mesenteric artery (SMA) and vein, colon situated on the left side of the abdomen, and small bowel on the right. When complicated by volvulus, CT shows a distended stomach and duodenum and an abrupt transition to decompressed bowel with a focal twist causing a “whirlpool" sign ( Fig. 13-18 ). There may also be occlusion of mesenteric vessels with associated bowel ischemia, indicated by bowel wall thickening, hypoenhancement, and/or pneumatosis with adjacent mesenteric edema and fluid.

Gallstones

Gastric outlet obstruction due to gallstones, termed Bouveret syndrome , is a rare subset of gallstone ileus that presents classically with a triad of pneumobilia, an ectopic gallstone, and bowel obstruction ( Fig. 13-19 ). Although the majority, approximately 85% of patients with cholecystenteric fistulas, have stones pass spontaneously, 15% of these patients will have a resulting bowel obstruction, most commonly in the terminal ileum and least commonly in the stomach and duodenum. Bouveret syndrome has a high mortality rate and is typically treated surgically.

Malignancy See Gastric Obstruction, Malignancy

Aortoduodenal Fistulas

Chronic perforation of the duodenum, similar to that of the esophagus, may result in fistulization to nearby structures, including small and large bowel, bile ducts, kidneys and ureters, inferior vena cava (IVC), and aorta. These fistulas can result from primary duodenal perforation, such as from malignancy, ulcer disease, or trauma, or from an extrinsic source, as is often the case with aortoduodenal fistulas. The duodenum is the most common site for aortoenteric fistulas, owing to the proximity of these two structures in the retroperitoneum. This condition most frequently occurs in the setting of an abdominal aortic aneurysm (AAA), either arising as a primary event or a complication of surgical repair. Uncommonly, fistulas between the aorta and duodenum may result from vasculitis or radiation. Clinically patients may present with abdominal pain, GI bleeding, and a pulsatile mass. Similar to those with aortoesophageal fistulas, affected patients may have a “herald bleed” preceding life-threatening voluminous hemorrhage. Although diagnostic imaging options for aortoenteric fistulas include barium studies, aortography, and tagged red blood cell (RBC) scintigraphy, these options have limitations compared to CT. Computed tomography findings of aortoduodenal fistulas include focal tethering of the duodenum to the aortic wall with associated duodenal wall thickening, ectopic perigraft gas and fluid remote from the perioperative period, pseudoaneurysm formation, and possibly active contrast extravasation into the bowel lumen ( Fig. 13-20 ).

Plain Radiography

Despite overall low diagnostic accuracy and specificity, the kidney, ureter, and bladder (KUB) radiographic examination is still sometimes used as an initial imaging examination in patients with abdominal symptoms. It is widely available, inexpensive, and reasonably sensitive for the diagnosis of high-grade bowel obstruction and radiopaque foreign bodies. Typical radiographic views include supine and upright views of the abdomen and an upright chest radiograph. The supine abdominal view demonstrates the bowel pattern to better extent, whereas air-fluid levels within the bowel are evident on the upright view. The upright view of the chest is best for the detection of free air under the diaphragm (pneumoperitoneum), which is an ominous sign of bowel perforation.

Although a fair amount of gas is normally seen within the stomach and colon, the small bowel should contain little gas. When bowel motility is affected by mechanical obstruction or nonobstructive adynamic ileus, gas accumulates within the small bowel. Small bowel obstruction is suspected when multiple gas- or fluid-filled loops of dilated small bowel are present. The presence of an unusual quantity of colonic gas in this setting usually indicates nonobstructive ileus, partial SBO, or early complete SBO. Common predisposing factors for ileus include sepsis, electrolyte disturbances, GI infection, and recent surgery. Differentiation between partial and early SBO can be challenging in the absence of clinical information. Although subjective, features favoring high-grade obstruction include (1) the presence of multiple air-fluid levels, particularly when discrepant levels are seen within the same loop, (2) dilated loops averaging more than 2.5 cm in diameter and/or exceeding 50% of the caliber of the largest visible colonic loop, and (3) a large number of distended loops of bowel. Although patients with SBO can present with normal KUB findings, a confident diagnosis can be made in 50% to 60% of cases when dilated gas or fluid-filled loops of small bowel are present in the setting of a gasless colon ( Fig. 13-21 ).

