Gastrointestinal Imaging

INTRODUCTION

This section serves as an introduction to the basic anatomy of the abdomen.

The human gastrointestinal tract can be divided into upper and lower portions. All structures proximal to the ligament of Treitz can be thought of as the upper GI tract, while structures found distal to it are considered the lower GI tract. We will begin with axial sections depicting the upper abdomen, including the liver and stomach, and work inferiorly toward the pelvis (Figs. 5.1 through 5.9).

Fig. 5.1

(A) Cross section demonstrating relative anatomy of stomach, liver, aorta, and inferior vena cava. (B) This section offers a clearer view of the hepatic veins, which can be seen within the liver, draining into the inferior vena cava. Axial CT sections correlating with the same level of anatomical cut section.

Fig. 5.2

(A) Cross-sectional anatomy of stomach, liver, left and right portal veins, and spleen together with correlating axial CT section (B) correlating with the same level of anatomical cut section. The portal vein is formed by the superior mesenteric vein, inferior mesenteric vein, splenic vein, gastric veins, and cystic veins. The main portal vein splits into the right and left portal vein, then further branches into venules (along with a hepatic arteriole and bile duct, forming a portal triad), and ultimately terminating in the liver sinusoids. (C) Illustration demonstrating the portal vein ascending into the liver, and the hepatic vein joining the IVC. The segments of the liver are demonstrated as well. There are eight segments, each with its own arterial supply, venous drainage, and biliary outflow.

Fig. 5.3

(A) Cross section revealing location of gallbladder in relation to liver, stomach, and pancreatic body and tail. The gallbladder drains into the common hepatic duct via the cystic duct, which later joins the pancreatic duct to form the ampulla of Vater. This empties through the sphincter of Oddi into the duodenum. The portal vein is seen prior to its branching into left and right portal veins. Note the presence of the splenic flexure of the colon as well. (B) Similar cross section revealing anatomy of the pancreatic tail and body. Axial CT section correlating with the same level of anatomical cut section is seen below each pertinent illustration.

Fig. 5.4

The superior poles of the kidneys and the adrenal glands become visible, along with portions of the jejunum, as well as the transverse colon. The splenic vein, which will empty into the portal vein, is seen here also.

Fig. 5.5

More of the kidney is visible, along with the left and right renal arteries and veins. Also the duodenum and the hepatic flexure of the colon become visible.

Fig. 5.6

More of the jejunum and ileum are seen along with the ascending and descending colon. The ureters can be seen as they ascend to the kidneys.

Fig. 5.7

(A) The cecum is visible here along with the ileocecal valve and the appendix.(B) The sigmoid colon is visible as we continue to move more inferiorly in the abdomen. Note the presence of the external iliac artery and vein, as we are below the level of the aorta and inferior vena cava.

Fig. 5.8

The rectum and its surrounding fat and fascia become visible, adjacent to the seminal vesicles and bladder. The external iliac artery and vein becomes the common femoral artery and common femoral vein, respectively, below the level of the inguinal ligament.

Fig. 5.9

Coronal CT demonstrating the normal anatomy of the GI tract, including the small intestine and ascending colon. The liver, abdominal aorta, and inferior vena cava are demonstrated as well.

CASE 1

PATIENT PRESENTATION

A 72-year-old man presented to an outpatient clinic with halitosis, regurgitation, aspiration, and dysphagia.

CLINICAL SUSPICION

Oropharyngeal dysphagia

IMAGING MODALITY OF CHOICE

Barium swallow examination is the mainstay for the diagnostic workup of dysphagia. The type of study used depends on the clinical presentation. For example, a patient recovering from a recent stroke (or any other disease with neurological sequelae), with a known cause of cough, pneumonia, or suspected aspiration, requires a modified barium swallow, which is performed by a speech pathologist and radiologist. In this, videofluoroscopy is used, usually only in the lateral projection, to evaluate oropharyngeal swallowing, mastication, and the presence and causes of aspiration. It does not evaluate the entire esophagus.

If the cause of oropharyngeal dysphagia is unknown, a more detailed barium study may be performed to assess the functional and structural abnormalities of the pharynx. As in the modified barium swallow, a dynamic examination of the oropharynx with videofluoroscopy allows assessment of the oral and pharyngeal phases of swallowing. However, static images of the pharynx can be obtained to detect structural abnormalities. This portion of the examination uses a double-contrast technique (thick, viscous barium for the mucosal coating and effervescent air crystals for air distention) with spot radiographs in the frontal and lateral projections. The same technique is used to image the entire esophagus and proximal stomach to exclude referred causes of oropharyngeal dysphagia.

STRUCTURAL PHARYNGEAL AND ESOPHAGEAL ABNORMALITIES

  • Zenker’s diverticulum: Zenker’s diverticulum is a pulsion diverticulum that occurs in the midline posterior pharynx, above the cricopharyngeus muscle (upper esophageal sphincter). It is believed to occur secondary to a lack of coordination of the cricopharyngeus during swallowing, resulting in increased intraluminal pressure, which creates a diverticulum at a specific anatomic weak point of the posterior pharynx known as Killian’s dehiscence. The resulting diverticulum usually extends inferiorly, with a small neck, frequently resulting in trapped food or liquid (Fig. C1.1). This can then compress the ventrally located upper esophagus, resulting in dysphagia. Associated symptoms include aspiration and halitosis due to retained liquids or food.

  • Killian-Jamieson diverticulum: Killian-Jamieson diverticulum is a pulsion diverticulum that arises from the anterolateral wall, beginning below the cricopharyngeus muscle and extending along the lateral aspect of the cervical esophagus. This is less common and is usually small and asymptomatic. The location beneath the cricopharyngeus muscle is felt to be a relative protection from aspiration (Fig. C1.2).

  • Cricopharyngeus hypertrophy: Patients with dysphagia may have a history of gastroesophageal reflux. Hypertrophy of the cricopharyngeus or upper esophageal sphincter is believed to represent a protective mechanism from aspiration in the setting of reflux. This should not be confused with a stricture because it has smooth margins (Fig. C1.3).

  • Epiphrenic diverticulum: An epiphrenic diverticulum is a rare diverticulum of the distal esophagus that is located above the lower esophageal sphincter. Because of the small opening neck, debris can become trapped; if large enough, this debris can compress the true lumen, resulting in dysphagia (Fig. C1.4).

Fig. C1.1

Zenker’s diverticulum. Lateral view from barium swallow of the esophagus showing the contrast pooling into the posteriorly positioned Zenker’s diverticulum (black arrow). This results in mass effect and effective narrowing of the upper esophagus located anterior to the diverticulum.

Fig. C1.2

(Left) Zenker’s diverticulum arising above the cricopharyngeus (upper esophageal sphincter) from the posterior midline. (Right) A Killian-Jamieson diverticulum arising from the lateral wall and below the cricopharyngeus in contradistinction from the Zenker’s diverticulum.

