2004 Vol.42 Issues 2 Emergency Ultrasound

Radiol Clin N Am 42 (2004) xi
Preface
Emergency ultrasound
Vikram Dogra, MD Guest Editor
Ultrasonography has undergone many technologic changes resulting in its present state-of-the-art equipment that is capable of high-resolution real-time gray-scale imaging and tissue harmonics, including color and power Doppler. These advances in ultrasound technology have resulted in improved work-up of patients undergoing evaluation in emergency departments because it is the first imaging performed on almost all patients presenting to an emergency facility. This easily available imaging modality remains the primary workhorse in diagnostic radiology not only in day-to-day practice but also in emergency situations. There has been a need for the Radiologic Clinics of North America to dedicate an issue solely to the practice of emergency ultrasound and I am honored to be the guest editor of this issue. Great care has been given to the selection of topics for this issue, and pertinent findings have been summarized in the form of tables for easy reference in most of the articles where problem-solving algorithms are also included. Relevant topics have been included that are helpful to all clinicians involved in emergency pa-
tient care. Most of the articles describe sonography techniques and pertinent sonographic anatomy to help those who are new to the field of ultrasonography. This issue on emergency ultrasound provides the reader with up-to-date information on what is new, exciting, and relevant in the practice of ultrasonography as it pertains to acutely ill patients. I wish to express my thanks to Joseph Molter for preparing the illustrations, to Bonnie Hami, MA, for her editorial assistance, and to Adrienne Jones for her secretarial assistance. In addition, my sincere thanks go to Barton Dudlick at Elsevier Science for his administrative and editorial assistance. Vikram Dogra, MD Division of Ultrasound Department of Radiology Case Western Reserve University University Hospitals 11100 Euclid Avenue Cleveland, OH 44106, USA E-mail address: Dogra@uhrad.com
0033-8389/04/$ see front matter D 2004 Elsevier Inc. All rights reserved. doi:10.1016/j.rcl.2004.01.004
Radiol Clin N Am 42 (2004) 257 278
Hepatobiliary imaging and its pitfalls

Deborah J. Rubens, MD
Departments of Radiology and Surgery, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642-8648, USA
Diagnosis of acute cholecystitis Acute cholecystitis is the result of obstruction of the gallbladder and accompanying inflammation of the gallbladder wall with associated infection and sometimes necrosis. Ninety percent to 95% of cases of acute cholecystitis are caused by obstruction by gallstones in either the gallbladder neck or the cystic duct [1]. Acute cholecystitis occurs in only approximately 20% of patients who have gallstones [2]. This means that many patients with gallstones have no symptoms, and their right upper quadrant pain may be caused by a different etiology [3]. Of patients who present with right upper quadrant pain, only 20% to 35% have acute cholecystitis [1,2]. As the definition of right upper quadrant pain becomes less specific, especially lacking an accompanying elevated white blood cell count and fever, the percentage of patients who actually have acute cholecystitis given the history of right upper quadrant pain diminishes further. Specific criteria for the diagnosis of acute cholecystitis are important, because many patients have gallstones but may not have acute cholecystitis. The primary diagnostic criterion is a positive sonographic Murphys sign in the presence of gallstones. Secondary signs of acute cholecystitis include gallbladder wall thickening more than 3 mm, a distended or hydropic gallbladder (loss of the normal tapered neck and development of an elliptical or rounded shape), and pericholecystic fluid.
Sonographic Murphys sign The sonographic Murphys sign is defined as specific reproducible point tenderness over the gallbladder as the transducer applies pressure. In a classic article by Dr. Phillip Ralls [4], which included only patients with right upper quadrant pain, fever, and an elevated white blood cell count, a sonographic Murphys sign was 87% specific for the diagnosis of acute cholecystitis. When a positive sonographic Murphys sign is used in conjunction with the presence of gallstones, it has a positive predictive value of 92% for diagnosing acute cholecystitis. Persons in whom a sonographic Murphys sign may be absent include persons who are medicated; therefore, careful attention to a patients clinical status is important. Denervated gallbladders in patients who have diabetes or gangrenous cholecystitis may result in the loss of a sonographic Murphys sign.
Gallstone diagnosis and pitfalls Gallstones are diagnosed by the presence of gravity-dependent, mobile intraluminal echoes within the gallbladder, which cast a posterior shadow (Fig. 1). Although ultrasound (US) has a high accuracy ( > 95%) for the diagnosis of gallstones, some stones may be missed [3]. False-negative results occur because of stones that are too small to cast a shadow (usually smaller than 1 mm), soft stones that lack strong echoes [1], and gallstones that are impacted in the gallbladder neck or in the cystic duct and may not be as readily visible (see Fig. 1) [5]. If the gallbladder is focally tender but no gallstones are appreciated, the patient should be examined from
E-mail address: Deborah_Rubens@urmc.rochester.edu
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Fig. 1. Gallstones. (A, left) Gallstone in the gallbladder neck (arrow) casts no significant shadow and is nearly invisible. Gas in the duodenum (arrowhead) obscures the fundus and casts a strong sharp shadow (asterisk). (Right) With patient in sitting position, stone (arrow) moves out of the neck and casts a clear shadow (asterisk). Adjacent duodenum (arrowheads) is separate from the gallbladder but still casts a strong shadow, equivalent to the gallstone. (B, left) Multiple gallstones (arrowheads), some of which cast shadows (arrows) and some of which do not. (Right) Normal caliber common duct (6 mm at the porta) with stones (arrows) in same patient. Choledocholithiasis may be difficult to detect, especially in the distal duct, if the stones do not shadow or are not outlined by the distal fluid. (C, left) Longitudinal US shows a normal gallbladder. (Right) Harmonic imaging reveals multiple small stones (arrows).
multiple positions, including prone position or upright position, to help stretch out the gallbladder [3,6]. Decubitus or intercostal scanning also may help visualize the neck, which may not be as easily apparent from a subcostal supine approach. Resolution of small stones in the gallbladder can be improved with use of harmonic imaging [7,8]. This approach uses the higher frequency of the returning sound beam for better resolution and decreases the scattering from superficial structures in the abdominal wall and in the adjacent liver. Harmonic imaging improves the echoes cast by stones and strengthens their posterior shadows. This improved resolution may permit visualization of stones not seen with conventional gray scale US (see Fig. 1).
Echogenicity of stones may be decreased in soft pigment stones. These stones are commonly associated with recurrent pyogenic cholangiohepatitis and are more often seen in the bile ducts than in the gallbladder. They look more like soft-tissue masses than stones and may or may not cast acoustic shadows. They may be misinterpreted as sludge or debris and give a false-negative diagnosis for gallstones. False-positive results may arise from side lobe artifacts, which give rise to echoes that seem to arise within the gallbladder lumen but are actually generated from the wall or outside the wall [1]. Similarly, partial volume artifacts from gas in the adjacent bowel may mimic stones with strong echoes and posterior shadowing (see Fig. 1A). A calcium bile salt precipi-
Fig. 2. Pseudo gallbladders. (A) Transverse image in the right upper quadrant with structure identified as the gallbladder (arrows) containing debris (asterisk). Note that the gallbladder does not extend anteriorly and that the aorta (A) is immediately adjacent. (B, left) CT image of the same area as in A shows a fluid-containing structure (arrows) with similar attenuation to blood in the aorta (A). This was a hematoma.(Right) The true gallbladder (GB) is lateral to the aorta and extends anteriorly. (C, left) Distended fluid- and debris-containing structure believed to represent an abnormal gallbladder in this patient with right upper quadrant pain. (Right) The true gallbladder (arrows) is compressed and displaced by the adjacent mass, a pancreatic pseudocyst. (D) CT of the pancreatic pseudocyst (P) displacing the gallbladder (arrows).
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tate may form with the use of Ceftriaxone and mimic gallstones on sonographic examination. These precipitates resolve after the patient ends therapy. Other fluid-containing structures may mimic the gallbladder, especially if the gallbladder is out of its normal position or is small and contracted. These structures include the duodenum, gastric antrum or colon, hematomas, pancreatic pseudocysts (Fig. 2), or even dilated vascular collaterals. Mistaking these structures for the gallbladder may result in missed pathology in the true gallbladder or a false-positive diagnosis of gallbladder disease (ie, obstructed gallbladder or acalculous cholecystitis).
associated with complications such as gangrenous cholecystitis [9]. A striated wall also is nonspecific, however, and may be seen in all the other causes of wall thickening, including hepatitis (Fig. 6) [10]. Similarly, pericholecystic fluid is a nonspecific finding; it may occur because of ascites or localized inflammation from other causes, such as peptic ulcer disease (see Fig. 4) [2]. Teefey et al [10] described two specific patterns of pericholecystic fluid. Type I, a thin, anechoic, crescent-shaped collection adjacent to the gallbladder wall, is nonspecific (see Fig. 4B). Type II, a round or irregular shaped collection with thick walls, septations, or internal debris, is associated with gallbladder perforation and abscess formation (Fig. 7) [10]
Gallbladder wall thickening and pericholecystic fluid Gallbladder wall thickening is defined as a wall diameter more than 3 mm and is present in 50% of patients with acute cholecystitis (Fig. 3) [1]. The gallbladder wall may be thickened because of hepatic congestion or edema from liver disease, right heart failure, or generalized edema from hypoproteinemia, which is often associated with renal disease or hepatic dysfunction [3]. A thickened gallbladder wall also can occur in association with adjacent inflammatory conditions, including hepatitis, peptic ulcer disease (Fig. 4), pancreatitis, perihepatitis (Fitz-Hugh-Curtis syndrome), and pyelonephritis (Fig. 5). A thickened, striated gallbladder wall consists of alternating hyper- and hypoechoic layers. When seen in the setting of acute cholecystitis, it is strongly Acute acalculous cholecystitis This is an acute inflammation of the gallbladder that occurs in up to 14% of patients with acute cholecystitis [11]. It is most frequently seen in posttrauma and postsurgical patients and other hospitalized patients and occurs because of conditions that lead to ischemia, hypotension, or sepsis [12]. These critically ill patients are often medicated with narcotics, are on ventilators, and receive hyperalimentation, which contributes to biliary stasis and functional cystic duct obstruction [2,12]. Gallbladder gangrene is associated in 40% to 60% of cases, with increased risk of perforation [2]. Mortality ranges from 6% to 44% but can be reduced by early diagnosis and therapy [12]. In the series by Cornwall et al [12], only 50% had a sonographic Murphys sign. This is a difficult clinical and ultrasonic diagnosis, because gallstones are absent and the sonographic Murphys sign may be limited because of other illnesses and medication. The diagnosis is made by gallbladder tenderness (if present) and is associated with gallbladder distension, intraluminal debris, and gallbladder wall thickening that is not caused by other etiologies, such as hypoalbuminemia, congestive heart failure, or hepatic congestion (Fig. 8). Because gallbladder wall thickening is nonspecific, CT can be used to visualize pericholecystic inflammation to improve diagnostic specificity [2,13].