Ultrasonography

The potential advantages of ultrasonography (US) include widespread availability, fast, dynamic real-time acquisition, low cost, and lack of ionizing radiation. Although US is often used in the diagnosis of intussusception in children, its role in the assessment of the small bowel in the adult population is very limited, particularly in the United States. Disadvantages include operator variability and incomplete evaluation of the small bowel due to intervening gas and obese habitus. However, it may be indicated in selected cases, such as in the follow-up of patients with inflammatory bowel disease (IBD) or critically ill patients.

Barium Contrast Studies

Although small bowel follow-through studies can provide spatial resolution in the evaluation of the mucosa that is superior to that of cross-sectional studies, and these studies have been performed in the past to triage patients with suspected SBO into surgical versus nonsurgical management, the widespread use of abdominal CT has largely replaced this practice. Rapid transit of contrast material within normal-caliber small bowel loops excludes SBO. However, in cases of SBO, the duration of the small bowel follow-through examination is lengthy, and retained fluid dilutes the barium, often limiting assessment of the point of obstruction, with delayed films needed if one wishes to identify the transition point or determine whether contrast passes distally.

Computed Tomography and Computed Tomography Enterography

The role of CT in the diagnosis of SBO cannot be overemphasized. It is fast and widely available, and it allows for the concurrent assessment of the mesentery, mesenteric vessels, and peritoneal cavity. In the setting of SBO, it can be performed without oral contrast administration, because the retained intraluminal fluid serves as a natural negative contrast agent (and delays transit of any ingested contrast). In the assessment of small bowel disease, CT enterography, with negative or neutral oral contrast material, can be used to achieve bowel distention and to improve evaluation of bowel wall morphologic characteristics, thickness, and enhancement. Multiplanar reformations (MPRs) and postprocessing techniques aid in a confident diagnosis and can be helpful to depicting findings. Coronal reformatted images are most intuitive because they are analogous to a frontal radiograph and the course of the bowel loops can be most readily followed in this plane. Maximum intensity projection images and other postprocessing techniques, such as volume-rendering techniques, can improve depiction of the vasculature and bowel anatomy and improve the communication of findings ( Fig. 13-22 ).

Magnetic Resonance Imaging

Magnetic resonance imaging provides accurate anatomic and functional information about the small bowel without the use of ionizing radiation. A potential advantage over CT that has been proposed is the characterization of malignant versus benign strictures. In addition, because MR enterography can be used to monitor small-bowel filling in real time without radiation exposure, it is an alternative to CT enterography as a means of evaluating low-grade obstruction. It is an exceptional technique to evaluate patients with IBD because these patients are often young and require serial examinations due to acute exacerbations. Magnetic resonance imaging is more controversial in the setting of suspected SBO but may have a role in children and pregnant patients.

Confirming the Presence and Severity of Obstruction

Typical findings of SBO include continuous loops of dilated (>2.5 cm) proximal small bowel, associated with normal caliber or collapsed bowel distal to a transition point. When oral contrast medium is used, the absence of contrast in distal loops of bowel is indicative of complete obstruction provided that enough time has been allowed for delayed passage. In selected cases, delayed scans can be performed to confirm complete obstruction, although this is rarely performed because the patient’s clinical progression is the primary determinant of management approach in the absence of clear signs of high-grade or closed-loop obstruction.

Multiple conditions can result in small bowel dilatation (or abdominal distention) and be confused with SBO, particularly before clinical and radiologic information are integrated. Adynamic ileus is associated with bowel distention that may include the colon, in addition to the small bowel and stomach. Shock bowel can present with dilated loops of small bowel, but history, involvement of the colon, and other imaging findings such as a flattened IVC, and hyperenhancement of the adrenal glands, should help differentiate it from SBO. Bowel ischemia can likewise cause significant distention of atonic small bowel loops and simulate the appearance of obstruction, but ancillary findings of bowel thickening, segmental bowel perfusion abnormalities, and evidence of arterial atherosclerotic disease help suggest an ischemic cause for the dilatation.

Differentiation between partial low-grade or high-grade obstruction is subjective. High-grade obstruction should be suggested when there is a substantive caliber difference between proximal and distal loops of bowel (and absent passage of contrast material through the transition point if delayed imaging is performed). The diagnosis of partial low-grade obstruction is more challenging and considered a relative “blind spot” for CT because the degree of caliber change is generally less striking.