Fig. C1.3

Cricopharyngeus hypertrophy. Lateral radiograph from esophagram shows round smoothly marginated indentation from the posterior wall of the upper esophagus representative of enlargement of the UES.

Fig. C1.4

Epiphrenic diverticulum. Upper GI examination shows large epiphrenic diverticulum (*) with mass effect significantly narrowing the lower esophagus (arrow).

DIFFERENTIAL DIAGNOSIS

Ultimately, many different etiologies can result in dysphagia, including neoplasms of the head and neck (most commonly squamous cell carcinoma) and inflammatory masses (eg, retropharyngeal abscess), trauma, diverticula, esophageal webs, anterior mediastinal masses, cervical spondylosis, or extrinsic structural lesions such as vascular rings. From an imaging standpoint, the differential diagnosis depends on the anatomical location.

REFERENCES AND SUGGESTED READING

Rubesin
 SE, Levine
 MS. Killian-Jamieson diverticula: radiographic findings in 16 patients. AJR. 2001;177:85-–89. 
[PubMed: 11418403]
Brant
 WE, Helms
 CH. Fundamentals of Diagnostic Radiology. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2006.

CASE 2

PATIENT PRESENTATION

A 33-year-old woman presented to a gastroenterology clinic with retrosternal dysphagia, relieved by repetitive swallowing, and several episodes of regurgitation.

CLINICAL SUSPICION

Esophageal dysphagia, achalasia

IMAGING MODALITY OF CHOICE

Barium studies are a vital tool in the initial diagnostic evaluation of dysphagia. When dysphagia is localized to the esophagus rather than the oropharynx and there are no reports of aspiration or coughing immediately after swallowing, videofluoroscopy of the swallowing reflex in combination with a speech pathologist (modified barium swallow) is usually not necessary. An esophagram study usually entails a double-contrast (thick barium for mucosal detail and effervescent air crystals for distention) examination in the upright position in multiple projections and a single contrast (thin barium) performed in the prone (right anterior oblique) position to evaluate for esophageal distensibility and peristalsis (Fig. C2.1).

Fig. C2.1

Normal esophagram. Normal double contrast esophagram with air distention and thick barium coating the mucosal surface. Normal GE junction (arrow).

Alternative methods for evaluating dysphagia include esophageal manometry, a pH probe, and endoscopy (Fig. C2.2).

Fig. C2.2

Distal esophagus with achalasia, scleroderma, and tumor. (A) Achalasia results in the most dilated esophagus frequently containing debris related to prior food which has not passed the tight “bird beak” appearance of the LES. (B) Scleroderma results in dilatation of the esophagus, but to a lesser degree than with achalasia. The LES is initially patulous and widened as illustrated, much different than achalasia, but eventually due to reflux esophagitis, can develop a stricture or worse Barrett’s esophagitis or adenocarcinoma. (C) Tumors of the GE junction are primarily adenocarcinoma and result in shaggy irregularity of the mucosa with abrupt shouldering and narrowing of the lumen.

NEUROMUSCULAR ESOPHAGEAL ABNORMALITIES

  • ACHALASIA: ACHALASIA is a well-known primary esophageal motility disorder that is characterized by incomplete relaxation of the lower esophageal sphincter (LES) and no primary peristalsis. Men and women are equally affected, with a mean age of 25 to 60 years. Primary achalasia refers to idiopathic loss of inhibitory ganglion cells, resulting in an unopposed excitatory and thus contracted state. Secondary achalasia has a similar appearance but is caused by an underlying disease, such as carcinoma of the gastric cardia or esophagus. Chagas disease is a parasitic infection that can induce secondary achalasia and has many cardiac manifestations.

Long-standing achalasia results in esophageal dilatation. This is often seen on a chest radiograph as a widened mediastinum with an air-fluid level. The classic sign is a dilated esophagus with smooth tapering at the LES, creating the “bird beak” appearance (Fig. C2.3). Other dynamic findings include loss of normal peristalsis.

Fig. C2.3

Achalasia. Classic bird beak appearance due to severe narrowing of the LES, with severe dilatation of the proximal esophagus. Notice the mottled appearance (white arrow) due to retained gas, debris, and contrast above the air-fluid level representing contrast mixed with undigested food residing in the dilated esophagus which cannot easily pass through the LES.

  • Scleroderma: Scleroderma is a collagen vascular disease with multiorgan involvement; it is due to immunologic and inflammatory changes. Women are more commonly affected, at a 3:1 ratio, and the mean age of onset is 30 to 50 years. Scleroderma is usually classified as one of two types:

    • Diffuse scleroderma: Diffuse scleroderma is more severe, with interstitial pulmonary fibrosis. It is associated with anti-topoisomerase 1 Ab (anti-Scl 70).

    • CREST syndrome (calcinosis of skin, Raynaud phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia): CREST syndrome is the more benign course. It is associated with anti-centromere Ab.

The radiographic findings include a lack of primary peristalsis of the lower two-thirds of the esophagus, which is controlled by smooth muscle (the proximal one-third is striated muscle). Early in the course of disease, there is a patulous or widened LES, with or without a hiatal hernia (Fig. C2.4). Chronic reflux may lead to reflux esophagitis, which may result in a fusiform peptic stricture at the LES. Proximal to the stricture, the esophagus will be dilated but to a lesser degree than with achalasia. Complications from long-standing reflux esophagitis include Barrett esophagus and adenocarcinoma.

Fig. C2.4

Scleroderma. Esophagram shows the dilated esophagus with a patulous LES which leads to chronic reflux and ultimately strictures. Axial CT in the same patient shows the associated pulmonary fibrosis with honey combing in the lung bases as well as a dilated esophagus.

  • Diffuse esophageal spasm: Diffuse esophageal spasm is an esophageal motility disorder that can present with chest pain. Similar disorders include nutcracker esophagus and nonspecific esophageal motility disorder. Cardiac disease must be excluded because patients present with anginalike symptoms. Radiographic evaluation plays a lesser role because of the intermittent nature of these diseases. A barium swallow will reveal a classic “corkscrew” esophagus in 30% of the patients. Esophageal manometry remains the gold standard.

  • Esophageal cancer: Two different subtypes of esophageal cancer exist: squamous cell carcinoma (SCC), involving the proximal two-thirds of the esophagus (Figs. C2.5A,B), and adenocarcinoma, involving the lower one-third (Figs. C2.6A,B). The risk factors for SCC include smoking and alcohol use, and the risk factors for adenocarcinoma are a history of gastroesophageal reflux disease (GERD) and Barrett’s esophagus. In the past, SCC was far more common than adenocarcinoma; however, this trend has changed significantly over the past few decades because of a higher incidence of GERD. Barium esophagography remains useful for the initial noninvasive evaluation of esophageal complaints; however, endoscopy is the gold standard for diagnosis. A multimodal approach can be used, with endoscopic sonography for T staging and computed tomography (CT) for excluding unresectable disease or diagnosing distant metastasis. PET is more useful for assessing distant metastasis and restaging after neoadjuvant therapy.