Fig. 3. Acute cholecystitis. This patient presented with right upper quadrant pain and a positive sonographic Murphys sign. Longitudinal US shows stones (arrows) and diffuse gallbladder wall thickening (cursors) that measures 5 mm.
Complicated cholecystitis Complications of acute cholecystitis include gangrenous cholecystitis, emphysematous cholecystitis,
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Fig. 4. Peptic ulcer perforation and thick gallbladder wall. (A) Patient with right upper quadrant pain, fever, and elevated white blood cell count. US shows focal gallbladder wall thickening (7-mm cursors) and gallstones (asterisks) and could be interpreted as cholecystitis. The free air with reverberation shadows (arrows) that leads to the correct diagnosis could be overlooked easily. (B) Transverse US shows wall thickening (cursors) and simple pericholecystic fluid (arrow). (C) CT image shows pericholecystic fluid (arrows), free air (arrowheads), and extraluminal accumulated air (paired arrowheads) in perforated duodenal ulcer.
and gallbladder perforation. These complications occur in up to 20% of patients [3]. Complications of acute cholecystitis are important to detect because they are associated with increased morbidity (10%) and mortality (15%) [14] and require emergency surgery [2]. There is also approximately a 30% conversion for laparoscopic cholecystectomy to an open procedure in the setting of complicated cholecystitis [14].
Gangrenous cholecystitis Gangrenous cholecystitis is defined histologically as coagulative necrosis of the mucosa or the entire wall associated with acute or chronic inflammation [10]. It occurs in up to 20% of patients with acute cholecystitis and has an increased risk of perforation [3]. Unfortunately, US is relatively nonspecific for the
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Fig. 5. Pyelonephritis with gallbladder wall thickening. (A) Gallbladder wall shows marked 1.3 cm thickening (cursors) and hypoechoic fluid within the wall. (B) Transverse US of the lower pole of the right kidney shows a 3-cm echogenic mass (arrows). (C) CT through the right lower pole shows the characteristic round, heterogeneous decreased attenuation area of pyelonephritis (arrows).
diagnosis of gangrenous cholecystitis because a sonographic Murphys sign is absent in two thirds of patients [15]. A relatively specific finding is intraluminal membranes caused by a fibrous exudate or necrosis and sloughing of the gallbladder mucosa (Fig. 9). This finding is present, however, in only 5% of patients [10].
Gallbladder perforation Gallbladder perforation occurs in 5% to 10% of patients with acute cholecystitis, most often in asso-
ciation with gangrenous cholecystitis [3]. The fundus is the most common site for perforation because it has the least blood supply. Acute perforation with free intraperitoneal bile results in peritonitis and is rare. More commonly, subacute perforation occurs, which results in pericholecystic abscess formation [2]. These abscesses may occur in or adjacent to the gallbladder wall in the gallbladder fossa, within the liver, or along the free margin of the gallbladder within the peritoneal cavity [10]. They are characterized by complex fluid collections with inflammatory changes in the adjacent fat on US or CT [2]. Patients with peritoneal or liver abscesses require immediate surgery and drainage, respectively, whereas abscesses
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in the gallbladder wall and fossa may respond to conservative management [16]. Pericholecystic fluid adjacent to the gallbladder wall may mimic perforation. Upon careful inspection, however, the wall is intact and the fluid anechoic (see Fig. 4B). Fluid that appears within the walls been noted to precede perforation in one case [17]; however, no specific US features predict which gallbladders will perforate.
Emphysematous cholecystitis This is a rare complication of acute cholecystitis (less than 1% of all complicated cases) and is associated with gas-forming bacteria in the gallbladder lumen or in the gallbladder wall. As many as 40% of patients with emphysematous cholecystitis have diabetes [2]. The clinical course is rapidly progressive, with 75% incidence of gallbladder gangrene and 20% incidence of perforation [18]. Emphysematous cholecystitis can be recognized by the antidependent gas echoes within the lumen (Fig. 10). Intramural gas may be more difficult to identify because it may mimic the calcified wall of a porcelain gallbladder. The type of shadowing (clean versus dirty) does not differentiate between calcium and air. The location of the echoes does. If the presence of gas is
Fig. 6. Hepatitis, with striated gallbladder wall thickening. Longitudinal US of contracted gallbladder with a thickened striated wall (arrows) with alternating echogenic and hypoechoic layers. This patient had right upper quadrant pain, fever, abnormal liver function tests, and a negative sonographic Murphys sign. She tested positive for hepatitis B and clinically had acute alcoholic hepatitis. The striated wall is not specific for gallbladder disease.
Fig. 7. Complicated cholecystitis with gallbladder perforation. (A) Longitudinal US of the gallbladder (GB) with adjacent irregularly marginated pericholecystic intrahepatic fluid (arrows). This patient presented with sepsis 2 weeks after prostate surgery and was found to have acute cholecystitis with an adjacent liver abscess. (B) Longitudinal US of gallbladder with stones shows a pericholecystic collection (arrow) that contains debris. The collection abuts the free wall of the gallbladder and is not contained within the gallbladder wall (double arrow). (C) CT shows an enhancing rim around the fluid (arrows) and inflammatory edema in the adjacent fat (arrowheads).
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Fig. 9. Gallbladder gangrene/mucosal sloughing. Longitudinal US of patient with acute cholecystitis secondary to stone (arrow) impacted in the gallbladder neck. Note the intraluminal membranes (arrowheads), which are associated with gallbladder gangrene.
Fig. 7 (continued).
extrinsic masses with biliary duct compression and obstruction. The diagnosis is made by evaluation of intra- and extrahepatic ducts, because one or both may be dilated, depending on the level of obstruction.
uncertain, either CT or plain film radiography can be used to differentiate between gas and calcification.
Ultrasound diagnosis of duct dilatation The extrahepatic common duct is measured from outer wall to outer wall at the level of the crossing of the right hepatic artery. The diameter at this level should not exceed 6 mm [1]. The diameter of the common duct is slightly greater distally as it approaches the pancreas, sometimes as much as 1 to 2 mm. There is still debate in literature as to whether the bile duct dilates with age or after cholecystectomy [1]. Most laboratories consider a duct smaller than 6 mm normal and a duct 8 mm or larger abnormal [1,19]. Clinically, if a patient has dilated ducts but no accompanying symptomselevated bilirubin, pain, sepsis, or elevated liver enzymes, including alkaline phosphatasethe dilated ducts are unlikely to be clinically relevant. Similar to the presence of gallstones, when assessing the ducts for biliary disease, the clinical scenario is of prime importance. Intrahepatic biliary ducts are normal if they are 2 mm or smaller in the porta or no more than 40% of the diameter of the accompanying portal vein [1]. With the advent of newer equipment, however, it is possible to see intrahepatic biliary ducts in normal patients, especially with the use of harmonic imaging, which diminishes scatter. Clinical correlation is important, because many young and slender patients may show normal ducts with high-frequency transducers (Fig. 11A). In general, intrahepatic biliary duct dila-
Biliary ducts Dilated biliary ducts in the acute patient represent a relative emergency because sepsis in association with dilated ducts requires rapid decompression. Biliary duct dilatation may be the result of multiple causes, including stones, tumor, stricture, or adjacent
Fig. 8. Acalculous cholecystitis. Longitudinal US of a debrisfilled (asterisk) gallbladder with a thick, striated wall (arrows). No stones are visualized. At surgery, this was acute acalculous cholecystitis.
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Fig. 10. Emphysematous cholecystitis. (A) Transverse supine view of the gallbladder reveals nondependent echoes anteriorly (arrowheads), which cast a dense posterior shadow. (B) When viewed longitudinally from the flank, the dependent echogenic gallstones (arrows) can be seen. Note that the shadow cast by the gas in (A) is denser and sharper than that from the stones (B). The bowel gas does not necessarily cast a dirty or reverberant echo-filled shadow. Thus, the shadow cannot distinguish gas from the stones.
Fig. 11. Normal ducts. (A) Normal intrahepatic ducts (cursors) in a post-cholecystectomy patient. Multicolored vessel in the center of the color box is the hepatic artery (HA), and dark red adjacent vessel is the portal vein (PV). (B,C) Patient with abdominal pain, nausea, and jaundice, 1 month after cholecystectomy. Note multiple anechoic irregularly branching tubes with confluence in the porta hepatis. Color Doppler image (C) confirms that some are avascular and represent ducts (arrowheads), and the portal veins (red), hepatic veins(blue) and hepatic arteries (HA) are correctly identified. The inferior vena cava (IVC) and hepatic vein (HV) as shown can be recognized by its anatomic position.
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Fig. 11 (continued).
tation can be diagnosed by irregular angular branching, a central stellate configuration, and acoustic enhancement posteriorly to the ducts (Fig. 11B) [1]. The use of color and power Doppler may be valuable to demonstrate that the dilated structures are ducts and that the normal portal veins and hepatic arteries course adjacent to them (Fig. 11C). Biliary duct necrosis is a critical complication that occurs after liver transplant. In this situation, the ducts may not be filled with bile but may be filled with pus or necrotic debris. They also may appear echogenic and irregular and enlarged without any fluid component (Fig. 12). If the diagnosis of biliary disease is in question on US, CT scan or transhepatic cholangiography may be helpful in posttransplant patients.
drink water to displace gas or by using large a footprint curvilinear transducer to compress bowel and bowel gas away from the distal duct. Ninety percent of obstruction occurs in the distal duct because of common duct stones, pancreatic carcinoma, or pancreatitis [1]. Obstruction also may occur at the level of the porta hepatis, usually because of tumor (cholangiocarcinoma) or adenopathy. Sclerosing cholangitis gives rise to segmentally dilated ducts, often only in one portion of the liver (Fig. 13). These patients may develop infection and present with sepsis. Other causes of obstruction between the pancreas and the porta hepatis include masses of the colon or duodenum (Fig. 14), primary biliary malignancy, or adenopathy. Pitfalls include patients who have obstruction without dilatation, which can occur in ascending cholangitis, intermittent obstruction from stones, or sclerosing cholangitis. As many as one third of common bile duct calculi are found in nondilated bile ducts (see Fig. 1B) [1]. In this group of patients, US is relatively insensitive to make the diagnosis. MR cholangiopancreatography (MRCP) and endoscopic retrograde cholangiopancreatography (ERCP) should be considered the alternative diagnostic modalities, especially for stone disease.
Acute hepatic disease processes Multiple abnormalities of the liver may present with right upper quadrant pain. Some of these situations involve medical emergencies, including lesions that are hemorrhagic or patients who have infection and sepsis. Space-occupying disorders that stress the liver capsule also may present with right upper quadrant pain. These disorders range from acute fatty infiltration to hepatitis to diffuse metastatic disease. The important clinical features to determine are whether the patient has infection or sepsis and if the pain is localized to the liver or is more diffuse (peritoneal signs). Anatomically the hepatic processes can be divided into diffuse disease, focal disease, and diseases that involve the vasculature.
