An abdominal aortic aneurysm (AAA) is a focal dilation of the aortic wall measuring greater than 1.5 times the normal diameter of the aorta. An aortic diameter of 3 cm at the level of the renal arteries meets the definition of an AAA. Most aneurysms produce little to no symptoms unless they rupture.
CT can accurately detect an AAA, mural thrombosis, aneurysmal leakage, and rupture. CT findings of a ruptured aneurysm include anterior displacement of the kidney, indistinct aortic wall, free intraperitoneal fluid, or a retroperitoneal hematoma in the presence of an aneurysm. Leakage and rupture of an AAA can be visualized without the use of IV contrast; however, contrast is necessary to delineate a patent aortic lumen from a mural thrombus and can provide anatomic information about the shape and location of the aneurysm. A normal aortic diameter on CT excludes the diagnosis of an AAA.
ED bedside ultrasonography is very accurate in establishing the presence of an AAA; however, it cannot reliably detect leakage or rupture. In a hemodynamically unstable patient, a ruptured AAA is presumed when it is visualized by ultrasonography.
An asymptomatic aneurysm may be detected during the evaluation of an unrelated medical problem, and can be followed closely as an outpatient. A leaking or ruptured AAA is a true emergency. Clinically stable patients should undergo CT scanning with IV contrast. If the patient is unstable, a bedside ultrasound can be obtained to determine if an aneurysm is present.
When performing bedside ultrasonography be careful to measure the aortic diameter from outer wall to outer wall. If the aneurysm contains a thrombus, take care not to mistake the edge of the thrombus for the aortic wall. Measuring the inner rim of the thrombus will result in a smaller measurement and may lead to the incorrect conclusion that an aneurysm is not present.
Aneurysms measuring greater than 5 cm, or demonstrating an increase in size of greater than 1 cm over a period of 6 months are at increased risk of rupture.
Figure 7.2 ▪ Abdominal Aortic Aneurysm.
A, B: Contrast-enhanced CTA demonstrates the extent of mural thrombus visible as low density (arrows) adjacent to the enhanced lumen of the vessel. The aneurysm extends throughout the suprarenal and infrarenal portions of the abdominal aorta. C, D: Transaxial and sagittal ultrasound images in the same individual. Mural thrombus is seen as echogenic material within the vessel.
Emphysematous cholecystitis is an acute infection of the gallbladder by gas-forming organisms. It is diagnosed radiographically by air within the gallbladder wall or the gallbladder lumen. Gallstones may or may not be present. Other evidence of gallbladder wall inflammation will likely be present, such as a thickened gallbladder wall (>3 mm) and pericholecystic fluid.
Emphysematous cholecystitis can be detected with ultrasound as a comet tail artifact seen within the gallbladder wall or as air artifact within the lumen. On CT, emphysematous cholecystitis will appear as radiolucent areas (gas) within the gallbladder wall or lumen.
Emphysematous cholecystitis occurs as a result of an ischemic and gangrenous gallbladder infected with gas-forming organisms. Emphysematous cholecystitis is uncommon and occurs in only about 1% of cases of acute cholecystitis. It is most often found in elderly men with diabetes mellitus. Patients are often febrile, ill appearing, and have a marked leukocytosis with a left shift. They may have evidence of sepsis or septic shock and require fluid resuscitation and vasopressor support.
Overall mortality rates for emphysematous cholecystitis are five times greater than those of nonemphysematous cholecystitis and range from 15 to 25%. Patients should receive early broad-spectrum antibiotics that cover anaerobic and gram-negative rod bacteria. Patients should be treated aggressively if signs of sepsis exist. Emergent surgical consultation for cholecystectomy should also be obtained.
Occasionally, asymptomatic gallstones may contain internal stellate collections of nitrogen gas (the Mercedes Benz sign). This should not be confused with emphysematous cholecystitis.
Cases require surgical consultation and operative management. In some instances, percutaneous drainage and IV antibiotics can serve as a temporizing measure in high-risk surgical candidates.