Fig. C2.5

Esophageal SCC. (A) Lateral radiograph showing mass in the middle mediastinum displacing the trachea anteriorly, with extension into the lumen (arrows). Esophageal SCC. (B) CT shows the diffuse circumferential thickening of the upper esophagus (yellow arrow), invading the trachea (white arrow).

Fig. C2.6

Esophageal adenocarcinoma. (A) Upper GI examination demonstrating an abrupt narrowing of the distal esophagus with shouldering (white arrow) extending to the cardia of the stomach with irregular mucosal nodularity through the strictured segment (bracket). Esophageal adenocarcinoma. (B) Coronal CT with oral and intravenous contrast demonstrates a large circumferential mass (*) centered at the lower esophagus extending to the GE junction. Oral contrast is visualized in the dilated esophagus (E). The mass narrows the esophageal lumen with shouldering proximally (white arrows). Oral contrast does reach the stomach (S). Due to lack of a surrounding serosa of the esophagus, early lymphatic spread occurs frequently; seen as the paraesophageal soft tissue masses representing mediastinal lymphadenopathy (black arrows) within the middle mediastinum.

DIFFERENTIAL DIAGNOSIS

Many other pathological conditions can result in dysphagia, including strictures, Schatzki rings, esophageal webs, foreign bodies, benign or malignant neoplasms, vascular compression, and mediastinal masses.

REFERENCES AND SUGGESTED READING

Levine
 MS, Rubesin
 SE. Update on esophageal radiology. AJR. 1990;155(5):933-–941. 
[PubMed: 2120962]
Marco
 G. Achalasia and other esophageal motility disorders. J Gastrointest Surg. 2001;15:703-–707.
Kim
 TJ. Multimodality assessment of esophageal cancer: preoperative staging and monitoring of response to therapy. RadioGraphics. 2009;29:403-–421. 
[PubMed: 19325056]

CASE 3

PATIENT PRESENTATION

A 42-year-old man with multiple episodes of vomiting and retching presented with severe epigastric and chest pain; he had no cardiac risk factors and normal electrocardiography results.

CLINICAL SUSPICION

Boerhaave’s syndrome

IMAGING MODALITY OF CHOICE

A chest radiograph should be the initial imaging study when evaluating patients with chest pain, regardless of whether the source is believed to be cardiac or noncardiac. The presence of air within the mediastinum, known as pneumomediastinum, would indicate a noncardiac process originating from either the esophagus or the lungs. Signs of pneumomediastinum on a chest radiograph are included in Table C3.1.

TABLE C3.1  

Signs of Pneumomediastinum

 

Many patients with chest pain are not initially suspected of having esophageal perforation and will undergo a standard CT of the chest, which will be more sensitive for pneumomediastinum than a chest radiograph (Fig. C3.1). Fluoroscopic water-soluble contrast esophagography has been the imaging modality of choice for esophageal perforation because extravasation of oral contrast into the mediastinum or pleural space is pathognomonic for perforation. The limitations of fluoroscopic esophagography include difficulty performing the examination in seriously ill patients, the need to transport the patient to a fluoroscopic suite, and potential false-negative results. To improve diagnostic capability for the detection of esophageal perforations, if no gross perforation is identified on initial studies performed with water-soluble agents, many advocate subsequent use of barium to detect subtle leaks that are more likely to be visualized with a high-density contrast agent.

Fig. C3.1

Pneumomediastinum. (A) Frontal chest radiograph demonstrating linear lucencies within the upper mediastinum and neck (black arrows) as well as the “continuous diaphragm” (white arrows) consistent with pneumomediastinum. (B) Same patient as chest radiograph demonstrating how visualizing pneumomediastinum on a CT chest is much easier. Air is tracking around the heart, esophagus, and aorta (back arrows). This was iatrogenic from endoscopic balloon dilatation of an esophageal stricture.

To expedite the diagnosis and minimize the number of examinations that need to be performed, CT esophagram protocols can be performed in several different ways. At our institution, an initial noncontrast examination of the chest is performed as the baseline, followed by a CT of the chest performed immediately after the patient swallows 1 cup of water-soluble contrast. Intravenous contrast can be added to the second scan if needed.

DIFFERENTIAL DIAGNOSIS

Esophageal perforation is an uncommon but potentially life-threatening event. The most common cause is iatrogenic perforation associated with endoscopy and thoracic surgery, which accounts for more than 50% of perforations. Other etiologies include idiopathic, foreign body, and traumatic perforations.

Boerhaave’s syndrome refers to the spontaneous rupture of the esophagus secondary to violent episodes of retching or vomiting. This involves a transmural or full thickness tear of the esophageal wall, typically posteriorly near the left diaphragmatic crus. Radiography may reveal pneumomediastinum, a left-sided pneumothorax, or a left pleural effusion (Fig. C3.2).

Fig. C3.2

Boerhaave’s syndrome. (A) Esophagram through NG tube using water-soluble contrast show the distal esophageal perforation with contrast leaking into the mediastinum and pleural spaces bilaterally (back arrows). (B) Coronal CT utilizing oral contrast with perforation distally resulting in extravasation of contrast into the left pleural space (black arrow).

In contrast to Boerhaave’s syndrome, Mallory-Weiss syndrome refers to partial or nontransmural tears of the esophageal wall. This may have a similar clinical presentation because it usually occurs after prolonged and forceful vomiting. However, because this is only a partial or nontransmural tear, it will not be radiographically detectable because no pneumomediastinum or contrast leak should be present.

DIFFERENTIAL DIAGNOSIS

First and foremost, whenever chest pain is the chief complaint, regardless of associated symptoms, cardiac etiologies must first be excluded. Other potential causes of acute noncardiac chest pain include disorders of the esophagus, including gastroesophageal reflux or motility disorders;
pulmonary disorders including pneumonia, pneumothorax or pulmonary embolism; and musculoskeletal pain.

Radiologically, a chest radiograph with pneumomediastinum would be suggestive of esophageal perforation in the proper clinical context. More commonly, pneumomediastinum occurs through a sequence of events known as the Macklin effect, which includes: (1) alveolar rupture, (2) air dissection along the interstitium of the bronchovascular sheath, and (3) free air reaching the mediastinum. This occurs not uncommonly with asthmatics, but can also occur from any form of barotrauma including forceful illicit drug inhalation, scuba diving, severe coughing, or in patients who are on assisted respiratory devices.