Diagnosis of biliary obstruction Assuming a patient has a dilated duct (6 mm or larger) associated with clinical signs of obstruction (including elevated bilirubin or elevated alkaline phosphatase), how well does US identify the level and cause of obstruction? With good technique, the level of obstruction can be defined in up to 92% of patients and the cause in up to 71% [1]. Important technical factors include positioning the patient in the erect right posterior oblique or right lateral decubitus position to minimize overlying bowel gas from the antrum or the duodenum and using transverse scans to follow the duct accurately [1]. Additional technical improvements sometimes can be achieved by having the patient
Hepatitis Hepatitis is a viral infection of the liver. The most common acute presentation is from hepatitis A, which is spread via oral ingestion with a 99% recovery rate [20]. Patients present acutely with jaundice, fever, and hepatomegaly. Sonographically,
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Fig. 12. Biliary duct necrosis. (A) Transverse US of a liver transplant patient who presented with sepsis. Amorphous echogenic debris (arrows) is seen on gray scale. (B) Two months later, the process has progressed. The echogenic areas (arrows) are more confluent and linear and cast acoustic shadows, which obscure the adjacent parenchyma. (C) Color Doppler image shows echogenic debris in a ductal distribution (arrows) and a low resistive index (less then 0.5) in the hepatic artery, which signifies hepatic arterial stenosis or thrombosis. (D) The extensive biliary duct necrosis (arrows) and the resulting liver abscess (arrowheads) are documented by CT. The abscess was obscured on the US because of shadowing from the ducts.
most often the liver parenchyma is normal [20,21]. Rarely, the liver may have diffusely decreased echogenicity with relatively increased echogenicity of the portal triadsthe starry-sky appearance [21]. The overall echogenicity of the liver is decreased relative to the adjacent kidney (Fig. 15). Confirmation should
be obtained by checking the echogenicity of the spleen relative to the left kidney to confirm that there is no medical renal disease [20]. More commonly, hepatitis has associated gallbladder findings, including gallbladder wall thickening (see Fig. 6) and sometimes a contracted gallbladder [20,21]. When
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Fig. 13. Sclerosing cholangitis. Patient presented with sepsis and abdominal pain. (A) Longitudinal US of the right lobe is normal, with a common duct (cursors) measuring 2 mm. (B) Longitudinal US of the left lobe shows multiple markedly enlarged ducts (arrows). (C) CT shows the asymmetrically enlarged ducts (arrows) with enhancing walls, which indicates inflammation. Emergent biliary drainage was performed, which alleviated the patients symptoms.
the patient recovers from hepatitis, the gallbladder wall and distention return to normal. Other viral infections that involve the liver, such as mononucleosis, may cause a similar pattern, with liver swelling, tenderness, and gallbladder wall thickening (Fig. 16).
Liver abscess The most common liver abscesses are pyogenic, caused by bacteria. Patients most often present with right upper quadrant pain, fever, and malaise. The cause may be biliary (ascending cholangitis or from the adjacent gallbladder), portal venous (from diverticulosis or Crohns disease), or arterial. Fifty percent of liver abscesses do not have a clear source [20]. The appearance of liver abscesses varies. Microabscesses,
lesions smaller than 2 cm, may be widely scattered in the liver or may cluster in a single focus. Pyogenic abscess cavities probably begin as a small cluster of microabscesses, which coalesce into a larger drainable collection [22]. Sonographically, abscess margins are often indistinct; which make abscesses less conspicuous than on contrasted CT scans. This is particularly true in small clustered microabscesses (Fig. 17A, B). Predominately abscesses are hypoechoic (see Fig. 7A) but also may be isoechoic, solid appearing, or even hyperechoic if they contain gas and debris (Fig. 17C). Fifty percent or less have enhanced through transmission. Because of this variable appearance, the differential diagnosis is large and includes tumor, simple cyst with hemorrhage, hematoma, or other forms of infection, including amebic abscess or ecchinococcal infection. The absence of flow centrally helps to
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Fig. 14. Duodenal mass with biliary, pancreatic, and bowel obstruction. Patient presented to the emergency department with nausea and rising bilirubin. (A) Transverse US of the pancreas shows a 1.8-cm common duct (CD) and a dilated pancreatic duct (arrowheads). (B) Longitudinal US shows a distended gallbladder with a soft-tissue mass (arrows) behind it. (C) On transverse imaging, the mass (arrows) obstructs the duodenum (Duod), which has a fluid-filled proximal lumen. GB, gallbladder. (D) CT confirms the circumferential duodenal tumor (arrows). Note distended gallbladder (GB) and common duct (CD).
confirm that these are not solid tumors; however, necrotic neoplasm remains in the differential diagnosis. The most helpful feature is a clinical scenario that includes signs of infection. Abscesses are frequently multiple, and US may be limited near the dome or underneath the ribs for identifying the extent of
abscess involvement. In this case, contrast-enhanced CT is often helpful in detecting the total abscess burden and may identify the cause, especially if the abscess arises from the bowel. After liver transplant, patients are particularly prone to abscesses, especially if biliary necrosis is present because of hepatic arterial
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Fig. 15. Acute hepatitis. Transverse image shows a hypoechoic liver relative to the kidney (K) and bright portal triads (arrowheads), the Starry Sky appearance. Although striking, this appearance is rare. Most often the hepatic echogenicity is normal.
thrombosis. If a transplant patient presents with a hepatic abscess, the patency of the hepatic arteries should be assessed (see Fig. 12).
Noninfectious diffuse enlargement of the liver Patients with diffuse metastatic disease may present with right upper quadrant pain, sometimes with fever and jaundice. When patients are questioned closely, their symptoms are usually not as acute as
that of cholecystitis or hepatitis. On imaging, metastatic disease may be of any type from cystic metastases of carcinoid to echogenic metastases from colon carcinoma or any other primary lesion. The liver is enlarged and tender to palpation, usually because of stretching of the liver capsule (Fig. 18A). Another disease process that causes rapid hepatic enlargement is acute fatty infiltration of the liver, which may be diffuse and homogenous fatty infiltration (Fig. 18B) of the liver or segmental fatty infiltration with areas of focal sparing. The liver may enlarge rapidly and give rise to the clinical symptoms of right upper quadrant tenderness. Vessels are not distorted, however, and if there are areas of focal fatty infiltration, they should have a geographic margin. If metastatic disease is in the differential diagnosis, a sulfur colloid nuclear medicine scan can be performed, which should produce normal results in the setting of fatty infiltration. An MR imaging scan with and without fat suppression also defines the cause of the US abnormalities. Acute fatty liver of pregnancy is a relatively rare but serious complication that occurs in the third trimester and peripartum. Two-thirds of patients have associated pre-eclampsia or the hemolysis, elevated liver enzymes and low platelets (HELLP) syndrome [23]. Patients present with various symptoms, most commonly nausea, vomiting, abdominal pain, fever, and jaundice [23,24]. Symptoms commonly mimic hepatitis. Laboratory abnormalities include elevated liver enzymes and coagulopathy (prolonged prothrombin time [PTT]). Disseminated intravascular coagulation occurs in up to 50% [23]. US and CT may have high false-
Fig. 16. Mononucleosis. (A) Initial longitudinal US in a patient 18 weeks pregnant with right upper quadrant pain, nausea, and vomiting. The gallbladder is thick walled (arrows) and contains debris. A diagnosis of acute acalculous cholecystitis was offered. (B) One week later the galbladder wall (arrows) has returned to normal and the sludge is diminishing. The patient tested positive for mononucleosis.
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Fig. 17. Liver abscesses. (A) Transverse US of nearly invisible microabscesses (cursors) within the liver. There are no specific US features to identify this as an abscess. The area is slightly heterogeneous and lacks a normal vessel pattern. (B) CT of the left lobe contains a typical rosette pattern diagnostic of clustered small abscesses with enhancing rims (arrows). A right lobe abscess (arrow) could not be seen by US. (C) Mixed abscesses and gas. Longitudinal US of a patient with multifocal abscesses. The fluid-containing abscess (A) anteriorly contains gas (arrow) with a reverberant echo posteriorly. The isoechoic abscess more posteriorly (arrowheads) with central gas is more difficult to detect. (D) CT scan shows both abscesses. The more central abscess (arrowheads) is much more extensive on CT than on US.
negative rates (as high as 80%), and the diagnosis largely depends on clinical features and biopsy, if necessary [23,24].
Focal lesions with hemorrhage Any focal hepatic lesion can potentially bleed, which leads to acute right upper quadrant pain with
subsequent presentation of the patient for emergency US. Even innocuous lesions, such as benign liver cysts, occasionally can hemorrhage with resultant symptoms. Hemangiomas, the most common benign tumors of the liver, are mostly small and asymptomatic and discovered incidentally. Lesions larger than 5 or 6 cm occasionally may present with either hemorrhage or thrombosis [20]. Hepatic adenoma, a benign tumor associated with estrogen or anabolic
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Fig. 18. Diffuse liver enlargement. (A) Carcinoid metastases. Longitudinal US of a patient with acute right upper quadrant pain to rule out (R/O) cholecystitis. The gallbladder is normal; however, the liver was enlarged at 21 cm and riddled with cystic thickwalled metastases (arrows) from a carcinoid primary. (B) Acute fatty infiltration. Longitudinal US in a patient with acute right upper quadrant pain and abnormal liver function tests. The liver is enlarged at 18.4 cm with diffusely increased echogenicity, loss of the normal vascular pattern, and increased attenuation, which causes poor delineation of the diaphragm posteriorly (arrows).
steroid therapy, does have a predisposition for bleeding [25]. The rate of intratumoral or intra-abdominal hemorrhage with adenomas is reported as high 50% to 65% [26]. Contrary to focal nodular hyperplasia and hemangioma, which are usually managed conservatively, except if the patient has significant symptoms, adenomas are usually resected, especially
if larger than 5 cm. On US, hepatic adenomas have a variable appearance that ranges from hypoechoic masses to mixed heterogeneous masses, which correspond pathologically with intratumoral hemorrhage and necrosis [25]. Masses also may be isoechoic to the liver with a hypoechoic rim or even hyperechoic if they contain fat. The mixed echogenic pattern is
Fig. 19. Hemorrhagic adenoma. (A) Transverse US in a patient with acute right upper quadrant pain who is taking oral contraceptive pills shows a mixed echogenicity mass (arrows) with through transmission (asterisk) displacing the gallbladder (arrowhead). The through transmission indicates fluid. (B) CT shows a heterogenous mass (arrows). The tumor portion (A) enhanced, whereas the remaining hemorrhage did not.
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most likely to correspond to hemorrhagic necrosis; however, it cannot be distinguished from other tumors that can hemorrhage (Fig. 19) [25]. After adenoma, the other hepatic tumor likely to present with hemorrhage is hepatocellular carcinoma. Similar to adenomas, the US appearance of these
lesions varies greatly and ranges from echogenic to hypoechoic or mixed [21]. Tumors even may be diffuse and infiltrative and relatively invisible by US. A clue to the presence of an underlying malignancy is increased hepatic arterial flow in the lesion compared with the remaining normal liver (Fig. 20).