The use of oral contrast for the diagnosis of SBO is controversial. Potential advantages include the indirect assessment of bowel transit time, which may aid in the diagnosis of partial low-grade obstruction, and the progressive dilution of contrast as the contrast column approaches the transition point, which may help to determine its location ( Fig. 13-23 ). Delayed images can provide confirmation of a complete obstruction in the appropriate setting. However, oral contrast delays the diagnosis in the emergency setting and is generally not tolerated by obstructed patients presenting with nausea and vomiting. In addition, the fluid within the distended loops of bowel acts like a natural neutral oral contrast, as long as nasogastric tube decompression is not performed before imaging ( Fig. 13-24 ).

Another helpful imaging feature in SBO is the “small bowel feces sign,” or the presence of mottled, particulate matter and gas within the lumen that simulates the appearance of feces. It is often associated with high-grade obstruction but has been described in nonobstructed patients. When present, it is generally located immediately proximal to the transition point and is thus extremely helpful to locating the site of obstruction, which is the next step in the evaluation of SBO ( Fig. 13-25 ).

Determining the Location and Cause

A transition zone or point is the region at which the bowel caliber changes and greatly increases confidence that a true mechanical obstruction is present by identifying the site of the obstruction. In the absence of a focal transition point, dilated loops are nonspecific and may be due to other conditions such as IBD, scleroderma, or ischemia. It is often easiest to identify a transition point by careful inspection of the course of the bowel loops, usually by an antegrade approach starting in the distended proximal loops. Distally located SBO can, however, be most readily evaluated by a retrograde approach starting at the decompressed terminal ileum. Careful and systematic travel through the bowel loops in multiple planes is the key to success. When the transition point is identified, a search for intraluminal, intrinsic, or extrinsic causes of obstruction should be performed. Intraluminal causes include foreign bodies, gallstones, and bezoar. Intrinsic bowel lesions typically manifest as mural or focal thickening. Extrinsic causes of obstruction, such as hernias and CD, are associated with other extraintestinal findings. It should be noted that adhesions, the most common cause of SBO in the United States, are typically not visible on CT and can be suggested in regions of an abrupt transition point when no clear cause is seen.

Determining the Presence of Closed-Loop Obstruction and Complications

In simple obstruction the bowel is occluded at one or more points along its course. The diagnosis of closed-loop obstruction is crucial because it carries a higher risk for strangulation and bowel infarction. Most often, an adhesion or hernia will cause partial or complete occlusion of a segment of bowel loop at two adjacent points. Computed tomography findings depend on the length, degree of distention, and orientation of the closed loop but include a characteristic fixed radial distribution of several dilated, usually fluid-filled bowel loops with stretched and prominent mesenteric vessels converging toward a point of torsion. The configuration is usually U shaped or C shaped. A narrow pedicle can be formed leading to torsion of the loops and producing a small bowel volvulus. A “beak" sign is seen at the site of the torsion as a fusiform tapering. Occasionally a “whirl" sign of the mesenteric vessels can be seen, reflecting the rotation of the bowel loops around the fixed point of obstruction. Strangulation is defined as closed-loop obstruction associated with intestinal ischemia, and its occurrence depends on the time and degree of rotation of the incarcerated loops. The findings that indicate strangulation include bowel wall thickening and hyperattenuation, a halo or target sign, mesenteric fat stranding and/or fluid, pneumatosis intestinalis, and mesenteric or portal venous gas, but these findings are not entirely specific. More specific findings include absent, asymmetric, or delayed bowel wall enhancement, with or without focal mesenteric fluid or hemorrhage ( Fig. 13-26 ).

Adhesions

Adhesions are the most common cause of SBO in the United States, ranging from 50% to 80% of cases. The diagnosis should not be excluded even in the absence of prior surgery because adhesions can occur as a result of prior peritonitis. Adhesions are typically not seen, and the diagnosis is one of exclusion. Computed tomography findings include an abrupt change in the caliber of the bowel, with focal kinking and tethering, in the absence of an underlying mass lesion, and significant inflammation or bowel wall thickening at the transition point ( Fig. 13-27 ).