REFERENCES AND SUGGESTED READING

ACR Appropriateness Criteria: ACR Practice Guideline for the Performance of Esophagrams and Upper Gastrointestinal Examinations in Adults. Revised 2008.
Swanson
 JO. Usefulness of high-density barium for detection of leaks after esophagogastrectomy, total gastrectomy, and total laryngectomy. AJR. 2003;181:415-–420. 
[PubMed: 12876019]
Farhan
 F. Helical CT esophagography for the evaluation of suspected esophageal perforation or rupture. AJR. 2004;182(5):1177-–1179. 
[PubMed: 15100114]

CASE 4

PATIENT PRESENTATION

A 58-year-old man presented with severe left upper quadrant and left chest pain and retching without vomiting; a nasogastric tube could not be inserted.

CLINICAL SUSPICION

Gastric obstruction or volvulus

IMAGING MODALITY OF CHOICE

An initial evaluation may include radiographs of the abdomen or chest. Preferably, a 2-view chest or acute abdominal series should be ordered. The latter includes both supine and upright views of the abdomen to identify gravity-dependent free air and air-fluid levels.

In the past, a diagnosis of gastric volvulus was made with an upper GI series with barium or water-soluble contrast, but the relative availability and timeliness of CT with multiplanar reconstructions may be more suitable in the acute setting. A CT of the chest and abdomen should be performed to image the entire region of interest, preferably with intravenous contrast (a lack of normal enhancement of the gastric mucosa indicates ischemia) and oral contrast. An advantage of an upper GI series is its ability to grade the degree of obstruction.

  • Gastric volvulus: Gastric volvulus is relatively rare and is an uncommon site of volvulus of the gastrointestinal tract. It is seen in children and adults, but it is far more common in the elderly. The Borchardt triad (acute onset epigastric pain, intractable retching, and an inability to pass a nasogastric tube) is highly suggestive of gastric volvulus. Delays in diagnosis and definitive surgical treatment can lead to serious complications such as gastric ischemia, perforation, internal hemorrhage, splenic rupture, and aspiration pneumonia. The nonoperative mortality rate reaches 80%.

FINDINGS

Gastric volvulus is subdivided into two subtypes, organoaxial and mesenteroaxial (Fig. C4.1). Organoaxial volvulus is far more common, accounting for almost two-thirds of cases; however, mesenteroaxial appears to be more common in children.

  • Organoaxial volvulus occurs when the stomach rotates along the long axis (line made from intersecting the gastroesophageal junction with the pylorus) and becomes obstructed. This results in the greater curvature being displaced superiorly and the lesser curvature inferiorly.

  • Mesenteroaxial volvulus occurs when the stomach rotates along its short axis, with subsequent displacement of the antrum or pylorus above the gastroesophageal junction.

Fig. C4.1

Gastric volvulus may be either mesenteroaxial (top) or organoaxial (bottom).

Radiographic Findings

Radiographs may demonstrate a large retrocardiac opacity with two separate air-fluid levels. If completely obstructed, there will be a relative paucity of gas in the small bowel.

An upper gastrointestinal series will reveal the abnormal orientation of the stomach and the degree of intraluminal obstruction or gross perforation. If high-grade obstruction is present, no contrast may enter the stomach. “Beaking,” or rapid tapering in the shape of a bird’s beak, may be seen at the point of volvulus (twisting).

Multidetector row CT, especially with coronal reformations, will demonstrate the abnormal position of the stomach and the size, location, and extent of commonly associated diaphragmatic defects (Fig. C4.2). More important, CT can illustrate complications such as gastric ischemia, pneumatosis, or perforation.

Fig. C4.2

Organoaxial volvulus. Coronal CT image of the chest/upper abdomen shows an organoaxial gastric volvulus, with the greater curvature along the superior border (white arrows).

DIFFERENTIAL DIAGNOSIS

Large sliding hiatal hernias can manifest on a chest radiograph as retrocardiac masses, which can have an air-fluid level. These usually only contain the gastroesophageal junction or cardia and not the entire stomach as in a volvulus (Fig. C4.3). In addition, most will be incidentally detected. Other conditions that can present as retrocardiac masses with an air-fluid level include paraesophageal hernia, epiphrenic diverticulum, large infected bronchogenic or cardiophrenic cyst, mediastinal abscess, and postsurgical changes after a prior esophagectomy with gastric pull-through.

Fig. C4.3

(A) Axial CT demonstrates a large hiatal hernia (white arrow). (B) Sagittal reconstruction of the same CT demonstrates the hernia through widened esophageal hiatus of the diaphragm (white arrow).

Besides volvulus, several other entities can result in gastric obstruction. The term gastric outlet obstruction can have several etiologies that result in narrowing and obstruction of the gastric antrum or pylorus which inhibit normal empting of the stomach. This process can be the result of tumors or infectious/inflammatory processes such as peptic ulcer disease or Crohn’s disease. The imaging appearance across all modalities is a grossly dilated stomach with narrowing at the antral region (Fig. C4.4).

Fig. C4.4

Gastric outlet obstruction. Coronal CT image with intravenous contrast demonstrating a very distended gastric body. No oral contrast was given, with all this fluid representing prior swallowed fluid. Not shown was dependent solid food debris layering posteriorly in the fundus. Focal wall thickening of the antrum (white arrow) is noted which was found to be due a large malignant ulcer from gastric adenocarcinoma.

Clinically, just as in the previous case, cardiac causes must be first eliminated. A similar differential of noncardiac chest pain would be included as well as well as epigastric and left upper quadrant pain including, gastritis, peptic ulcer disease, pancreatitis, and/or pyelonephritis or nephrolithiasis of the left kidney.

REFERENCES AND SUGGESTED READING

Miller
 DL, Pasquale
 MD, Seneca
 RP. Gastric volvulus in the pediatric population. Arch Surg. 1991;126(9):1146-–1149. 
[PubMed: 1929847]

[Archives of Surgery Full Text]
Peterson
 CM. Volvulus of the gastrointestinal tract: appearances at multimodality imaging. RadioGraphics. 2009;29:1281-–1293. 
[PubMed: 19755596]

CASE 5

PATIENT PRESENTATION

A 47-year-old man with a 2-week history of dull, gnawing, intermittent epigastric pain that was progressively worsening. The patient was self-medicating his chronic right shoulder pain with ibuprofen as needed.