Fig. 20. Hepatocellular carcinoma with hemorrhage. (A) Transverse US shows a heterogeneous liver echogenicity with hypoechoic fluid (F) and an echogenic region that has a straight-line margin (arrows) with the more superficial hypoechoic tissue (H). (B) Color Doppler image from the liver shows an area with high velocity (1.6 m/second) and low resistance (resistive index of 0.49) flow, which indicates tumor shunt flow. (C, D) CT confirms enhancing tumor at the dome (arrows), and a more caudal image (D) shows the acute clot (H) bordering the lateral liver margin (arrows). This accounted for the straight margin seen in Fig. 19A. F, fluid.
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Most patients with hepatocellular carcinomas also have predisposing risk factors, including cirrhosis or hepatitis B or C. The important feature to remember about acute hemorrhage is that it may mimic the adjacent liver parenchyma. Color Doppler imaging is useful for showing vessels in a normal liver or in the tumor, whereas the hemorrhage has no vascularity within the hematoma. Straight lines and geographic margins are also a clue to the presence of hemorrhage (Fig. 20). Usually this indicates a subcapsular component with compression of the adjacent liver capsule. Because US can have difficulty differentiating between the acute blood and the adjacent liver, CT scan is often used to map the extent of the process and differentiate hepatic tissue from blood and tumor.
Abnormalities of hepatic vasculature Pathologic processes that involve the hepatic vasculature may result in acute symptoms and emergent presentations of the patient for US examination. The liver has three vascular systems: the hepatic arterial and portal venous for incoming blood and the hepatic venous for outgoing blood.
Acute portal vein thrombosis Acute portal venous thrombosis has multiple causes, including septic thrombophlebitis [27], associated pancreatitis, and hypercoagulable states,
including stem cell transplantation [28]. Septic thrombophlebitis has a mortality rate as high as 50% [27]. The most common cause is diverticulitis, with inflammatory bowel disease, bowel perforation, and suppurative pelvic and pancreatitis infections as potential sources. Most patients present with sepsis, fever, chills, and upper abdominal pain because the primary bowel source is often asymptomatic [27]. Patients without sepsis and acute portal vein thrombosis present with nonspecific right upper quadrant or epigastric pain. Some patients also have abnormal liver function tests without hyperbilirubinemia [29]. On US, the portal vein is dilated and may be completely anechoic, but it is more often filled with low-level echoes and shows no flow on color or power Doppler (Fig. 21). The main portal vein is seen on 97% of upper abdominal US [30]. Failure to visualize a patent main portal vein on gray scale and Doppler US should indicate portal vein thrombosis. False-positive results may occur in patients with slow flow caused by portal hypertension. In these cases, maximum Doppler sensitivity should be achieved with low wall filter and lower Doppler angles and lower Doppler frequencies to improve penetration at depth. Spectral Doppler always should be used to confirm absent flow on color or power Doppler images [29]. If flow remains absent but no thrombosis can be visualized, contrast-enhanced US, CT, or MR imaging could be used to confirm the presence of thrombosis [31]. In the subacute to chronic phase, older thrombosis becomes hyperechoic and recanalizes, or the patient forms collaterals. These smaller multiple portal channels are called cavernous transformation of the portal vein. On
Fig. 21. Portal vein thrombosis. (A) Longitudinal US in a patient with right upper quadrant pain on oral contraceptives. The portal vein (arrows) is distended and hypoechoic with no flow on color Doppler. (B) Contrasted CT scan shows low-attenuation portal vein (arrow), which fails to enhance. Thrombus also involves the splenic vein (paired arrows).
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spectral Doppler they have the typical monophasic spectral waveform of the portal system.
Acute hepatic venous thrombosis Acute hepatic venous thrombosis is otherwise known as Budd-Chiari syndrome. This rare entity results from venous obstruction usually caused by thrombosis of the hepatic veins, although proximal suprahepatic webs or obstruction of the inferior vena cava (IVC) also can cause it [30,31]. Etiologic factors include hypercoagulable states, including pregnancy, birth control pill use, and post bone marrow transplant status, and other malignancies, including hepatoma, which may directly invade the veins [30]. Patients present with abdominal pain, ascites, and liver enlargement. US findings include abnormal flow in one or more hepatic veins [32]. Flow may be absent or completely monophasic on spectral Doppler, which indicates loss of cardiac pulsatility because of interruption between the vein and the heart. Reversed or to and fro flow also may be seen in these excluded segments if they form collaterals with the portal veins or the IVC [30,33]. Nonvisualization of the veins on color or power Doppler is nonspecific because they may be compressed in the setting of cirrhosis [32]. Portal venous flow is present, although it may be biphasic or reversed in fairly severe cases [30]. Obstruction of the suprahepatic IVC also can be documented by US, visualization of the thrombus, or absent flow in the obstructed segment. The inferior IVC and iliacs may be patent but should have a monophasic spectral Doppler waveform and lack the normal re-
sponse to a Valsalvas maneuver [30]. Findings may be confirmed with either CT or MR imaging. CT in acute cases shows global ascites and liver enlargement with decreased attenuation in the affected areas before contrast and heterogeneous patchy enhancement after contrast with rim enhancement of the hepatic veins [34]. MR imaging may show heterogeneous enhancement of the hepatic parenchyma with edema and relative caudate sparing because the caudate drains directly into the IVC and does not go through the hepatic veins [35]. Severe involvement of the veins may lead to liver failure, which requires transplantation.
Hepatic artery thrombosis Hepatic arterial thrombosis is a major contributor to acute hepatic dysfunction in patients after liver transplant. In particular, the biliary ducts depend on adequate hepatic arterial perfusion for oxygenation. Hepatic arterial thrombosis or stenosis occurs in up to 13% of patients after liver transplant and is a major cause of graft failure [36]. Clinically, hepatic arterial thrombosis is suspected when liver function studies deteriorate, fever of unknown origin occurs, or the biliary tract is involved, with either a delayed biliary leak secondary to ischemia or development of liver abscesses [37]. Without treatment, mortality rate may be as high as 70%. Graft salvage may be achieved by arterial revision, or retransplantation may be required [38]. The diagnosis could be made by Doppler US in as many as 10% of patients who are clinically asymptomatic by using aggressive US screening in the early postoperative period (days 1 3) [37]. US
Fig. 22. Hepatic artery thrombosis with infarction postpartum. A liver transplant patient presented with acute pain and liver failure 3 days postpartum. (A) US shows a diffusely disorganized liver pattern with no discernable vessels anteriorly (arrowheads). Echogenic lines (arrows) represent gas. (B) CT scan shows the large infarct (arrowheads) and the gas in the biliary ducts (arrows).
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Fig. 23. Hemorrhagic adrenal adenoma. Patient presented with fever and acute right upper quadrant pain. Clinically the attending surgeon was convinced she had acute cholecystitis. (Left) Longitudinal US shows mass (M) posterior to retroperitoneal reflection (arrows) and separate from kidney (K). The gallbladder was normal. (Right) Transverse CT shows non-enhancing adrenal mass (M) caused by hemorrhage of an adrenal adenoma.
diagnosis consists of color Doppler and spectral Doppler examination. Absent hepatic arteries indicate thrombosis, although vessels may be small and difficult to visualize in the immediate postoperative patient. This may be a situation in which US contrast is useful. If flow is visualized in the vessels, a resistive index is obtained (peak systolic velocity = end diastolic velocity divided by systolic velocity). A resistive index of less than 0.5 or acceleration from beginning of systolic to systolic peak of more than 0.08 seconds yields 73% to 81% sensitivity for hepatic thrombosis or stenosis [39,40]. Additional diagnostic criteria include a resistive index of 1 in the extrahepatic artery with no flow visualized in the intrahepatic arteries [37]. Confirmation of US findings is usually performed angiographically. Prompt revascularization or retransplantation is desirable because asymptomatic patients may achieve up to an 80% graft salvage rate versus 43% on symptomatic patients [37]. Massive acute hepatic arterial thrombosis may result in liver infarction (Fig. 22).
renal infarction, renal obstruction, and renal or adrenal hemorrhage (Fig. 23), also can present occasionally with right upper quadrant pain, which mimics acute cholecystitis.
Summary In summary, US is the initial imaging modality for the evaluation of acute right upper quadrant pain. It permits accurate diagnosis of acute cholecystitis and successfully identifies multiple other causes of patient symptomatology. Some of these processes lie outside the hepatobiliary system and include renal infection and obstruction, pancreatitis and its sequelae, duodenal or colonic perforation or mass lesions, peritoneal tumor spread, adrenal hemorrhage, and even remote problems, such as pneumonia. The limitations on US include incomplete imaging of the liver, most often at the dome or beneath ribs on the surface, and incomplete visualization of lesion boundaries, particularly with some infections and tumors. For these clinical scenarios, contrast-enhanced CT is complementary to US and should be encouraged. In the biliary tree, US has limitations in situations in which the ducts are not dilated and sometimes with imaging the extrahepatic ducts, especially distally. For these patients, CT or MR imaging (MRCP) is especially useful. If one keeps the clinical scenario in mind and always images a patient where he or she hurts, US is a powerful and effective diagnostic method for evaluating acute right upper quadrant pain.
Acute right upper quadrant pain, outside the hepatobiliary system The differential diagnosis for patients with right upper quadrant pain is extensive and includes pneumonia, appendicitis, peritoneal tumor, primary bowel disease, pancreatitis, and peritonitis caused by either bowel or pelvic pathology, such as hemorrhagic adnexal masses. Retroperitoneal processes, such as
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References
[1] Laing FC. The gallbladder and bile ducts. In: Rumack CM, Wilson SR, Charboneau JW, editors. 2nd edition. Diagnostic ultrasound, volume 1. St. Louis: MosbyYear Book; 1998. p. 175 223. [2] Gore RM, Yaghmai V, Newmark GM, Berlin JW, Miller FH. Imaging benign and malignant disease of the gallbladder. RCNA 2002;40(6):1307 23. [3] Coopersberg PL, et al. Imaging of the gallbladder. Radiology 1987;163:605 13. [4] Ralls PW, Colletti PM, Lapin SA, et al. Real-time sonography in suspected acute cholecystitis. Radiology 1985;155:767 71. [5] Laing FC, Jeffrey Jr RB. Choledocholithiasis and cystic duct obstruction: difficult ultrasonographic diagnosis. Radiology 1983;146:475 9. [6] Hough DM, Glazebrook KN, Paulson ER, et al. Value of prone positioning in the ultrasonographic diagnosis of gallstones: prospective study. J Ultrasound Med 2000;19:633 8. [7] Choudry S, Gorman B, Charboneau JW, et al. Comparison of tissue harmonic imaging with conventional us in abdominal disease. Radiographics 2000;20: 1127 35. [8] Hong HS, Han JK, Kim TK, et al. Ultrasonic evaluation of the gallbladder. J Ultrasound Med 2001;20: 35 41. [9] Teefey SA, Baron RL, Bigler SA. Sonography of the gallbladder: significance of striated (layered) thickening of the gallbladder wall. AJR Am J Roentgenol 1991;156:945 7. [10] Teefey SA, Baron RL, Radke HM, et al. Gangrenous cholecystitis: new observations on sonography. J Ultrasound Med 1991;10:603 6. [11] Kalliafas S, Ziegler DW, Flancbaum L, et al. Acute acalculous cholecystitis: incidence, risk factors, diagnosis, and outcome. Am Surg 1998;64(5):471 5. [12] Cornwell EE, Rodriguez A, Mirvis SE, et al. Acute acalculous cholecystitis in critically injured patients. Ann Surg 1989;219(1):52 5. [13] Blankenberg F, Wirth R, Jeffrey RB, et al. Computed tomography as an adjunct to ultrasound in the diagnosis of acute acalculous cholecystitis. Gastrointest Radiol 1991;196:149 53. [14] Habib FA, Kolachalam RB, Khilnani R, et al. Role of laparoscopic cholecystectomy in the management of gangrenous cholecystitis. Am J Surg 2001;181: 71 5. [15] Simeone JF, Brink JA, Mueller PR, et al. The sonographic diagnosis of acute gangrenous cholecystitis: importance of the Murphy sign. AJR Am J Roentgenol 1989;152:289 90. [16] Takada T, Yasuda H, Uchiyama K, et al. Pericholecystic abscess: classification of us findings to determine the proper therapy. Radiology 1989;172:693 7. [17] Forsberg L, Andersson R, Hederstrom E, et al. Ultrasonography and gallbladder perforation in acute cholecystitis. Radiology 1988;29(2):203 5.