Patients who have orally ingested a foreign body or inserted a foreign body into the rectum or vagina will frequently seek medical care in the Emergency Department. Conventional abdominal radiographs can be used to locate the object if it is radiopaque, such as metal and glass. Wood and plastic are generally not radiopaque. CT and MRI may be used with variable success.
“Mules” or “body packers” transport illegal drugs by ingesting drug-filled packets or inserting packets into the rectum or vagina. The packets are often condoms or balloons filled with heroin or cocaine, and vary in their imaging characteristics. On plain abdominal radiographs, the packets may appear as multiple objects of varying radio-opacity throughout the GI tract. A crescent-shaped collection of air may surround condom-wrapped packets, and is described as the “double condom sign.”
Abdominal foreign bodies that are smooth and less than 2 cm in width and 6 cm in length will generally pass without incident. Large or sharp objects located in the stomach should be referred for endoscopic removal. If such an object has already passed into the duodenum, progress through the GI tract should be followed by serial radiographs. Sharp, long objects can lodge in the GI tract at sites of anatomic sharp angulations, such as the duodenal loop, duodenal–jejunal junction, appendix, and ileocecal valve.
Patients who have swallowed packets of drugs are at risk for fatal overdose if one of the packets ruptures. Removal of the drug packets in the ED should be expedited by whole bowel irrigation.
The presence of blood seen on rectal or vaginal exam indicates laceration and possible perforation, and necessitates a surgical consultation.
The majority of ingested foreign bodies will pass spontaneously through the gastrointestinal tract without any intervention. Subsequent radiographs are not needed unless the patient develops abdominal pain, fever, vomiting, or constipation.
Rectal foreign bodies found on abdominal radiographs to be more than 10 cm from the anal verge are more likely to require surgical intervention for removal.
Rectal exam should not be performed on patients complaining of a rectal foreign body until an imaging study has excluded the presence of a sharp object, which could harm the examiner.
An abdominal wall hernia is defined as an abnormal protrusion of peritoneal contents through a fascial defect in the abdominal wall. Plain abdominal radiography is generally nondiagnostic of an abdominal wall hernia unless the patient has a complication such as a bowel obstruction, pneumatosis intestinalis as a result of bowel strangulation and infarction, or pneumoperitoneum as the result of a bowel perforation. Plain radiographs may visualize loops of bowel projecting into scrotum or over the obturator foramen.
CT is the test of choice for evaluation of an abdominal wall hernia as it provides accurate detail of the abdominal wall and hernia contents. CT allows visualization of bowel and omentum protruding through the peritoneum. An incarcerated hernia can be identified by fat stranding around the hernia sac. CT findings of a strangulated hernia include bowel wall thickening, extraluminal fluid, marked fat stranding, and engorged mesenteric vessels suggesting vascular compromise.
Ultrasound can also be used to evaluate hernias, and has the added benefit of avoiding ionizing radiation. Color Doppler flow can help differentiate between an incarcerated or strangulated hernia.
A patient may be discharged to home if the hernia is reducible and if the patient has minimal to no symptoms after hernia reduction. These patients can be referred to a surgeon without any further imaging.
Patients with suspected incarcerated or strangulated hernias should undergo prompt surgical evaluation. Radiographic imaging should be obtained if there is clinical concern for bowel obstruction, ischemia, and perforation.
An ultrasound can be used to differentiate masses in the abdominal wall and inguinal canal, which do not clearly present as hernias on physical exam.
Ultrasound may be used as an aid to hernia reduction. The ultrasound probe can visualize the abdominal fascial defect, allowing the clinician to directly guide the hernia back through the fascial opening into the abdominal cavity.
Figure 7.10 ▪ Inguinal Hernia.
A: On this plain radiograph, bowel containing fecal material is seen projecting over the right obturator foramen. This location is outside of the expected normal confines of the abdominal cavity and is highly suggestive of an inguinal hernia. There are no distended loops of bowel to suggest obstruction at this time. B: CT scan on the same patient demonstrates the bowel-containing inguinal hernia.