CLINICAL SUSPICION

Gastritis or gastric or duodenal ulcers

IMAGING MODALITY OF CHOICE

The choice of test to diagnose peptic ulcer disease may depend on the clinical setting. Epigastric pain may be seen in the setting of cardiopulmonary disease; thus, as always, the initial cardiopulmonary workup tests should be performed before the radiologic workup. In the acute setting of severe epigastric pain, an initial radiographic workup may include an acute abdominal series to identify free air from perforation. Free air or pneumoperitoneum has a variable appearance that depends on the position of the patient, with free air rising to the nondependent portion of the peritoneal cavity. For that reason, upright chest radiographs will reveal subdiaphragmatic air as crescentic lucencies (Fig. C5.1); decubitus views will reveal air along the paracolic gutter, which becomes nondependent in this position. Free air on supine films is more difficult to detect because it rises to the anterior abdominal wall and therefore will not be tangential to x-rays. Only when larger volumes of air are present are both the inner and outer bowel walls visible. The inner mucosal wall is always visible, but the outer wall is not because there is no interface between the surrounding peritoneal fat and bowel. The double wall sign, also known as Rigler’s sign, is indicative of pneumoperitoneum. Occasionally, the falciform ligament can be visualized when free air outlines both margins of the ligament, resulting in the so-called football sign.

Fig. C5.1

Pneumoperitoneum. Upright chest radiograph demonstrating pneumoperitoneum with subdiaphragmatic free air (arrows) due to perforated duodenal ulcer found at exploratory laparotomy.

Alternatively, CT of the abdomen and pelvis with intravenous and oral contrast can be performed, especially when the cause of epigastric pain is not readily evident. If there is a possibility of perforation of the gastrointestinal tract, water-soluble contrast (eg, gastroview, omnipaque, or visipaque) should be used in place of barium. Barium is a nonabsorbable substance that can cause chemical peritonitis and remain in the peritoneum indefinitely. The advantages of CT include rapid acquisition time; high sensitivity for pneumoperitoneum; small, contained perforations; and alternative diagnoses. The disadvantages include limited evaluation of the gastric mucosa and frequency of underdistention of the gastric lumen, limiting evaluation of gastric wall thickening.

In the less acute or chronic outpatient setting, an upper gastrointestinal series may be performed as a less invasive test than an endoscopic gastroduodenoscopy. An upper gastrointestinal series consists of a double-contrast evaluation (thick consistency barium and effervescent air crystals) to distend the esophagus, stomach, and proximal small bowel as well as to thinly coat the mucosal surface, followed by single-contrast barium (thin, watery consistency) to identify distention and peristalsis (Fig. C5.2).

Fig. C5.2

Normal stomach. Upper GI examination utilizing double contrast demonstrating normal contours and mucosa of the stomach. Normal folds are visualized (white arrow). Areae gastricae are normal features of the gastric mucosa producing the fine reticular pattern (black arrow). This image was obtained with the patient in the supine position with the liquid barium layering dependently in the most posterior portion of the stomach, the fundus.

Other tests that test for presence of Helicobacter pylori, one of the causes for gastritis, are the nuclear medicine C-14 urea breath test, which is based on the principle that H pylori produces urease that breaks down the radioactive urea into C-14 containing CO2, which can be collected and quantified. Alternative noninvasive tests include the H pylori stool antigen test and serum antibodies for H pylori; however, antibodies may be positive up to 3 years after eradication.

FINDINGS

Gastritis

Gastritis is inflammation of the stomach; however, it includes numerous disorders with different etiologies, histological types, and clinical presentations. Different forms of gastritis include:

  • H pylori gastritis (most common)

  • Erosive or NSAID-induced gastritis

  • Phlegmonous (acute bacterial) gastritis

  • Emphysematous gastritis

  • Granulomatous gastritis

  • Eosinophilic gastritis

  • Atrophic gastritis

All forms of gastritis have variable radiological presentations, but in general, they share several common features: thickening of gastric folds, scalloping or nodularity of antral folds, and erosions surrounded by radiolucent halos of edematous, elevated mucosa. CT can reveal a thickened gastric wall (>5 mm) and thickened rugae, with decreased attenuation of submucosa related to edema (Fig. C5.3).

Fig. C5.3

Gastritis. Axial CT image without intravenous contrast, but with oral contrast demonstrates diffusely thickened gastric folds. The oral contrast can faintly be seen between the thickened folds (white arrow).

Ulcers

An ulcer is a focal area of mucosal disruption that penetrates through the muscularis mucosae. Benign gastric ulcers are predominantly caused by H pylori infections (approximately two-thirds); the remaining are mostly due to nonsteroidal anti-inflammatory drugs (NSAIDs). On the other hand, 95% of duodenal ulcers are caused by H pylori infections. Approximately 20% of gastric ulcers are multiple, whereas multiple postbulbar duodenal ulcers are unusual and raise suspicion for Zollinger-Ellison syndrome.

Gastric ulcers can usually be categorized as benign or malignant, but ultimately, any gastric ulcer identified by imaging would need to be evaluated by endoscopy and most likely a biopsy for definitive diagnosis. Imaging features of both benign and malignant ulcers are included in Table C5.1. Most benign gastric ulcers are located on the lesser curvature or posterior wall (Fig. C5.4). NSAID-induced benign ulcers have a propensity for being located on the greater curvature, making location less reliable for distinguishing benign from malignant. The major complications of ulcers are bleeding, gastric outlet obstruction, and perforation (Fig. C5.5). Bleeding can occur in up to 20% of patients and can present as melena, hematemesis, or hematochezia.

Fig. C5.4

Benign gastric ulcer. Water-soluble contrast upper GI examination showing smooth ovoid ulcer (white arrow) collection as well as Hampton’s line with smooth ulcer collar (black arrows) of biopsy-proven benign ulcer.

Fig. C5.5

Ruptured duodenal ulcer. Axial CT with intravenous contrast demonstrates a focal disruption of the lateral wall of the second portion of the duodenum with a contained perforation with extraluminal air-fluid level (white arrow). Because the duodenum has portions that are either intraperitoneal or retroperitoneal, depending on the location of the ulcer, perforation could result in pneumoperitoneum or pneumoretroperitoneum.

TABLE C5.1  

Gastric Ulcer Characteristics

 

DIFFERENTIAL DIAGNOSIS

Clinically, many disorders can have similar symptoms including functional dyspepsia, GERD, gastroenteritis, esophagitis, cholecystitis, cholangitis, biliary colic, acute coronary syndrome, and pancreatitis.

On imaging, thickened gastric folds can be found with gastritis, lymphoma, Ménétrier disease, and gastric varices (Fig. C5.6).

Fig. C5.6

Varices. Double-contrast upper GI examination demonstrates prominent gastric folds as well as serpiginous esophageal folds related to gastric and esophageal varices (white arrows) due to portal hypertension.

REFERENCES AND SUGGESTED READING

Rubesin
 SE, Levine
 MS. Double-contrast upper gastrointestinal radiography: a pattern approach for diseases of the stomach. Radiology. 2008;246:33-–48. 
[PubMed: 18096527]
Brant
 WE, Helms
 CA. Fundamentals of Diagnostic Radiology. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2006.