Hernias

Hernias are the most common cause of SBO in developing countries. An external hernia occurs as a result of a defect in the abdominal wall at sites of congenital weakness or previous surgery. Although the diagnosis can be obvious at clinical examination, it may be challenging in very obese patients ( Fig. 13-28 ).

The less common internal hernia occurs when there is protrusion of the viscera through a defect in the peritoneum or mesentery into another compartment within the abdominal cavity. Closed-loop obstruction can result ( Fig. 13-29 ). Early diagnosis in this scenario becomes critical because these patients will often not benefit from conservative management because the involved segment will not be decompressed with nasogastric drainage, and bowel ischemia and necrosis can rapidly develop ( Fig. 13-30 ).

Endometriosis

Endometriosis is common and underdiagnosed. It is estimated to affect approximately 5% of women of reproductive age. Endometrial implants may manifest as contiguous or penetrating soft tissue nodules along the antimesenteric border of the bowel wall.

Malignancy

Metastatic involvement is far more common than primary disease. It can result in SBO by different mechanisms (intrinsic and extrinsic). It can be secondary to intraperitoneal seeding, hematogenous spread, or direct extension from an adjacent visceral malignancy. Although SBO can result from intrinsic obstruction from submucosal implants, such as from malignant melanoma and breast cancer, it most often occurs in the setting of peritoneal carcinomatosis, when extensive serosal disease will determine extrinsic compression and/or circumferential involvement at the transition point ( Fig. 13-31 ).

Primary small bowel neoplasms are rare. Advanced cases of adenocarcinoma can present with SBO, with pronounced asymmetric and irregular mural thickening noted at the transition point ( Fig. 13-32 ). Conversely, primary lymphoma of the small bowel, even when extensive or annular, is a soft tumor and does not generally cause obstruction unless it is associated with adhesions or posttreatment change ( Fig. 13-33 ). Small bowel carcinoid is a relatively rare cause of SBO because the primary lesion is often occult, and it usually will manifest as spiculated mesenteric masses with calcification resulting from a desmoplastic reaction ( Fig. 13-34 ).

Intussusception

Intussusception is a benign and common condition in children younger than 3 years old, but a rare cause of bowel obstruction in adults. When found in older children and adults, it should trigger a search for a lead point, such as an underlying neoplasm, inciting adhesion or foreign body. Computed tomography findings include the pathognomonic bowel-within-bowel configuration, with or without mesenteric fat and mesenteric vessels. The finding of a leading mass should be interpreted with caution because the intussusception itself can present as a pseudotumor ( Fig. 13-35 ).

Functional disturbances that affect bowel motility, such as scleroderma, celiac disease, and cystic fibrosis, can cause transient intussusception. Clinical history can be helpful in these patients, and careful evaluation of the intussusception will confirm the absence of a neoplastic lead point. When multiphasic CT is performed, resolution of the intussusception can be often observed, confirming the transient nature of this phenomenon ( Fig. 13-36 ).

Inflammation and Fibrosis

Acute and chronic inflammation, such as CD and radiation enteritis, can lead to fibrosis, strictures, and, in more severe cases, obstruction. Small bowel obstruction can occur during the acute phase of CD when the intense acute transmural inflammation causes narrowing of the bowel lumen, during the chronic phase due to fibrotic stenosis, postoperative adhesions, incisional hernias, and exacerbation of the inflammatory condition (acute flare). Small bowel obstruction occurs in the late phase of radiation enteritis, most often in the distal small bowel as a result of adhesive and fibrotic changes that develop several months after therapy. Radiation serositis can lead to narrowing of the lumen and abnormal peristalsis. Computed tomography findings include adhesions, narrowing of the lumen secondary to mural thickening, mesenteric retraction, and abnormal bowel enhancement within the radiation field.

Hematoma and Vascular Causes

Hematoma can mimic neoplasm and result in significant luminal narrowing. It is usually associated with anticoagulant therapy, iatrogenic intervention, or trauma. In the setting of severe stenosis or occlusion of the mesenteric arterial or venous supply, bowel ischemia can lead to significant bowel wall thickening, resulting in SBO. Although relatively benign, in advanced cases, pneumatosis and portomesenteric venous gas can signal the presence of infarction.