[18] Bloom RA, Libson E, Lebensart PD, et al. The ultrasound spectrum of emphysematous cholecystitis. J Clin Ultrasound 1989;17(4):251 6. [19] Ralls PW, Jeffrey RB, Kane RA, Robbin M. Ultrasonography. Gastroenterol Clin North Am 2002;31: 801 25. [20] Withers CE, Wilson SR. The liver. In: Rumack CM, Wilson SR, Charboneau JW, editors. 2nd edition. Diagnostic ultrasound, volume 1. St. Louis: Mosby-Year Book; 1998. p. 87 154. [21] Tchelepi H, Ralls PW, Radin R, et al. Sonography of diffuse liver disease. J Ultrasound Med 2002;21: 1023 32. [22] Ralls PW. Inflammatory disease of the liver. Clin Liver Dis 2002;6(1):203 25. [23] Usta IM, Barton JR, Amon EA, et al. Obstetrics: acute fatty liver of pregnancy. An experience in the diagnosis and management of fourteen cases. Am J Obstet Gynecol 1994;171(5):1342 7. [24] Castro MA, Fassett MJ, Reynolds TB, et al. Reversible peripartum liver failure: a new perspective on the diagnosis, treatment, and cause of acute fatty liver pregnancy, based on 28 consecutive cases. Am J Obstet Gynecol 1999;181(2):389 95. [25] Hung CH, Changchien CS, Lu SN, et al. Sonographic features of hepatic adenomas with pathologic correlation. Abdom Imaging 2001;26(5):500 6. [26] Terkivatan T, de Witt J, de Man RA, et al. Indications and long-term outcome of treatment for benign hepatic tumors: a critical appraisal. Arch Surg 2001;136(9): 1033 8. [27] Balthazar EJ, Gollapudi P. Septic thrombophlebitis of the mesenteric and portal veins: CT imaging. J Comput Assist Tomogr 2000;24(5):755 60. [28] Grigg A, Gibson R, Bardy P, et al. Acute portal vein thrombosis after autologous stem cell transplantation. Bone Marrow Transplant 1996;18:949 53. [29] Sheen CL, Lampareli H, Milne A, et al. Clinical features, diagnosis and outcome of acute portal vein thrombosis. QJM 2000;93(8):531 4. [30] Zwiebel WJ. Sonographic diagnosis of hepatic vascular disorders. Semin Ultrasound CT MR 1995;16(1): 34 8. [31] Grant EG, Schiller VL, Millener P, et al. Color Doppler imaging of the hepatic vasculature. AJR AM J Roentgenol 1992;159(5):943 50. [32] Millener P, Grant EG, Rose S, et al. Color Doppler imaging findings in patients with Budd-Chiari syndrome: correlation with venographic findings. AJR Am J Roentgenol 1993;161(2):307 12. [33] Ralls PW, Johnson MB, Radin DR, et al. Budd-Chiari syndrome: detection with color Doppler sonography. AJR Am J Roentgenol 1992;159(1):113 6. [34] Didier M, Vasile V, Menu Y, et al. Budd-Chiari syndrome: dynamic CT. Radiology 1987;165(2):409 13. [35] Noone TC, Semekla RC, Woosley JT, et al. Case report: US and MR findings in acute Budd-Chiari syndrome with histopathologic correlation. J Comput Assist Tomogr 1996;29(5):819 22.
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Venous protocols, techniques, and interpretations of the upper and lower extremities
James D. Fraser, MDa,*, David R. Anderson, MDb
Department of Diagnostic Radiology, Dalhousie University, Queen Elizabeth II Health Sciences Centre, 3rd Floor, Victoria Building, 1278 Tower Road, Halifax, Nova Scotia, Canada B3H 2Y9 b Division of Hematology, Department of Medicine, Dalhousie University, Queen Elizabeth II Health Sciences Centre, Victoria General Site, 4th Floor, Bethune Building, 1278 Tower Road, Halifax, Nova Scotia, Canada B3H 2Y9
a
Deep venous thrombosis (DVT) and pulmonary embolism (PE), collectively known as venous thromboembolism, are common problems and are frequently in the differential diagnosis of patients presenting to the emergency department and in the acute care setting. In the United States, the annual combined incidence of DVT and PE is at least 70 per 100,000 individuals [1,2]. Clinical signs and symptoms of both of these entities are nonspecific and it is important to perform objective testing to confirm the diagnosis and initiate appropriate therapy. This approach leads to a demand for emergent diagnostic studies. Compression ultrasonography (CUS) is the diagnostic procedure of choice for the assessment of patients with suspected DVT. It has been shown to be highly sensitive and specific for the diagnosis of DVT, particularly in the lower extremities in symptomatic patients. Bilateral leg CUS combined with assessment of the clinical pretest probability and D-dimer testing has also been shown safely to reduce the need for pulmonary angiography in patients with suspected PE. This article reviews the clinical indications, diagnostic techniques, and interpretation of CUS for the assessment of DVT in the upper and lower extremities and evaluates the role of CUS in the assessment of patients with suspected PE.
Clinical presentations Patients who eventually require assessment for potential venous thromboembolic disease may present with symptoms suggestive of DVT of the upper or lower extremity, PE, or both. Most commonly, DVT begins in the veins of the calf and moves proximally with time. Patients who present with acute calfpopliteal vein thrombosis experience pain and swelling in the calf of one leg, which is exacerbated with ambulation and improved with rest. There may be associated warmth, redness, and tenderness in the calf area [3]. Over time, these symptoms tend to become more severe and may progress proximally to the popliteal fossa and into the medial thigh area. On average, these patients symptoms persist for about 7 days before presenting for medical assessment [4,5]. Less than 20% of patients who are confirmed to have lower-extremity DVT have thrombi isolated to the calf veins. In approximately 10% of patients with lowerextremity DVT, the thrombus is isolated in the iliofemoral region (Fig. 1) [6]. These patients initially present with symptoms of pain in the buttock or groin region, which over time extend to the medial thigh and cause swelling and dusky discoloration of the proximal leg. Superficial veins in the groin and proximal thigh become prominent because of venous engorgement [7]. Iliofemoral disease is a common presentation of DVT during pregnancy with over 90% occurring on the left side usually caused by extrinsic compression of the left iliac vein. Iliofe-
* Corresponding author. E-mail address: J.D.Fraser@Dal.Ca (J.D. Fraser).
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Fig. 1. Iliofemoral DVT. A 35-year-old pregnant woman with isolated iliofemoral DVT, who presented with left buttock pain. (A) Longitudinal image with color flow Doppler shows a small amount of spontaneous venous flow around the thrombus (T). (B) A transverse image of the iliac with compression was obtained with the maximum compressed anteroposterior diameter measured. Normal compressibility of the (C) superficial femoral vein and (D) popliteal veins (arrowheads), which are free of thrombus. Arrowheads in (A) and (B) delineate the left iliac vein. The arrows in (C) and (D) designate the accompanying artery. The asterisk in (C) denotes the deep femoral artery branch. Note the superficial position of the vein relative to the artery in the popliteal fossa.
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Fig. 1 (continued).
moral DVT is associated with pelvic masses, recent pelvic surgery, oral contraceptive use, and the antiphospholipid antibody syndrome. In contrast, patients presenting with upper-extremity DVT (Fig. 2) usually have thrombosis initiating in the proximal veins (subclavian and brachiocephalic). Pain and swelling of the proximal arm and superficial vein distention in the upper chest and proximal arm are commonly seen. Functional impairment also may be present. Upper-extremity DVT most commonly occurs in patients with malignancy and incidence is much higher when they have indwelling central venous catheters. It occasionally occurs in otherwise healthy individuals or following strenuous upperextremity exercise, such as weight lifting [8]. Patients with acute PE may present with dyspnea, pleuritic chest pain, dizziness, and loss of consciousness with or without symptoms of DVT. Tachypnea, tachycardia, and hypotension may be noted on physical examination. The range of presentation of PE is great, from minimal chest symptoms to life-threatening shock.
The role of ultrasound in the evaluation of thromboembolic disease Because of the nonspecific nature of the presentation of venous thromboembolic disease, clinical assessment is certainly not sufficient to make a diagnosis. Given the possible serious consequences of a misdiagnosis, objective testing for DVT and PE is crucial. In the lower extremities, CUS is the method of choice to evaluate patients with symptoms suspected to be DVT. The sensitivity and specificity exceeds 97% for the diagnosis of DVT involving the proximal
leg veins. Accuracy studies using CUS for evaluation of the calf veins have been relatively few and have demonstrated much greater variation. The range of sensitivities varies between 11% and 100%, whereas the specificity ranges between 90% and 100% [9 12]. A meta-analysis of methodologically high-quality studies reported the sensitivity of CUS for the diagnosis of DVT isolated to the calf to be 73% [11]. The rate of technically inadequate studies has been reported to be much higher than those for the evaluation of proximal DVT (ie, in the range of 20% 40%) [12,13]. In contrast to patients with suspected DVT of the lower extremities, the validity of ultrasound for the evaluation of upper-extremity DVT is less well established. In a recent systematic review of the sensitivity and specificity of ultrasonography in the diagnosis of upper-extremity DVT, Mustafa et al [14] found only six original prospective studies, only one of which met their predefined criteria for adequately determining sensitivity and specificity and included a total of 58 patients [8]. The sensitivity of duplex ultrasound from this review ranged from 56% to 100% with a specificity ranging from 94% to 100%. None of these studies evaluated the safety of withholding anticoagulation therapy in a patient with a negative result on ultrasound evaluation who did not undergo further testing and concluded that the safety of this approach is uncertain [14]. More recently in a prospective study published in 2002 comparing color Doppler with contrast venography in 126 patients, Baarslag et al [15] reported a sensitivity and specificity of 82%. He also noted that incompressibility of the vein during ultrasound correlated well with thrombus, whereas only 50% of isolated flow-related abnormalities proved to be thrombus-related. He concluded that patients with isolated flow abnormal-
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Fig. 2. Upper-extremity DVT. Cancer patient who developed a painful swollen right arm secondary to extensive DVT of the upper extremity. (A) Longitudinal color flow image of the internal jugular vein with spontaneous flow above the thrombus. (B) Thrombus (arrow) can be seen within the distal jugular vein (arrowheads). (C) Clot is seen (arrowheads) extending down to the confluence with the subclavian vein (arrows). (D) Color flow Doppler demonstrates complete occlusion of the subclavian vein (arrowheads). The presence of clot in the axillary (arrowhead) vein (E) and basilic vein (arrowhead) (F) is confirmed because of the inability to compress the vein in the transverse plane. The arrows denote the associated arteries.