CASE 6

PATIENT PRESENTATION

A 62-year-old woman with a history of right breast cancer treated 2 years earlier with mastectomy and adjuvant chemoradiation therapy presented with progressive nausea, occasional vomiting, a 15-lb unintentional weight loss, and anorexia.

CLINICAL SUSPICION

Gastric cancerz

IMAGING MODALITY OF CHOICE

Upper endoscopy has mostly supplanted the routine use of upper gastrointestinal series for initial diagnosis, largely because of the ability to confirm diagnosis with biopsy, but upper gastrointestinal series are still a useful, inexpensive, safe, and noninvasive diagnostic tool.

Multidetector CT has remained the modality of choice for the preoperative staging of gastric cancer and for follow-up. Several newer staging techniques include multiphase dynamic imaging during the arterial and later portal venous phases. The arterial phase is the most useful for determining the arterial supply and the depth of tumor invasion; it is similar to endoscopic ultrasound (EUS). The portal venous phase is the most adequate for detecting distant metastasis. In addition, these techniques use a neutral oral contrast, such as water or a 0.1% barium suspension (VoLumen), for the optimal evaluation of mucosal and mural enhancement, and multiplanar reconstructions and 3-D processing. Gastric distension may be optimal with the use of negative contrast, and gas-producing crystals.

The combination of FDG-PET and CT is useful in the preoperative staging of stomach cancer and in restaging after treatment, but it is still limited in initial locoregional staging.

FINDINGS

Gastric carcinoma is the fourth most common malignancy worldwide and a common cause of cancer mortality. The incidence varies highly across different geographic locations, with much higher rates (5 times higher) seen in Japan, Finland, Chile, and Iceland than in the United States. One reason for a large difference in mortality rate and incidence between developed and undeveloped countries is that gastric cancer is one of a few cancers with can develop due to an infection (H pylori), and therefore without treatment of the underlying infection, more cancers can develop. The mortality rate is dismal because most patients are not diagnosed until the later stages; the 5-year survival rate is 20%.

Adenocarcinoma is the most common malignant gastric neoplasm, comprising more than 90% of cases. Other malignant gastric neoplasms include lymphoma, mucosa-associated lymphoid tissue (MALT) lymphoma, GIST, leiomyosarcoma, carcinoid, small cell carcinoma, and metastasis (lungs, breast, melanoma, colon, prostate, and pancreas). The risk factors for gastric adenocarcinoma include H pylori infection, adenomas, polyposis syndromes, pernicious anemia, atrophic gastritis, and prior partial gastrectomy (Billroth II>I).

Gastric neoplasms have several different radiological presentations. Approximately one-third present as a polypoid mass extending into the gastric lumen, either papillary or broad based (Fig. C6.1). Another one-third present as malignant ulcers, previously characterized in Table C5.1. The remaining tumors present as scirrhous carcinoma or superficial spreading. Scirrhous carcinoma is a cause of “linitis plastica” or “water bottle stomach.” These terms describe a narrowed and nondistensible stomach due to diffuse infiltration of the gastric wall with poorly differentiated or undifferentiated neoplastic cells (Fig. C6.2).

Fig. C6.1

Gastric adenocarcinoma. Axial CT of the abdomen with IV and oral contrast demonstrates a round polypoid mass (*) within the stomach.

Fig. C6.2

Linitis plastica. (A) Upper GI radiograph demonstrating the nondistensible stomach with a water bottle shape consistent with linitis plastica. (B) Same patient with axial CT showing the thickened nondistensible stomach (white arrow) due to a scirrhous carcinoma.

Gastric cancer usually spreads by local invasion through the gastric wall into the perigastric fat and adjacent organs, via the lymph nodes, or by seeding the peritoneal cavity. The primary role of CT in imaging of gastric cancer is staging. Newer CT techniques, however, have improved T staging, which is now comparable to EUS. A CT criterion for local staging closely mirrors the American Joint Committee on Cancer’s TNM staging system.

AJCC T Staging

  • T1: Tumor invades the lamina propria or submucosa

  • T2: Tumor invades the muscularis propria or subserosa

  • T3: Tumor penetrates the serosa, with no invasion of adjacent structures

  • T4: Adjacent organs involved

CT Staging

  • T1: Nontransmural enhancement; inner or middle wall enhancement only

  • T2: Transmural enhancement with smooth outer wall

  • T3: Transmural enhancement with irregular wall or reticular or linear perigastric opacities

  • T4: Extension to adjacent organs

The local lymph nodes that are commonly involved include the perigastric, gastrohepatic, gastrocolic, celiac, and para-aortic nodes. A Virchow node is a metastatic, enlarged left supraclavicular node that receives drainage from lymph vessels in the abdomen. Hematogenous spread is usually to the liver. Intraperitoneal spread or seeding can result in peritoneal carcinomatosis or a Krukenberg ovarian tumor (Fig. C6.3), the original name given for ovarian masses from “drop” gastric metastasis.

Fig. C6.3

Krukenberg tumors. Axial CT of the pelvis with large bilateral adnexal masses (*) as well as a large volume of ascites due to metastatic gastric cancer consistent with Krukenberg tumors, gastric cancer metastatic to ovaries.

  • Lymphoma: Lymphoma comprises approximately 2% of gastric malignancies. Most cases are non-Hodgkin’s B-cell type. Infection with H pylori is a risk factor for MALT gastric lymphoma, which has a better prognosis than the B-cell type because of a more indolent course. Lymphoma has a wide variety of presentations, but marked wall thickening is characteristic of gastric lymphoma; this thickening does not result in luminal narrowing (Fig. C6.4).

  • Gastrointestinal stromal tumors (GISTs): GISTs are the most common mesenchymal neoplasm from the gastrointestinal tract. GISTs express KIT (CD117), a tyrosine kinase receptor; this distinguishes them from other mesenchymal tumors, such as leiomyomas, leiomyosarcomas, schwannomas, and neurofibromas. These tumors are highly receptive to treatment with KIT tyrosine kinase inhibitors such as imatinib. Common radiologic features include a large predominantly exophytic mass, heterogeneous enhancement, and little lymphadenopathy (Fig. C6.5).

Fig. C6.4

Gastric lymphoma. Axial CT postcontrast (A) and PET/CT axial fusion (B) images shows an endoluminal polypoid mass (arrows) within the cardia that is FDG avid. This appearance is nonspecific from other gastric malignancies.

Fig. C6.5

Gastrointestinal stromal tumor. Axial CT with contrast demonstrates an exophytic GIST arising from the antrum (*).