Gallstone Ileus

Gallstone ileus is a rare complication of chronic cholecystitis. It is the result of migration of a gallstone into the small bowel with subsequent impaction, most often at the ileocecal valve. The imaging features of the “Rigler triad” include SBO, an ectopic gallstone, and pneumobilia because a cholecystenteric fistula is needed for the migration of a large obstructing gallstone to occur ( Fig. 13-37 ). In the event of proximal obstruction, at the level of the stomach or duodenum, gastric outlet obstruction may result (Bouveret syndrome).

Bezoar

Bezoar was considered a rare cause of SBO, but the number of reported cases is increasing in recent years as a result of gastric outlet surgery, because it prevents adequate digestion of vegetable fibers, which may become impacted. Computed tomography findings include an elongated and intraluminal mass demonstrating a mottled appearance at the transition point ( Fig. 13-38 ).

Foreign Bodies

A wide range of foreign bodies can cause SBO with variable imaging appearances. Clinical history is very important in helping to establish preoperative diagnosis ( Fig. 13-39 ). In children and, emotionally disturbed, or mentally disabled patients, foreign bodies should be suspected.

Iatrogenic SBO can occur as a result of endoscopic capsule retention because they have been used more often in the evaluation of the small bowel, particularly in patients with CD. Diagnosis is made by identifying an ovoid metallic object impacted at the transition point.

Infectious Enteritis

Infectious enterocolitis can cause mild symptoms resembling common viral gastroenteritis, but it can present with clinical findings that are indistinguishable from appendicitis and other surgical conditions. Although imaging findings are often nonspecific, including mural thickening, mesenteric fat stranding, and moderate mesenteric lymphadenopathy, the clinical history and distribution can be helpful in narrowing the differential diagnosis. Giardia lamblia is a protozoan known to cause severe diarrhea and malabsorption. The organism tends to inhabit the duodenum and jejunum. Imaging findings consist of mural thickening involving the proximal small bowel, increased luminal secretions, and disordered motility.

Immunocompromised patients can be affected with systemic infection with Mycobacterium avium-intracellulare . It affects multiple organs and has been called pseudo-Whipple disease because of clinical, histologic, and radiologic similarities. Computed tomography findings include thickened small bowel more pronounced in the jejunum, hepatomegaly, and splenomegaly. Focal, low-density lesions can be present in the spleen. Cytomegalovirus can be reactivated in the setting of immunosuppression and can result in hemorrhagic enteritis. Definitive diagnosis may require biopsy with immunohistochemical stains. Cryptosporidium is a GI parasite that results in watery diarrhea in patients with acquired immunodeficiency syndrome (AIDS). Clinical history is important in establishing the diagnosis. Computed tomography findings demonstrate wall thickening more often involving the proximal small bowel and stomach, similar to that of giardiasis. Other common pathogens that often affect the small bowel, typically the distal ileum and cecum, include Yersinia , Campylobacter , and Salmonella species ( Fig. 13-40 ).

Crohn Disease

Inflammatory bowel disease and infectious enteritis can have similar imaging findings, with distinction made based on the clinical history, as well as the distribution of findings within the bowel. Crohn disease is part of the IBD spectrum, characterized by chronic, relapsing inflammation of unknown cause. Despite abundant research in this field, it remains a diagnostic and therapeutic challenge. Crohn disease can affect any part of the GI tract but predominantly affects the small bowel (up to 80% of cases) and right colon. As opposed to ulcerative colitis (UC), rectal involvement is very rare in CD.

Crohn disease is characterized by the presence of granulomatous inflammation at histologic evaluation, with chronic erosions, ulceration, and transmural bowel inflammation, which predisposes to complications such as fistulas and abscess formation. The presence of “skip lesions” is one of the hallmarks of the disease. Crohn disease has a tendency toward remission and relapse, and acute and chronic changes often coexist within the same affected bowel segment. Fatty infiltration of the bowel wall may occur in chronic IBD and was thought to be pathognomonic of this disease. However, it has been demonstrated in healthy individuals, particularly in association with obesity.