Cholelithiasis is the presence of gallstones within the gallbladder. Sonographically, gallstones greater than 2-3 mm will appear as bright echogenic structures within the gallbladder with an anechoic area just underneath them as a result of acoustic shadowing. Mobile gallstones are differentiated from an impacted stone or gallbladder mass by demonstrating that they are freely mobile when the patient is rolled to the lateral decubitus or prone position. CT is less sensitive than ultrasound in detecting gallstones, which will appear as radio-opaque round structures within the gallbladder.
A contracted gallbladder with multiple stones may appear sonographically as wall-echo-shadow sign. Because little to no bile is present in the gallbladder, a bright, echogenic area representing both the wall and the gallstone with subsequent acoustic shadowing will occur. In patients with wall-echo-shadow complex it is not possible to ascertain whether a gallstone may be impacted in the neck of the gallbladder and may be difficult to ascertain for other signs of gallbladder wall inflammation.
While gallstones are present in approximately 15% of the population, most are asymptomatic and require no treatment or intervention. Each year, approximately 3% of patients with gallstones will have an episode of biliary colic with 20% of these patients eventually developing acute cholecystitis. Smaller gallstones (3-4 mm) are less likely to cause acute cholecystitis, but may pass through the cystic duct and into the common bile duct where they can cause obstruction. Depending on the location of that obstruction, these small stones lodged within the common bile duct can lead to gallstone pancreatitis or cholangitis.
Gallstones require no treatment if they are asymptomatic, but may be a marker of hemolytic diseases if found in children or adolescents.
Biliary colic lasts less than 6 hours; if symptoms persist greater than 6 hours a diligent search should be made for an impacted stone in the neck of the gallbladder, cystic duct, or common bile duct.
Acute cholecystitis is the rapid development of inflammation of the gallbladder. It is manifested on ultrasound and CT by inflammation and thickening of the gallbladder wall and pericholecystic fluid. In calculous disease, an impacted stone is seen in the gallbladder neck or cystic duct. In acalculous disease, no stones are present. Biliary sludge may be present in either calculous or acalculous cholecystitis and is evidence of biliary stasis from gallbladder dysfunction. Gallbladder wall inflammation is present if the wall measures more than 3 mm in thickness, has surrounding pericholecystic fluid, or is tender with direct compression of the ultrasound probe (sonographic Murphy’s sign). However, these findings take time to develop. In early acute cholecystitis, the only sonographic manifestation may be an immobile gallstone lodged within the neck of the gallbladder and a sonographic Murphy’s sign. In acalculous disease, a large distended gallbladder with a transverse diameter measurement >4 cm is also indicative of acute cholecystitis.
Acute cholecystitis is a clinical diagnosis supported by sonographic or radiographic findings. The majority of cases (>90%) are the result of an impacted gallstone in the neck or cystic duct of the gallbladder. Acute cholecystitis is first differentiated clinically from symptomatic cholelithiasis by symptoms that persist for more than 6 hours.
Patients often present with right upper quadrant abdominal pain that radiates to the back, nausea, and vomiting. Laboratory values will often be normal in patients with early acute cholecytitis. As time and inflammation progress, a leukocytosis and mild transaminase elevation will occur reflecting the inflammatory process.
Patients with acute cholecystitis should receive broad-spectrum antibiotics that cover gut microorganisms. A surgeon should be consulted for cholecystectomy. Patients who are high-risk surgical candidates may be candidates for percutaneous gallbladder drainage.
Acute cholecystitis frequently occurs in patients who are fair, female, fat, and fertile.
Can occur in younger patients with sickle cell disease, spherocytosis, G-6PD deficiencies, and other hemolytic disorders.
A small and contracted gallbladder (commonly seen after eating a fatty meal) may have a gallbladder wall that appears >3 mm in thickness only because it is contracted. In these cases, the gallbladder wall will have three distinct layers representing the adventitia, muscular layer, and mucosa.