REFERENCES AND SUGGESTED READING

Hargunani
 R, Maclachlan
 J. Cross-sectional imaging of gastric neoplasia. Clin Radiol. 2009;64:420-–429. 
[PubMed: 19264188]
Van
 Cutsem E. The diagnosis and management of gastric cancer: expert discussion and recommendations from the 12th ESMO/World Congress on Gastrointestinal Cancer, Barcelona, 2010. Ann Oncol. 2011;22(suppl 5):v1-–v9. 
[PubMed: 21633049]
Lim
 JS. CT and PET in stomach cancer: preoperative staging and monitoring of response to therapy. RadioGraphics. 2006;26:143-–156. 
[PubMed: 16418249]
Canon
 C. McGraw-Hill Specialty Board Review: Radiology. New York: McGraw-Hill Companies; 2010.
Fishman
 EK, Urban
 BA, Hruban
 RH,
 et al. CT of the stomach: spectrum of disease. RadioGraphics. 1996;16:1035-–1054. 
[PubMed: 8888389]

CASE 7

PATIENT PRESENTATION

A 32-year-old man presented with nausea, vomiting, generalized abdominal pain, and distention; he had a history of open appendectomy. His abdomen was tympanic to percussion, with high-pitched bowel sounds.

CLINICAL SUSPICION

Small bowel obstruction (SBO)

IMAGING MODALITY OF CHOICE

The choice of imaging modality for a suspected SBO varies among experts and is based on the clinical presentation. Abdominal radiography may be the first modality used because it is relative easy and inexpensive; however, its effectiveness at diagnosing SBO ranges from 30% to 90%. An important early differentiation in SBO is complete or high grade versus low grade, equivocal, or normal. Common radiographic findings include multiple dilated loops more than 2.5 cm in caliber, multiple air-fluid levels, and collapsed distal bowel. Two specific radiographic findings on upright plain films that are predictive of severe SBO are differential air-fluid level heights in the same small bowel loop and a mean air-fluid level width of 2.5 cm or greater (Fig. C7.1).

Fig. C7.1

Small-bowel obstruction. (A) AP supine radiograph of the abdomen with SBO with multiple dilated loops. In contrast to large-bowel obstruction (LBO), notice the more central position and mucosal folds extending completely across the loop of bowel, representative of the valvulae conniventes (white arrow). (B) Upright AP radiograph of the abdomen of same patient showing multiple differential air-fluid levels with dilated loops of bowel. Given enough time, with a high grade SBO, the distal bowel including the colon and rectum will be devoid of air as in this case.

Standard multidetector CT of the abdomen and pelvis with intravenous contrast and multiplanar reformatting is the American College of Radiology (ACR)’s Appropriateness Criteria Committee’s recommended imaging modality. Oral contrast is no longer believed to be necessary in routine cases because of the delay in diagnosis. Intraluminal fluid in the obstructed segment acts as a natural neutral contrast agent, facilitating visualization of the bowel wall. The CT criteria for SBO include dilated SB loops greater than 2.5 cm, with air-fluid levels. A helpful but nonpathognomonic sign is the “small bowel feces” sign, which refers to small gas bubbles intermixed with particulate matter in the dilated loops of small bowel, usually proximal to the transition point. CT can accurately confirm the diagnosis; it can also characterize the severity, identify the cause and the transition point, and most important, identify any complications (Figs. C7.2 and C7.3). Table C7.1 lists the signs of bowel ischemia. Mesenteric ischemia can be due to a variety of causes including strangulating obstruction or volvulus (Fig. C7.4), as well as arterial occlusion due to embolic disease or thrombosis at sites of atherosclerosis, venous occlusion, or hypoperfusion associated with nonvascular disease. Mesenteric ischemia has a high mortality rate.

Fig. C7.2

Pneumatosis intestinalis. (A) Axial postcontrast CT images showing pneumatosis intestinalis (white arrow) of the proximal jejunum. Air can be seen along the nondependent wall, but never along the dependent wall as visualized posteriorly in this case. (B) Images slightly superior demonstrate a small amount of linear air collection within the liver representative of portal venous air (white arrow).

Fig. C7.3

Bowel ischemia. Small bowel ischemia with diffusely thickened bowel wall. Notice target sign of end on bowel (arrow).

Fig. C7.4

(A) Small bowel volvulus. Axial CT postcontrast showing the “whirl” sign from mesenteric torsion due to the twisting of the mesentery (arrows). This resulted in acute mesenteric ischemia with partial infarction of the small bowel. At surgery an ileal duplication cyst was found as the lead point for the volvulus. (B) Mesenteric ischemia. 3-D reconstruction from the same patient with mesenteric torsion, showing abrupt occlusion of the SMA (white arrow).

Table C7.1  

Signs of Strangulation

 

As a problem-solving tool for partial or low-grade small bowel obstructions, small bowel follow through exams may be performed. This entails administration of oral contrast with intermittent spot overhead radiographs or direct fluoroscopy to evaluate the contrast transit through the bowel, looking for focal narrowing or strictures. Limitations include overlap of bowel segments and incomplete distention of the small bowel. Other imaging techniques advocated by the ACR Appropriateness Criteria for intermittent or low grade SBO include CT or MR enterography or enteroclysis. Enteroclysis studies are slightly more invasiveness requiring placement of an enteric tube to inject contrast directly into the small bowel which results in greater intraluminal pressure and distention of the bowel to visualize focal narrowing and strictures.

DIFFERENTIAL DIAGNOSIS

Clinical Differential

  • Adhesions: Adhesions are the most common cause of SBO; most of them are postoperative. Adhesions are usually not identified on imaging but instead are a diagnosis of exclusion.

  • Hernia: Hernias are also a common cause of SBO. External hernias usually occur in congenital or surgically weakened defects in the abdominal or pelvic wall and are commonly clinically apparent (Fig. C7.5). Internal hernias occur through defects in the mesentery or peritoneum.

  • Crohn’s disease: SBO in Crohn’s disease can occur in several ways, including acute inflammatory, cicatricial stenosis from long-standing disease, and secondary to postoperative adhesions, strictures, and incisional hernias.

  • Mass: Primary neoplasms rarely cause SBO. Metastasis to the small bowel is more common and may occur hematogenously or by direct spread from peritoneal carcinomatosis.

  • Intussusception: A condition in which a part of the gastrointestinal tract has invaginated into another section. Intussusception is usually found in children and most commonly is ileum invaginating into the ascending colon (ileocolic). In adults, intussusception may occur and be due to a lead point such as a polyp or other mass. The classic sign of bowel-within-bowel, with or without mesenteric fat and vessels, resulting in the “bulls-eye sign” is pathognomonic. In children, intussusceptions may be imaged initially with ultrasound, which involves no radiation to the child. It can also be imaged and treated with air or contrast enemas. Transient intussusceptions in adults are commonly incidentally identified in the proximal jejunum, but should not be confused with pathologic cases that result in obstruction.