Endoscopy and classic barium studies are critical in the initial diagnosis and staging of IBD in general because they are superior to cross-sectional imaging in the evaluation of the mucosa, particularly in early-stage disease. However, CT and MRI can depict several abnormalities that are associated with acute bowel inflammation, such as mural thickening and stratification, thickened folds and/or reduction or distortion of folds due to ulceration and cobblestoning. Additional findings include pseudosacculations or pseudodiverticulum formation, which occur as a consequence of relative sparing of the antimesenteric border within an affected segment. The major advantage over endoscopy and classic barium studies is the assessment of extraenteric findings, which are relatively common in CD. In addition, cross-sectional imaging is reserved for the follow-up evaluation of established disease, assessment of treatment response, diagnosis of relapse, detection of complications, and assessment before surgical intervention. In the presence of abscesses, percutaneous drainage under CT guidance is favored over surgery.

Computed tomography findings of active inflammation in CD include significant mural enhancement and stratification due to submucosal edema (target or “double-halo” appearance), adjacent mesenteric fat stranding, and engorged vasa recta (“comb” sign). The presence of fibrofatty proliferation along the mesenteric border of the affected bowel is considered pathognomonic of this disease. Extraintestinal manifestations include mesenteric inflammatory changes and the presence of phlegmon, abscess, or lymphadenopathy. As described earlier, deformity of bowel loops, such as pseudodiverticulum formation, is caused by asymmetric involvement by longitudinal ulcers and scars, both of which are well demonstrated on both axial and coronal images. Lymphadenopathy is not uncommon, and although controversial, it has been suggested that lymphadenopathy can allow differentiation between active inflammatory and chronic (fibrostenosing) disease. Nonetheless, lymph nodes larger than 10 mm in short axis should prompt evaluation for superimposed lymphoma or carcinoma ( Figs. 13-41 and 13-42 ).

Magnetic resonance enterography is an attractive modality for the assessment of CD because it can offer dynamic evaluation of bowel motility, superior soft tissue contrast, and excellent depiction of fluid and edema, without associated ionizing radiation. Magnetic resonance enterography can be particularly useful in young patients that require serial examinations. Protocols are variable but generally include multiphasic coronal fluid-sensitive sequences. Optimal bowel distention is achieved by use of enteric contrast material, but the type of contrast material and method of administration are controversial. Most patients require a delay of at least 40 to 60 minutes from contrast material ingestion to imaging.

Magnetic resonance enterography can play an important role in the follow-up of patients with established IBD, or it can be used to exclude IBD in a young patient who presents with symptoms suggesting the disease. Although early changes, such as aphtoid ulceration, are beyond the resolution of MR, it can be useful in the evaluation of fixed stenoses and segmental dilatation and to detect adhesions. Because of high contrast, CT can better assess extent of fistulas in penetrating disease, mesenteric vascularity, and lymphadenopathy. Fistulas, sinus formation, and abscesses are features of penetrating disease. They are visible as wall-enhancing structures. Adhesions can be differentiated from fistulas because they are fibrotic and tend to be thinner and enhance later. Over time, chronic inflammation within the bowel wall leads to stricture formation, and bowel obstruction may develop. These findings are important to identify because they are not responsive to medical therapy and typically require surgical resection if associated with symptomatic bowel obstruction. On dynamic images, fibrotic strictures appear as aperistaltic bowel segments that often demonstrate fixed mural thickening and luminal narrowing. T2 hyperintensity is typically absent in these fibrotic regions, unless there is associated mural inflammation and edema ( Fig. 13-43 ).

Radiation Enteritis

Radiation-induced enteropathy has distinct acute and chronic manifestations. Acute radiation enteritis occurs within the first few days or weeks after exposure. The most characteristic findings include mucosal hyperenhancement, submucosal edema, and bowel wall thickening. Chronic radiation enteritis is a transmural process that develops months to years after exposure in up to 16% of patients after radiation treatment to the pelvis. It is characterized by stricture formation and obstruction. Typical morphologic changes include diffuse bowel wall thickening, strictures and fistula formation, tethering, and impaired peristalsis.