ities on duplex color ultrasound should have contrast venography performed for further evaluation. The optimal strategy to diagnose PE remains controversial. Spiral CT and ventilation-perfusion scanning are used routinely for the evaluation of patients with suspected PE, but neither test is particularly sensitive. Ultrasonography may be added to diagnostic algorithms for suspected PE to increase the sensitivity of noninvasive testing because most
PEs are believed to originate in the veins of the legs. Patients with nondiagnostic pulmonary investigation may be confirmed to have venous thromboembolism by leg ultrasonography and thereby avoid the need for angiography [16]. A definitive diagnosis or exclusion of PE may not be possible at the initial presentation using noninvasive testing. Most cases of DVT (approximately 90%) start in the calf and rarely cause clinically important PE unless they
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Fig. 2 (continued).
extend into the proximal deep venous system. Eighty percent of clots isolated to the calf are asymptomatic; however, if left untreated approximately 25% extend to involve the proximal veins. This usually occurs within the first week or so after presentation. Seventy-five percent of patients diagnosed with PE have DVT, two thirds of which are located in the proximal veins (Fig. 3). Up to one-quarter of patients with symptomatic PE have clinical evidence of DVT [17]. Given this information, various algorithms have been developed that incorporate the use of CUS in the work-up of patients with suspected PE (Fig. 4).
Clinical assessment and the use of D-dimer Clinical assessment Although the clinical presentation of DVT is nonspecific and clinical assessment alone is unreliable, recent studies have shown that with explicit clinical criteria, patients can be categorized accurately into high, moderate, or low pretest probability groups based solely on a clinical evaluation [18]. These criteria combine the signs and risk factors for DVT and take into consideration the likelihood of an
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Fig. 2 (continued).
alternate diagnosis as the cause for the patients presentation. A simple, nine-point clinical criteria scoring system has been developed to determine the pretest probability for DVT (Table 1) [19]. Using such criteria, patients with a high pretest probability have a greater than 75% prevalence of DVT confirmed by objective testing. Patients in whom the diagnosis of DVT cannot be excluded on clinical grounds but who have a low pretest probability have less than a 5% prevalence of DVT. The use of this clinical categorization tool has proved to be a valuable adjunct to noninvasive testing for the evaluation of patients with suspected DVT and PE [16,20,21].
D-dimer Several serologic markers of thrombosis have been investigated for their predictive value in the diagnosis of DVT. The test that has emerged as the most useful is the D-dimer test. D-dimer represents a breakdown product of the cross-linked fibrin clot. Several D-dimer assays have been validated to be sensitive but nonspecific markers of DVT and PE, indicating that a positive test has a low predictive value but a negative test has a reported negative predictive value of more than 97% [16,22 29]. Combinations of clinical assessment and D-dimer
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Fig. 3. Lower-extremity DVT with PE. Patient presenting with shortness of breath and chest pain who underwent chest CT as per PE protocol. (A) It revealed bilateral pulmonary emboli (arrowheads). CUS of the legs confirmed DVT involving the popliteal and superficial femoral veins (arrowheads) to the mid thigh (B,C) with normal venous flow and no clot present within the superficial femoral veins (arrowheads) above the mid thigh (D). Arrows in (B) and (C) designate the accompanying arteries.
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Fig. 3 (continued).
results have been shown safely to reduce or eliminate the need for noninvasive testing in certain patient groups [30,31]. For example, patients with a low suspicion of DVT or PE but in whom a diagnosis cannot be excluded on clinical assessment alone may safely avoid the need for radiographic imaging on the basis of a negative D-dimer study (see Figs. 4 6). Ddimer is less useful for excluding venous thromboembolism in hospital patients, particularly those having had major surgery or trauma in whom the test is highly likely to be positive [32]. A variety of D-dimer assays have been validated for diagnostic testing for venous thromboembolism. The accuracy parameters of these assays (sensitivity, specificity) vary and physicians need to be aware of these and of the validated laboratory cut-off points for defining a positive and negative test.
Non-diagnostic Ventilation Perfusion (VQ)/ Computerized axial Tomography (CT) Scan Bilateral Compression Ultrasound (CUS)
Ultrasound technique for the evaluation of deep venous thrombosis of the extremities Lower extremities The venous anatomy of the lower extremity is shown in Fig. 7. CUS of the deep venous system of the lower extremities is performed with the patient in the supine position ideally with the head elevated
Table 1 Clinical evaluation table for predicting pretest probability of deep vein thrombosis Clinical characteristics Active cancer (treatment ongoing, within previous 6 mo or palliative) Paralysis, paresis, or recent plaster immobilization of the lower extremities Recently bedridden > 3 d or major surgery within 12 wk requiring general or regional anesthesia Localized tenderness along the distribution of the deep venous system Entire leg swollen Calf swelling 3 cm larger than asymptomatic side (measured 10 cm below tibial tuberosity) Pitting edema confined to the symptomatic leg Collateral superficial veins (nonvaricose) Alternative diagnosis at least as likely as deep vein thrombosis Score 1 1 1
1 1 1 1 1 2
Pretest Probability (PTP) + D-dimer (DD) Low PTP or - DD PE excluded Mod/High PTP and + DD +
Pulmonary angiogram or 1 wk CUS
Treat for PE
Fig. 4. Algorithm for investigation of patients with suspected PE. CUS, compression ultrasound; DD, D-dimer; PE, pulmonary embolism; PTP, pretest probability.
A score of 3 or higher indicates a high probability of deep vein thrombosis; 1 or 2, a moderate probability: and 0 or lower, a low probability. In patients with symptoms in both legs, the more symptomatic leg is used.

Clinically Suspected Deep Vein Thrombosis (DVT) Pretest Probability (PTP) Low + D-dimer (DD) DD/PTP Low PTP or - DD Mod/High PTP and + DD + Compression Ultrasound (CUS) Moderate/High
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DVT Excluded
1 wk CUS
Treat for DVT
Fig. 5. Algorithm for clinically suspected DVT. CUS, compression ultrasound; DD, D-dimer; DVT, deep vein thrombosis; PTP, pretest probability.
20 to 30 degrees to promote venous pooling and distention of the veins. A linear transducer with a frequency in the 5- to 10-MHz range is used, ideally with duplex and color Doppler capability, although these are not required but can be helpful in localizing the vessels and characterizing their flow. The leg is rotated externally and flexed slightly at the knee. The transducer is placed transversely in the groin area to identify the common femoral vein just medial to the common femoral artery. Gentle pressure is applied to the vessels with the transducer and in the absence of DVT, the lumen of the vein should collapse with complete apposition of the anterior and posterior walls (see Fig. 1C, D). In the presence of DVT, the lumen does not collapse completely even with enough pressure to occlude the adjacent artery (Fig. 8). This compression is performed at 1-cm intervals moving down the leg following the common femoral vein, superficial femoral vein, and popliteal vein until it divides into the three calf branches at the popliteal trifurcation. Compression of the veins within the muscular adductor (Hunters) canal is often difficult and visualization limited because of the depth of the vein. This can usually be overcome by placing one hand underneath the medial aspect of the distal thigh and compressing the vein between the fingers and the transducer. This not only aids in compressing the vein but also brings the vein closer to the transducer head, allowing better visualization. Scanning along the axis of the vein is often advantageous for following the course of the vein and for assessing flow (see Figs. 2A, 3D). It is important, however, to confirm compressibility in the transverse
plane; compression in the longitudinal plane is unreliable because the transducer may slide off the vessel, possibly resulting in a false-negative interpretation. In a mobile patient, the popliteal vein is assessed most easily with the patient in the lateral decubitus or prone position with the knee passively flexed to approximately 10 to 15 degrees to avoid collapse of the vein. Very often the patient is not able to move from the supine position but the popliteal vein can usually be assessed adequately by lifting the affected leg with a hand sufficiently under the distal thigh to place the transducer behind the knee. The popliteal vein is superficial to the popliteal artery (see Fig. 1D) in the popliteal fossa and can be compressed easily by the extended knee. It is important to keep the knee slightly flexed while interrogating the popliteal vein. There remains controversy over the value of performing CUS of the calf veins if the more proximal veins are normal. Approximately 10% to 20% of patients with symptomatic DVT have thrombus isolated to the calf veins of, which 20% to 30% eventually extend into the proximal venous system [33,34]. The positive predictive value of CUS for detecting DVT in the calf is significantly lower than it is for proximal DVT, and there are a relatively large number of cases in which the studies are considered nondiagnostic or inadequate. Reported rates of nondiagnostic studies vary in the literature from 9.3% to 82.7%. Gottlieb et al [35] had a nondiagnostic rate of 41% for the evaluation of calf veins. The same study found no significant difference in adverse outcomes in patients undergoing a protocol in which the deep calf veins were routinely evaluated or a protocol in which the calf was evaluated only if physical signs or symptoms were present.
Clinically Suspected DVT Pretest Probability (PTP) Low + D-dimer (DD) DD/PTP Low PTP or - DD Mod/High PTP and + DD + Compression Ultrasound (CUS) Moderate/High
DVT Excluded
Venogram
Treat for DVT
Fig. 6. Algorithm for suspected DVT in the upper extremity. CUS, compression ultrasound; DD, D-dimer; DVT, deep vein thrombosis; PTP, pretest probability.
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Inferior vena cava Common iliac vein External iliac vein Common femoral vein
Superficial femoral vein Great saphenous vein (superficial)
Popliteal vein Popliteal vein Anterior tibial vein Peroneal vein Anterior tibial vein Peroneal vein Small Saphenous (superficial) Posterior tibial vein
Fig. 7. Diagrammatic representation of the veins of the lower extremity.