  • Others: Radiation enteritis, hematomas, vascular causes (mesenteric ischemia or small mesenteric vein thrombosis), foreign body (bezoar), and gallstone ileus.

  • Closed-loop obstruction: A closed-loop obstruction occurs at 2 points, usually with mesenteric involvement, and is often overlooked because of a lack of dilatation of the upstream proximal bowel loops; it should not be missed because it tends to progress rapidly to ischemia. The involved bowel segment may be completely filled with fluid, with no air-fluid level. A characteristic C- or U-shaped bowel configuration is often present, with a “beaking sign” at the point of torsion or obstruction (Fig. C7.6).

Fig. C7.5

SBO from ventral hernia. Axial CT with small bowel obstruction due to ventral hernia. This ventral hernia has a narrow neck (arrowhead) and could not be reduced manually. The incarcerated segment of bowel perforated resulting in the subcutaneous air throughout the anterior wall (arrows).

Fig. C7.6

Closed loop small bowel obstruction. Coronal CT with closed loop obstruction due to adhesions. Notice the U-shaped loop of bowel beaking converging to same point (arrow).

Imaging Differential

The differential diagnosis includes multiple air-distended bowel loops: an adynamic or paralytic ileus, aerophagia, or a large bowel obstruction.

REFERENCES AND SUGGESTED READING

ACR Appropriateness Criteria. Suspected small-bowel obstruction.
Lappas
 JC. Abdominal radiography findings in small-bowel obstruction: relevance to triage for additional diagnostic imaging. AJR. 2001;176:167-–174. 
[PubMed: 11133561]
Boudiaf
 M. CT evaluation of small bowel obstruction. RadioGraphics. 2001;21:613-–624. 
[PubMed: 11353110]
Silva
 AC. Small bowel obstruction: what to look for. Radio–Graphics. 2009;29:423-–439.

CASE 8

PATIENT PRESENTATION

A 24-year-old man presented with acute-onset abdominal pain that was localized to the right lower quadrant and was associated with fever and leukocytosis.

CLINICAL SUSPICION

Acute appendicitis

IMAGING MODALITY OF CHOICE

Acute appendicitis is a common cause of acute abdominal pain and requires surgery. Several imaging modalities are available for evaluating right lower quadrant pain; the modality of choice depends on the patient’s demographics. In adults, CT is, by far, the best diagnostic test. In children, a few factors favor initial evaluation with sonography, including a small body size, with less body fat, and a high radiosensitivity to ionizing radiation. For similar reasons, in pregnant women, sonography or magnetic resonance imaging (MRI) may initially be used to minimize ionizing radiation exposure (Fig. C8.1).

Fig. C8.1

Algorithm for RLQ pain depending on age.

Abdominal and pelvic CT with intravenous contrast and multiplanar reconstructions is the preferred protocol. The addition of intravenous contrast has been found to increase the sensitivity and specificity, but no significant difference has been found if oral or rectal contrast are used. Contrast is institutional dependent and is favored at our institution. The routine use of CT for appendicitis has been found to decrease the negative appendectomy rate from 43% to 7% among women aged 18 to 45 years.

Findings

The pathogenesis of appendicitis relates to appendiceal lumen obstruction, which results in progressive luminal distention, bacterial overgrowth, and inflammatory cascade activation. If left untreated, the increasing intraluminal pressure and inflammatory changes of the appendiceal wall can lead to perforation and generalized peritonitis. Early CT findings reflect these changes and include a dilated appendix (>6 mm), thickening and enhancement of the appendiceal wall, and surrounding periappendiceal fat stranding (Fig. C8.2). Other helpful signs include an obstructing appendicolith. If rectally or orally administered contrast material opacifies the appendiceal lumen, this in most cases would exclude the diagnosis of appendicitis. Late appendicitis after rupture may no longer demonstrate a dilated appendix, but adjacent inflammatory changes, including a disorganized phlegmonous collection or an abscess, may be identified. Gross free intraperitoneal air may be present, but is uncommon. In patients with little intra-abdominal fat, the bowel loops are commonly not separated and visualization of the appendix can be difficult; this is particularly true in children. However, nonvisualization of the appendix on an otherwise normal CT scan has a negative predictive value of 98.7%.

Fig. C8.2

Acute appendicitis. Axial CT of the lower abdomen with intravenous and oral contrast. Acute appendicitis with a dilated appendix with enhancing walls within the right lower quadrant (white arrow). Notice the surrounding inflammation manifested by the stranding or increased density of the periappendiceal fat (black arrow) as opposed to the near uniform black subcutaneous fat.

DIFFERENTIAL DIAGNOSIS

Numerous disorders present with right lower quadrant pain. The differential considerations are much larger in women because several gynecologic disorders can mimic appendicitis, including pelvic inflammatory disease, tubo-ovarian abscess, ectopic pregnancy, ovarian torsion, ruptured ovarian cyst, and endometriosis. Other differentials include Crohn’s disease, diverticular disease, gastroenteritis, renal calculi, and urinary tract infection.

Omental infarct or torsion is another cause of lower abdominal pain; it most commonly occurs on the right side, can mimic appendicitis clinically. Omental torsion occurs when the greater omentum becomes twisted over itself, leading to vascular compromise and infarction. CT may demonstrate swirling fatty tissue around a vessel, indicating torsion or focal fat stranding with hazy soft tissue infiltration of the involved omental fat (Fig. C8.3). The appendix is not expected to be dilated, but the adjacent stranding may be misinterpreted as periappendiceal fat stranding.

Fig. C8.3

Omental torsion/infarct with extensive stranding in the right abdomen (white arrow) inferior to the right hepatic lobe.

A few neoplasms can mimic appendicitis, including a mucocele of the appendix that is formed by a mucus-producing tumor and can result in a dilated, mucus-filled appendix. This usually lacks surrounding inflammatory changes unless it becomes secondarily infected. Other tumors include carcinoid and adenocarcinoma of the appendix; carcinoid is more common. These can infiltrate the adjacent fat, mimicking inflammatory stranding and regional lymphadenopathy. The mass can eventually obstruct the lumen, resulting in acute appendicitis.

REFERENCES AND SUGGESTED READING

Yoo
 E. Greater and lesser omenta: normal anatomy and pathologic processes. RadioGraphics, 2007;27:707-–720. 
[PubMed: 17495288]

CASE 9

PATIENT PRESENTATION

A 72-year-old woman presented with left lower quadrant pain that was rated 8 on a 10-point pain scale; it had progressively worsened over the past day. The patient was febrile, with slight leukocytosis, guarding, and minimal rebound.

CLINICAL SUSPICION

Diverticulitis

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Jun 12, 2016 | Posted by in GENERAL RADIOLOGY | Comments Off on Gastrointestinal Imaging

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