An iliopsoas abscess is a collection of pus located in the iliopsoas muscle compartment. CT is the modality of choice for the evaluation of a suspected iliopsoas abscess. Findings on CT include a focal hypodense lesion, infiltration of surrounding fat, and gas or air fluid levels within the muscle belly. Ultrasound may be diagnostic in up to 50% of cases; however, overlying bowel gas and the pelvic bones may prevent visualization of the abscess. In cases of long-standing iliopsoas abscesses, MRI should be performed to rule out the spread of infection to, or from adjacent soft tissue and vertebral structures.
The iliopsoas muscle has a rich blood supply and may develop an abscess as the result of hematogenous or lymphatic seeding from a distal infection. In addition, the iliopsoas muscle lies in close proximity to the sigmoid colon, appendix, pancreas, and kidney and an abscess may develop from the direct spread from one of these contiguous organs. Iliopsoas abscesses may develop as a complication of infectious spondylitis or sacroilitis.
Common bacterial organisms implicated in the formation of iliopsoas abscess are Staphylococcus aureus, Streptococci, or E. coli, although infections spreading from contiguous organs may be polymicrobial. Mycobacterium tuberculosis may cause an iliopsoas abscess in regions of the world where TB infections are endemic. Management of iliopsoas abscesses includes initiation of broad-spectrum antibiotics to cover Staphylococcus aureus and enteric organisms as well as abscess drainage.
CT-guided aspiration may be used to confirm the diagnosis and guide therapy.
Tuberculous iliopsoas abscesses may show marked abscess wall thickening, rim calcification, and multiple cavities with the muscle belly when visualized by CT scanning.
Ultrasound can miss a small phlegmon or abscess of the iliopsoas muscle.
Acalculous cholecystitis is inflammation of the gallbladder in the absence of gallstones. Sonographically or on CT, it appears as a large gallbladder with a transverse diameter measuring greater than 4 cm with evidence of a gallbladder wall inflammation. Gallbladder wall inflammation is manifested by a gallbladder wall thickness greater than 3 mm and/or the presence of pericholecystic fluid. Pericholecystic fluid is more likely to be present with advanced disease but may not be present early in the disease process. In some cases, biliary sludge can be seen layering in the dependent portions of the gallbladder as a result of biliary stasis and gallbladder dysfunction.
In patients with persistent right upper quadrant pain and no evidence of gallstones on sonography, hepatobiliary scan (Tc-99m HIDA) may have utility in establishing the diagnosis of acalculous cholecystitis. Failure to visualize the normal gallbladder on hepatobiliary imaging is consistent with the diagnosis.
Figure 7.22 ▪ Acalculous Cholecystitis.
A, B: Longitudinal and transverse ultrasound images demonstrate gallbladder wall thickening and dependent sludge (arrow). There is distension of the gallbladder lumen. There are no calculi present. C: CT scan in the same patient demonstrates gallbladder wall thickening and pericholecystic stranding.
Acalculous cholecystitis accounts for approximately 5% of cases of acute cholecytitis and most often occurs in elderly or debilitated patients. It is often a complication of other severe illnesses and most notably occurs in the ICU or in patients receiving TPN. Acalculous cholecystitis is associated with higher mortality (10-50%) and has a higher incidence of gangrene and perforation.
Surgical cholecystectomy is preferred; however, percutaneous drainage may be the only option in patients who are poor surgical candidates. Regardless, patients with suspected acalculous cholecystitis should receive broad-spectrum antibiotics that cover gut flora and have emergent surgical consultation for definitive management.
Acute cholangitis is a bacterial superinfection of the biliary tree caused by distal bile duct obstruction. It is manifested on CT or ultrasound as intrahepatic biliary duct dilation with associated distal bile duct obstruction. Evidence of intrahepatic abscess formation or air within the biliary tree (pneumobilia) may also be present.
Ultrasound and CT will show bile duct dilation and at times a gallstone within the lumen of the common bile duct. Rarely, common hepatic duct compression as a result of a large intraluminal gallstone or an impacted stone in the cystic duct (Mirizzi syndrome) can also lead to acute cholangitis as a result of obstruction to drainage from the biliary tree. Overall, CT is the test of choice and is superior to ultrasound as it can also exclude a compressive mass arising from the bile duct or surrounding structures (i.e., pancreas).