The authors have previously described the technique for the evaluation of the calf veins [1]; however, their present protocols for the evaluation of patients with suspected thromboembolic disease do not include evaluation of the calf and the technique is not discussed in this article. It should be stressed, however, that when assessing the proximal venous system, one should ensure that the examination includes the distal popliteal vein all the way down to its trifurcation point to have the highest possible sensitivity for DVT. In addition, if there is focal tenderness or swelling within the calf region, it is useful to scan this area to evaluate for nonvenous focal pathology,
such as a hematoma, which might explain the patients symptoms. Upper extremities The venous anatomy of the upper extremity is shown in (Fig. 9). The technique for evaluating the upper extremities for DVT is similar to that for the lower extremities; however, compression of the deep venous system is more limited particularly in the area where the subclavian vein passes beneath the clavicle. Because of this limitation, technical modifications are required, such as the use of adjunctive procedures
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and the findings of Doppler and color flow Doppler analysis (see Fig. 2). Once again, a linear transducer with a frequency in the 5- to 10-MHz range with Doppler or color flow Doppler is preferable. With the patient in the supine position, the head is tilted slightly away from the side of interrogation. It is often easiest to begin by evaluating the internal jugular vein, following this down to the confluence with the subclavian vein (see Fig. 2C), which is located under the proximal third of the clavicle, and is best visualized by placing the transducer longitudinally along the
course of the vessel just below the clavicle and angling it slightly cephalad. The vein can be differentiated from the adjacent artery by its generally larger size, lack of internal pulsations, and its vascular flow pattern as assessed by Doppler. Attempts to compress the vein with the transducer in the transverse plain often fail because of the presence of the clavicle. Attempts should then be made to compress the vein with the transducer along the length of the vessel. If compression is not possible, one must evaluate with spectral or color flow Doppler to determine if the lack
Fig. 8. Extensive lower-extremity DVT involving the iliac vein. Patient with painful swollen left leg with extensive DVT involving the popliteal vein (A) and extending up to involve the superficial femoral veins (not shown), CFV (B), and the iliac vein (C) (arrowheads), all of which are not compressible despite sufficient pressure to partially compress the adjacent artery (arrows).
290
Fig. 8 (continued).
of compressibility is caused by thrombus or by overlying structures preventing adequate force to be transmitted to the vein. The subclavian vein is followed distally to the axillary, cephalic, brachial, and basilic veins, which are assessed with transverse compression similar to the evaluation of the lower-extremity veins (see Fig. 2E, F). Assessment of the axillary, brachial, and basilic veins is performed using an axillary approach by raising the arm. High in the axilla, the vein is superficial to the artery [36]. In such areas as the subclavian where the vein may not be accessible to com-
pression and color Doppler is used for assessment of patency, it is important to pay close attention to the color flow gain settings to avoid oversaturation, which may obscure small intraluminal clots or areas of incomplete thrombosis [37]. Similar to assessment of the leg, if thrombosis is discovered it is important to document the full extent of the disease including evaluation of the contralateral neck and proximal arm because this information may be important for subsequent evaluation for progression or recurrence of disease or for the effectiveness of treatment.
Internal jugular vein External jugular vein Subclavian vein BCP vein SVC Axillary vein Cephalic vein Brachial vein Basalic vein
Median cubital vein
Fig. 9. Diagrammatic representation of the veins of the upper limb and thoracic inlet. BCP vein, brachiocephalic vein; SVC, superior vena cava.
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Diagnostic criteria for the diagnosis of deep venous thrombosis of the extremity In the absence of DVT, the vein being evaluated should collapse and the walls of the vein should be completely apposed with less pressure than required to occlude the adjacent artery. The inability completely to compress the vein lumen is the principal criterion for the diagnosis of DVT [6,7,38 40]. Other adjunctive findings are often observed in the presence of DVT but have much poorer sensitivities and specificities. These include distention of the involved vein in acute DVT and the absence of or reduced spontaneous blood flow on Doppler evaluation (see Fig. 8). In patients with incomplete obstruction, there is usually loss of the normal phasic respiratory venous flow pattern, often giving a reduced continuous flow pattern (monophasic flow), which is minimally affected by the Valsalvas maneuver or attempts to augment flow, such as gently squeezing the calf. The monophasic pattern indicates some degree of obstruction to venous flow returning to the right side of the heart and should increase ones suspicion for the presence of DVT. This pattern can also be seen, however, in the absence of thrombosis when sufficient external compression on the deep venous system exists. The appearance of the vein alone is unreliable because acute thrombus is often anechoic mimicking a patent vein and internal echoes are not infrequently seen within a patent vein lumen in the presence of slowflowing blood. The ultrasound appearance of DVT changes over time with the clot retracting and becoming more echogenic. The vein wall in the area of previous thrombus may become thickened, echogenic, and resistant to compression [41]. Over a 12- to 24-month period, only about 50% of patients have complete resolution of thrombus and normal compressibility of the proximal leg veins [41 43]. Although the ultrasound appearance in patients with previous DVT may be suggestive of chronic disease, it is usually difficult to rule out acute or chronic disease unless the patient has a posttreatment baseline study available for comparison. In the latter setting, unequivocal evidence of thrombosis in a venous segment previously demonstrated to be free of disease or increase in compressed venous diameter greater than 4 mm from a baseline study may be considered diagnostic of recurrent DVT in the appropriate clinical setting. Compression ultrasound occasionally diagnoses an alternative cause for pain and swelling of the lower extremity in the absence of DVT, such as a ruptured Bakers cyst or a calf hematoma (Fig. 10).
Adjunctive procedures, pitfalls, and limitations There are a number of procedures that may be helpful when examining a patient whose deep venous system is difficult to localize. Placing the patient in a position that promotes venous pooling in the extremity of interest distends the veins, making them easier to localize and assess. Similarly, having the patient perform a Valsalvas maneuver also results in venous distention [7]. When duplex or color flow Doppler is available, it can be used to localize the venous system based on its flow characteristics. The presence of spontaneous flow, normal respiratory phasic flow variation, and flow augmentation with manual compression of the limb suggests patency. It is, however, important to remember that spontaneous flow and flow augmentation can occur in the presence of incomplete thrombosis (see Fig. 1A), adequate collateralization, and in patients with duplication of the deep venous system. Augmentation may even force blood around an area of complete thrombosis and should probably be used only to aid in the localization of venous segments that are difficult to visualize. Patients in whom adequate compression studies of the proximal deep venous system may be difficult to perform include obese patients, patients with tense swollen extremities, burn patients, and patients with recent surgery in the area of interest. These limitations seldom preclude evaluation of the areas where DVT most commonly occurs (ie, the common femoral and popliteal veins). Pitfalls occasionally encountered include missing a thrombosed vein segment when a nonthrombosed duplicated vein segment is present (Fig. 11) and occasionally mistaking a large collateral for a patent venous segment when thrombosis is present in the underlying vein. The latter can usually be avoided by confirming the normal course of the vein in relationship to the adjacent artery.
Suggested protocols Diagnosis of acute deep venous thrombosis of the lower extremities To maximize patient safety and the efficiency of resources, clinicians should be encouraged to follow validated nomograms that encompass consideration of clinical probability, D-dimer testing, and venous ultrasound imaging. The algorithm outlined in Fig. 5 has been demonstrated to be safe for patients with low pretest probability for DVT because only less than 1% of these patients, if left untreated, develop
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Fig. 11. Duplicated superficial femoral and popliteal veins. Patient with symptomatic DVT who has duplication of the popliteal veins (A) and the superficial femoral veins (B) of the leg. Noncompressible clot is seen within the more superficial of the two deep veins at both levels (2), with the deeper vein (1) demonstrating normal compressibility (A,B). Duplication of the artery within the popliteal fossa is appreciated only on the color Doppler images with a more superficial artery (A) and a deeper
objective evidence of DVT or PE in follow-up over a 3-month period. The ultrasound examination in this algorithm is restricted to the proximal venous system. Pretest probability should be judged either by experienced clinicians or by using a validated clinical model. D-dimer testing should be done using a validated assay for the diagnosis of venous thromboembolism.
Using this approach, most patients can have a diagnosis of DVT confirmed or excluded on initial testing. Recognizing that a small proportion of patients may have DVT isolated to the calf veins, it is advisable that these higher-risk patients as defined by moderate or high pretest probability and positive D-dimer should have the ultrasound repeated approximately 1 week following their initial evaluation.
Fig. 10. Calf hematoma. Patient who presented to the emergency department with a painful swollen calf area suspicious for DVT. The deep venous system (arrowheads) within the common femoral (A) and popliteal regions (B) demonstrates patency with normal compressibility. A hematoma was discovered (arrows) between the heads of the gastrocnemius and the soleus muscles (C), explaining the patients calf pain and tenderness.
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This is to detect patients whose calf DVT may have extended to the proximal venous system, which has thereby increased the risk of PE. Diagnosis of deep venous thrombosis of the upper extremities Unfortunately, validated diagnostic algorithms are not available for patients presenting with DVT of the upper extremity. There also are no models to assist clinicians in determining pretest probability. Fig. 6 contains an algorithm based on one of the principles of DVT investigation of the lower extremities with the recognition that CUS is less sensitive in the evaluation of the upper extremities. This algorithm is based on the opinion and clinical experience of the authors. It is their opinion that venography should be performed in patients in whom the clinical suspicion of upper extremity DVT is moderate or high, D-dimer is positive, and the ultrasound is negative. As a second option, a repeat ultrasound may be performed 1 week later; however, the safety of this approach has not been demonstrated in controlled trials.
ography, particularly if the clinical pretest probability is high.
Other considerations Frequently, patients with suspected venous thromboembolism present at inopportune times when immediate access to diagnostic testing may not be available. With the advent of low-molecular-weight heparin, diagnostic testing can be scheduled safely within 24 hours of presentation. Such patients may receive a single dose of subcutaneous low-molecularweight heparin designed to treat DVT or PE while awaiting diagnostic testing [16,30]. The only restriction to this regimen is that patients are at increased risk of major bleeding.
References
[1] Fraser JD, Anderson DR. Deep venous thrombosis: recent advances and optimal investigation with US. Radiology 1999;211:9 24. [2] Anderson DR, Wells PS. Improvements in the diagnostic approach for patients with suspected deep vein thrombosis for pulmonary embolism. Thromb Haemost 1999;82:878 86. [3] Cogo A, Lensing AWA, Prandoni P, Hirsh J. Distribution of venous thrombosis in patients with symptomatic deep vein thrombosis: implications for simplifying the diagnostic process with compression ultrasound. Arch Intern Med 1993;153:2777 80. [4] Birdwell BG, Raskob GE, Whitsett TL, et al. The clinical validity of normal compression ultrasonography in outpatients suspected of having deep venous thrombosis. Ann Intern Med 1998;128:1 7. [5] DeBaleu ME, Ochner A. Phlegmasia cerulea dolens associated with thrombophlebitis: case reports and review of the literature. Surgery 1966;59:997 1007. [6] Cronan JJ. Venous thromboembolic disease: the role of US. Radiology 1993;186:619 30. [7] Cogo A, Lensing AWA, Wells P, Prandoni P, Buller HR. Noninvasive objective tests for the diagnosis of clinically suspected deep-vein thrombosis. Haemostasis 1995;25:27 39. [8] Prandoni P, Polistena P, Bernardi E, et al. Upperextremity deep vein thrombosis: risk factors, diagnosis and complications. Arch Intern Med 1997;157:57 62. [9] Simons GR, Skibo LK, Polak JF. Utility of leg ultrasonography in suspected symptomatic isolated calf deep venous thrombosis. Am J Med 1995;99:43 7. [10] Atri M, Herba MJ, Reinhold C, et al. Accuracy of sonography in the evaluation of calf deep vein thrombosis in both postoperative surveillance and symptomatic patients. AJR Am J Roentgenol 1996;166:1361 7. [11] Kearon C, Julian JA, Newman TE, Ginsberg JS.