Angioedema of the Bowel

Angioedema is not a true inflammatory disease, but it can mimic inflammation because it presents with bowel wall thickening. It is characterized by episodes of increased capillary permeability, with extravasation of intravascular fluid and subsequent edema of the skin, mucosa of the upper airways, or GI tract. Gastrointestinal involvement sometimes mimics an acute abdomen or rarely can cause life-threatening hypovolemic shock. Characteristic imaging features include reversible bowel and mesenteric edema, characterized by multiple dilated small-bowel loops with regular thickened mucosal folds, a stacked-coin appearance with bowel wall thickening, and thumbprinting. The small and large intestine may be involved, including jejunum, ileum, duodenum, and colon, in descending frequency of involvement. The findings are usually transient and segmental, returning to normal after an acute attack. A high degree of clinical suspicion is needed, particularly in patients using angiotensin-converting enzyme inhibitors and a variety of other medications, in the setting of typical imaging findings. A definite diagnosis can be confirmed by elevated serum levels of C4 and C1 esterase inhibitor and C1 esterase inhibitor functional activity complement levels ( Fig. 13-44 ).

Celiac Disease

Celiac disease in now recognized as a common but largely underdiagnosed disease, with typical diagnostic delay of more than 10 years from the onset of symptoms. It is a chronic autoimmune disorder induced in genetically susceptible individuals after ingestion of gluten proteins. The small bowel mucosa is primarily affected, resulting in progressive villus inflammation and destruction, with resulting induction of crypt hyperplasia. It may be asymptomatic or characterized by diverse symptoms of malabsorption with varying severity. Characteristic findings include duodenitis with dilution, slow transit, and flocculation of oral contrast, small bowel dilation, transient small bowel intussusception, villous atrophy and reversal of the fold pattern, with jejunization of the ileum, as reflected by a decrease in normal jejunal folds in contrast to the increasing fold pattern in the ileum.

Whipple Disease

Whipple disease is a rare multisystemic bacterial infection caused by the Whipple bacillus (Tropheryma whipplei) , involving the small bowel (particularly the jejunum), lymph nodes, joints, and central nervous system. Barium studies can demonstrate to better extent the thickened, irregular folds and tiny nodules in the jejunum and, to a lesser degree, the ileum, due to accumulation of the Whipple bacilli and periodic acid-Schiff–positive macrophages in the submucosa and lamina propria. Characteristic imaging findings include mesenteric and retroperitoneal lymphadenopathy and fat-attenuation lymph nodes measuring between 10 and 20 HU. Whipple disease is an infectious condition, and these patients often demonstrate significant response to treatment with antibiotics.

Small Bowel Diverticulitis

Small bowel diverticulosis is far less common than colonic diverticulosis and characterized by the presence of multiple saclike mucosal herniations, or pseudodiverticula, through weak points in the intestinal wall. Duodenal diverticula are relatively common and have been found in up to 5% of the population undergoing barium studies. Jejunoileal diverticula are less common but usually multiple and localized to the proximal jejunum. They are frequently associated with disorders of intestinal motility such as scleroderma and visceral neuropathies. The major clinical manifestation of jejunoileal diverticula is malabsorption. Complications are more common in jejunoileal diverticula than duodenal diverticula and, similar to their colonic counterpart, include bleeding, intestinal obstruction, and diverticulitis.

Meckel diverticulum is the most common congenital anomaly of the GI tract, occurring in 2% of the population. It is a true diverticulum that contains all layers of the intestinal wall and has its own blood supply. It results from incomplete absorption of the omphalomesenteric duct and is frequently associated with heterotopic gastric or pancreatic mucosa in up to 50% of cases, with gastric heterotopia being most common. It is typically located in the distal ileum approximately 2 feet from the ileocecal valve. Although usually asymptomatic, approximately 2% of patients can present with complications, more common in children than adults. Inflammation (Meckel diverticulitis) is one of the most common complications, after hemorrhage and SBO. Computed tomography diagnosis relies on the identification of a blind-ending, tubular, round, or oval structure in the right lower quadrant or periumbilical region, with surrounding inflammation. The diverticulum can be associated with mural thickening and hyperenhancement, with focal calcifications at the base (enteroliths), and adjacent mesenteric fat stranding and fluid collections. In some instances the diverticulum will extend toward the umbilicus. The identification of a normal appendix can be very helpful because patients will often present with right lower quadrant pain. A Meckel scan can confirm the presence of gastric mucosa within the diverticulum in equivocal cases ( Fig. 13-45 ).

Other Inflammatory Conditions of the Small Bowel

There are numerous additional inflammatory conditions of the small bowel that will present with nonspecific bowel wall thickening, including eosinophilic gastroenteritis, amyloidosis, Behçet syndrome, and primary lymphangiectasia. Differentiation will depend on the clinical history, distribution pattern, and often biopsy.