Acute cholangitis is inflammation of the biliary tree. This is most often the result of an ascending bacterial infection that arises when an impacted gallstone or mass prevents drainage of bile from the biliary tree. Classically, Charcot’s triad (RUQ pain, fever, and jaundice) or Reynold’s Pentad (addition of altered mental status and sepsis) have been used to describe acute cholangitis. However, the complete triad or pentad is absent in the majority of patients who present with acute cholangitis. Accurate and timely diagnosis requires a combination of clinical suspicion and CT or ultrasound findings.
Treatment surrounds removing the obstruction and administering broad-spectrum antibiotics. Emergent Gastroenterology consultation for ERCP is the treatment of choice to relieve the obstruction and has reduced the near 100% historical mortality rate to the current mortality rate of 5-10%.
Figure 7.24 ▪ Pneumobilia.
Gas in the biliary ducts is seen overlying the liver shadow centrally (arrows). The location of biliary gas is distinguished from portal venous gas, which is typically seen in the periphery of the liver. Pneumobilia is rarely attributable to acute cholangitis, and is more commonly related to prior instrumentation of the Sphincter of Oddi.
Consider acute cholangitis in elderly patients with altered mental status, sepsis, and an elevated bilirubin.
Patients who present with acute cholangitis are ill-appearing with fever being present in more than 90% of patients.
Figure 7.25 ▪ Acute Cholangitis.
A-C: Peripheral low-attenuation defects are seen in the liver indicating early abscess formation (arrows). Prominent central biliary ducts are seen adjacent to intrahepatic portal vein branches (arrowhead). D, E: Ultrasound of the same patient shows dilation of intrahepatic ducts. The ducts are distinguished from intrahepatic vasculature by lack of flow on color Doppler imaging (arrows).
Appendicitis is the inflammation of the vermiform appendix generally caused by obstruction of the appendiceal lumen. Acute appendicitis is the most common reason for emergency abdominal surgery.
CT has become the gold standard for the radiographic evaluation of acute appendicitis. CT findings suggestive of acute appendicitis are enlarged appendiceal diameter >6 mm with an occluded lumen, appendiceal wall thickening >2 mm, pathologic appendiceal wall enhancement, and periappendiceal fat stranding. Appendicitis is not present if the scan does not demonstrate appendiceal enlargement, obstruction, and abnormal enhancement. A nonvisualized appendix does not rule out acute appendicitis.
Ultrasonography has proven to be reliable in the evaluation of acute appendicitis as well. Ultrasonography is particularly useful when avoidance of ionizing radiation is desirable, especially in children and women of childbearing age.
Ultrasound findings suggestive of acute appendicitis are noncompressible blind-ended tubular structures arising from the cecum, appendiceal diameter >6 mm, presence of an appendicolith, periappendiceal fluid collection, and echogenic prominent pericecal fat. The challenge with ultrasound is finding the appendix. Ultrasound diagnosis of appendicitis is very accurate when the appendix is completely visualized, compressed, measured and the surrounding tissue is scanned to detect any inflammation of the periappendiceal fat. As with CT scanning, appendicitis cannot be ruled out unless a normal appendix is visualized.
The correct diagnosis of appendicitis can occasionally be made from history, physical exam, and laboratory studies, without the aid of radiographic studies. Radiographic studies have decreased the rate of false-negative exploratory surgery from 20% to 3% and proven beneficial when the cause of the abdominal pain is not clear, and in those populations prone to atypical presentations of appendicitis such as young children, elderly, women of childbearing age, diabetics, obese, and immunocompromised patients.
CT remains the preferred study for the detection of appendicitis. Ultrasound has the advantage of imaging without ionizing radiation and is useful for the detection of gynecologic pathology.
A nonvisualized appendix on CT scan or ultrasound does not rule out appendicitis.
Among experienced radiologists, MRI without gadolinium has been found to be extremely accurate in the diagnosis of appendicitis, and may be used in pregnant patients to avoid ionizing radiation.
10% of adults presenting with appendicitis will have an appendolith visualized by plain abdominal radiographs. When present, an appendicolith has a 90% positive predictive value for acute appendicitis.
Figure 7.28 ▪ Normal Appendix.
A-D: The terminal ileum is identified at its junction with the cecum (arrow). Inferiorly, a blind-ended tubular structure is seen arising from the cecum (arrowheads). In contrast to the prior two cases, there is no surrounding standing, enlargement or enhancement of the normal appendix.
Diverticulitis occurs when colonic diverticula become inflamed or infected. In the United States, the majority of cases are located in the sigmoid colon.
CT scan of the abdomen is the preferred radiographic imaging modality for the diagnosis of diverticulitis. Diverticula are identified on CT scan as gas-filled outpouchings of the colonic wall. The CT diagnosis of diverticulitis is contingent on colonic inflammation in the presence of diverticula. CT will show stranding of pericolic fat due to inflammation, bowel wall thickening >1 cm, and pathologic colonic wall enhancement. Intramural abscesses may be identified as small fluid collections within the bowel wall. Extramural intraabdominal abscesses may occur if a diverticulum perforates.
CT of the abdomen can detect complications of diverticulitis including abscess formation, perforation, fistula, and sinus tract formation. An unenhanced CT scan is generally sufficient to allow for the diagnosis of uncomplicated diverticulitis. Addition of IV contrast is necessary to detect the presence of diverticular abscesses, fistulas, and colonic wall inflammation. CT can also be used to guide percutaneous drainage of localized diverticular abscesses.
Acute diverticulitis can be classified as complicated or uncomplicated. Complicated diverticulitis occurs when there is abscess formation, obstruction, perforation, or fistula formation. While acute diverticulitis can often be diagnosed on the basis of history, physical exam, and laboratory exam, consideration should be given to obtaining a CT scan to rule out complicated disease.
Findings on CT scan can predict which patients can be successfully managed without the need for procedural intervention. Uncomplicated acute diverticulitis is managed with bowel rest, intravenous fluids, and antibiotic therapy. CT findings that are classified as mild, that is, localized bowel wall thickening and stranding of the pericolic fat, predict a high success rate with medical management alone. ED patients with complicated diverticulitis should be evaluated by a surgeon.
In 10% of patients, CT scan alone cannot differentiate diverticulitis from colon carcinoma; therefore, the need for close follow-up after resolution of the acute episode of diverticulitis should be emphasized to each patient.
Infarcted appendage epiploica or “epiploic appendigitis” may mimic diverticulitis clinically and on CT. Both will demonstrate pericolic stranding adjacent to the bowel. In cases of epiploic appendigitis however, a fat density, rather than a diverticulum will be seen in association with the pericolonic inflammation and nearby diverticula are often absent.
Small bowel obstruction is the result of a mechanical or functional obstruction, which does not allow passage of the intestinal contents through the small bowel. The most common causes of small bowel obstruction are postoperative adhesions and hernias.
On plain abdominal radiographs, findings characteristics of a small bowel obstruction include dilated air-filled small bowel >3 cm in diameter and the presence of differential air-fluid levels within the same small bowel loop whose levels are separated by at least 2 cm. The presence of air in the distal bowel denotes a partial or early complete small bowel obstruction, whereas the absence of gas in the distal bowel indicates a complete obstruction.
On CT a small bowel obstruction will appear as dilated, fluid-filled loops of bowel proximal to the obstruction, and nondilated, collapsed loops of bowel distal to the obstruction. The change in the caliber, or “transition point” of the bowel at the site of obstruction can often be quite marked. The presence of the “small bowel feces sign” indicates stasis and small bowel obstruction. This sign describes the appearance of gas mixed with stagnant fluid within the obstructed small bowel lumen, resembling feces normally seen in the large bowel only.
Figure 7.37 ▪ Small Bowel Obstruction.
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