Acute Appendicitis

Acute appendicitis is the most common acute abdominal emergency requiring surgery and typically presents as periumbilical pain that migrates to the right lower quadrant with other characteristic clinical signs and symptoms, including nausea, anorexia, and fever, although the clinical presentation is highly variable. Initially the appendiceal lumen becomes obstructed by fecal material (appendicolith or fecalith), undigested material such as vegetables or seeds, hypertrophied Peyer patches, or neoplasm, and progressive accumulation of secretions leads to intraluminal distention and increased intramural pressure. The initial periumbilical abdominal pain represents referred pain from visceral innervation due to appendiceal luminal distention, and localized right lower quadrant pain is secondary to inflammation of the parietal peritoneum. Ongoing luminal distention and bacterial overgrowth result in lymphatic and venous obstruction leading to mucosal ischemia.

Plain abdominal radiographs have limited utility in the diagnosis of acute appendicitis. However, appendicoliths may be seen on abdominal radiographs and, in the appropriate clinical setting, are suggestive of acute appendicitis. In addition, free intra-abdominal air and bowel obstruction may readily be excluded on plain abdominal radiographs. In certain patients, such as young women or generally thin patients, US of the right lower quadrant may be the first-line imaging modality. Acute appendicitis on US is seen as a noncompressible, thick-walled, dilated, blind-ending tubular structure in the right lower quadrant measuring 7 mm or more in diameter with graded compression, with or without a visible appendicolith. The utility of US for the diagnosis of acute appendicitis is highly operator dependent, and this modality is limited in obese patients and in the presence of gas-filled bowel. Typically, in cases of ongoing clinical suspicion, negative or inconclusive US examination results warrant a subsequent CT examination. In the majority of patients, CECT represents the first-line imaging modality of choice and is the most accurate imaging study with well-demonstrated sensitivity, specificity, and diagnostic accuracy exceeding 95% for the diagnosis of acute appendicitis. On CT, acute appendicitis is seen as a distended, circumferentially thickened, fluid-filled structure with mucosal hyperenhancement and surrounding fat stranding consistent with periappendiceal inflammation ( Fig. 13-47 ). Although a strict size limit for normal appendices, similar to ultrasonographic imaging, is not applicable to CT given the lack of compression, acutely inflamed appendices are typically dilated and approach or exceed 1 cm in diameter. Furthermore, CECT is the imaging modality of choice to detect complications of acute appendicitis such as appendiceal perforation and periappendiceal abscess formation. On unenhanced CT examinations, a thickened appendix with surrounding inflammatory changes, with or without a calcified appendicolith (see Fig. 13-47 ), is diagnostic of acute appendicitis. In cases in which positive oral contrast agents are administered, opacification of the appendiceal lumen with oral contrast effectively excludes a diagnosis of appendicitis. However, the converse does not hold true, and a lack of appendiceal opacification with oral contrast material does not definitively indicate a diagnosis of acute appendicitis because this is often the case with normal appendices.

In cases of suspected acute appendicitis in pregnant women, an abdominal US is often the initial imaging study obtained to evaluate for possible appendicitis. However, because the sensitivity of this modality for the detection of acute appendicitis is limited, especially in pregnant women, a noncontrast MRI of the abdomen is often employed after an inconclusive US. With a reported sensitivity and specificity comparable to that of CT, with the benefits of a lack of ionizing radiation exposure to the fetus, MRI has gained wide acceptance for this application. With the use of MRI, the need for CT in cases of suspected acute appendicitis may be markedly decreased or eliminated altogether. Typically MRI examinations in cases of suspected appendicitis include multiplanar T1- and T2-weighted sequences. In pregnancy, intravenous gadolinium should not be administered for this application and the utility of oral contrast is a subject of ongoing investigation. Appendicitis on MRI is readily depicted on T2-weighted sequences acquired with and without fat suppression. The inflamed and edematous appendix is dilated and fluid filled and exhibits surrounding periappendiceal edema and fat inflammation ( Fig. 13-48 ).

Appendectomy is the treatment of choice in simple acute appendicitis, and laparoscopic appendectomy is increasingly common. Antibiotic treatment for small abscesses is feasible, whereas image-guided percutaneous drainage may be performed for larger abscesses.