Diagnosis of pulmonary embolism Ultrasonography is particularly valuable in the investigation of patients in whom PE is not conclusively confirmed or refuted by other radiographic imaging techniques. Patients with high-probability ventilation-perfusion lung scans or positive spiral CT may be treated for PE. Those with normal ventilation-perfusion scans may be considered to have PE excluded. For patients with abnormal ventilation-perfusion scans that are not high probability or with normal spiral CT scans, however, a significant proportion may have underlying PE. It is recommended that these patients undergo bilateral ultrasound imaging of the proximal venous system of the lower extremities. Those with positive studies may be treated for venous thromboembolism. Those patients with negative ultrasound investigations have a much lower likelihood of having PE responsible for their symptoms. Clinical trials have demonstrated that patients with suspected PEs who have the combination of negative spiral CT and bilateral CUS may safely have the diagnosis of PE excluded [44 46]. Patients with non high-probability ventilation-perfusion scans with normal spiral CT may have the diagnosis of PE excluded if clinical pretest probability is low or the D-dimer is negative. Other patients should be considered for 1-week follow-up CUS or pulmonary angi-
J.D. Fraser, D.R. Anderson / Radiol Clin N Am 42 (2004) 279296 Noninvasive diagnosis of deep venous thrombosis: McMaster diagnostic imaging practice guidelines initiative. Ann Intern Med 1998;128:663 77. Rose SC, Zwiebel WJ, Nelson BD, et al. Symptomatic lower extremity deep venous thrombosis: accuracy, limitations, and role of color duplex flow imaging in diagnosis. Radiology 1990;175:639 44. Noren A, Ottosson E, Rosfors S. Is it safe to withhold anticoagulation based on a single negative color duplex examination in patients with suspected deep venous thrombosis? A prospective 3-month follow-up study. Angiology 2002;53:521 7. Mustafa BO, Rathbun SW, Whitsett TL, Raskob GE. Sensitivity and specificity of ultrasonography in the diagnosis of upper extremity deep vein thrombosis: a systematic review. Arch Intern Med 2002;162:401 4. Baarslag H-J, van Beek EJR, Koopman MWM, Reekers JA. Prospective study of color duplex ultrasonography compared with contrast venography in patients suspected of having deep venous thrombosis of the upper extremities. Ann Intern Med 2002;136:865 72. Wells PS, Anderson DR, Rodger M, Stiell I, Dreyer J, Barnes D, et al. Excluding pulmonary embolism at the bedside without diagnostic imaging: management of patients with suspected pulmonary embolism presenting to the emergency department using a simple clinical model and D-dimer. Ann Intern Med 2001; 135:98 107. Kearon C. Natural history of venous thromboembolism. Circulation 2003;107:I22 30. Wells PS, Hirsh J, Anderson DR, et al. Accuracy of clinical assessment of deep-vein thrombosis. Lancet 1995;345:1326 30. Anderson DR, Wells PS, Stiell I, MacLeod B, Simms M, Gray L, et al. Use of a clinical diagnosis model to safely avoid the need for urgent radiological investigation. Arch Intern Med 1999;159:477 82. Wells PS, Anderson DR, Bormanis J, et al. Value of assessment of pretest probability of deep-vein thrombosis in clinical management. Lancet 1997;350: 1795 8. Kearon C. Diagnosis of pulmonary embolism. CMAJ 2003;168:183 94. Wells PS, Anderson DR, Rodger M, Forgie M, Kearon C, Kovacs G, et al. Evaluation of D-dimer in the diagnosis of suspected deep-vein thrombosis. N Engl J Med 2003;349:1227 35. Bounameaux H, Cirafici IP, de Moerloose P, et al. Measurement of D-dimer in plasma as diagnostic aid in suspected pulmonary embolism. Lancet 1991;337: 196 200. Turkstra F, van Beek JR, ten Cate JW, Buller HR. Reliable rapid blood test for the exclusion of venous thromboembolism in symptomatic outpatients. Thromb Haemost 1996;76:9 11. Bounameaux H, Schneider PA, Reber G, Moerloose P, Krahenbuhl B. Measurement of plasma D-dimer for diagnosis of deep venous thrombosis. Am J Clin Pathol 1989;91:82 5.
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[26] Boneu B, Bes G, Pelzer H, Sie P, Boccalon H. D-Dimers, thrombin antithrombin III complexes and prothrombin fragment 1 + 2: diagnostic value in clinically suspected deep vein thrombosis. Thromb Haemost 1991;65:28 32. [27] Heaton DC, Billings JD, Hickton CM. Assessment of D-dimer assays for the diagnosis of deep vein thrombosis. J Lab Clin Med 1987;110:588 91. [28] Wells PS, Brill-Edwards P, Stevens P, et al. A novel and rapid whole-blood assay for D-dimer in patients with clinically suspected deep vein thrombosis. Circulation 1995;91:2184 7. [29] Wells PS, Anderson DR, Bormanis J, Guy F, Mitchell M, Lewandowski B. Simpli-RED D-dimer can reduce the diagnostic tests in suspected deep vein thrombosis. Lancet 1998;351:1405 6. [30] Anderson DR, Kovacs MJ, Kovacs G, Stiell I, Mitchell M, Khoury V, et al. Combined use of clinical assessment and D-dimer to improve the management of patients presenting to the emergency department with suspected deep vein thrombosis (The EDITED Study). Journal of Thrombosis and Haemostasis 2003;1:1 7. [31] Anderson DR, Wells PS, Stiell I, MacLeod B, Simms M, Gray L, et al. Management of patients with suspected deep vein thrombosis in the emergency department: combining use of a clinical diagnosis model with D-dimer testing. J Emerg Med 2000;19:225 30. [32] Schutgens REG, Esseboom EU, Haas FJLM, Nieuwenhuis HK, Biesma DH. Usefulness of a semiquantitative D-dimer test for the exclusion of deep venous thrombosis in outpatients. Am J Med 2002;112:617 21. [33] Kakkar VV, Howe CT, Flanc C, Clarke MB. Natural history of postoperative deep-vein thrombosis. Lancet 1969;2:230 2. [34] Lagerstedt CI, Olsson CG, Fagher BO, Oqvist BW, Albrechtsson U. Need for long-term anticoagulant treatment in symptomatic calf-vein thrombosis. Lancet 1985;2:515 8. [35] Gottlieb RH, Voci SL, Syed L, Shyu C, Fultz PJ, Rubens DJ, et al. Randomized prospective study comparing routine versus selective use of sonography of the complete calf in patients with suspected deep venous thrombosis. AJR Am J Roentgenol 2003;180: 241 5. [36] Talbot SR. B-mode evaluation of peripheral veins. Semin Ultrasound CT MR 1988;9:295 319. [37] Machi J, Sigel B, Roberts AB, Kahn MB. Oversaturation of color may obscure small intraluminal partial occlusions in color Doppler imaging. J Ultrasound Med 1994;13:735 41. [38] Lensing AW, Prandoni P, Brandjes D, et al. Detection of deep-vein thrombosis by real-time B-mode ultrasonography. N Engl J Med 1989;320:342 5. [39] Raghavendra BN, Rosen RJ, Lam S, Riles T, Horii SC. Deep venous thrombosis: detection by high-resolution real-time ultrasonography. Radiology 1984;152: 789 93. [40] Raghavendra BN, Horii SC, Hilton S, Sabramanyam BR, Rosen RJ, Lam S. Deep venous thrombosis: detec-
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J.D. Fraser, D.R. Anderson / Radiol Clin N Am 42 (2004) 279296 tion by probe compression of veins. J Ultrasound Med 1986;5:89 95. Cronan JJ, Leen V. Recurrent deep venous thrombosis: limitations of US. Radiology 1989;170:739 42. Prandoni P, Lensing AWA, Cattelan AM, Cogo A, Cuppini S, Ruol A. Outcome of abnormal compression ultrasonography after acute deep venous thrombosis (DVT) and its implications for diagnosis of recurrent DVT [abstract]. Thromb Haemost 1991;66:1175. Killewich LA, Bedford GR, Beach KW, Strandness DE. Spontaneous lysis of deep venous thrombi: rate and outcome. J Vasc Surg 1989;9:89 97. Kearon C. Excluding pulmonary embolism with helical (spiral) computed tomography: evidence is catching up with enthusiasm. CMAJ 2003;168:1430 1. [45] Musset D, Parent F, Meyer G, Maitre S, Girard P, Leroyer C, et al. Diagnostic strategy for patients with suspected pulmonary embolism: a prospective multicentre outcome study. Lancet 2002;360:1914 20. [46] van Strijen MJ, de Monye W, Schiereck J, Kieft GJ, Prins MH, Huisman MV, et al. Single-detector helical computed tomography as the primary diagnostic test in suspected pulmonary embolism: a multicenter clinical management study of 510 patients. Ann Intern Med 2003;138:307 14.
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Sonographic evaluation of first-trimester bleeding

Raj Mohan Paspulati, MD*, Shweta Bhatt, DMRD, DMRE, Sherif Nour, MD
Department of Radiology, University Hospitals of Cleveland, Case Western Reserve University, 11100 Euclid Avenue, Cleveland, OH 44106, USA
Vaginal bleeding in the first trimester of pregnancy is a common presentation in emergency care facilities. About 25% of all gestations present with vaginal spotting or frank bleeding in the first few weeks of pregnancy; half of these progress into miscarriage or abortion [1]. The acuity of these symptoms may vary from occasional spotting to severe hemorrhage, associated with cramping and abdominal pain. The bleeding often is self-limited and is most likely caused by implantation of the conceptus into the endometrium. The important causes of first-trimester bleeding are spontaneous abortion, ectopic pregnancy, and gestational trophoblastic disease. The clinical assessment of pregnancy outcome is unreliable and ultrasound (US) evaluation combined with quantitative beta human chorionic gonadotropin (b-hCG) is an established diagnostic tool in these patients. This article reviews the role of ultrasonography in the evaluation of patients presenting with first-trimester bleeding.
Sonographic anatomy The uterus is a pear-shaped, muscular organ that varies greatly in size and shape depending on age and prior pregnancies. The normal postpuberty uterus in an adult measures approximately 7.5 to 8 cm in length, 4 to 5 cm in width, and about 2 cm in anteroposterior dimension. The normal cervix is 3.5 to 4 cm in length. The cervix is comprised of internal
* Corresponding author. E-mail address: paspulati@uhrad.com (R.M. Paspulati).
and external cervical os. The internal os is the junction of the uterine cavity and the cervical canal and the external os is the junction of the cervical canal and the vagina. Transvaginal US (TVUS) of the normal myometrium reveals three distinct layers. Arcuate vessels separate the thin outer layer from the thick middle layer, and both layers are homogeneous with the outer layer more hypoechoic relative to the middle layer [2]. The inner layer consists of a thin hypoechoic halo that surrounds the endometrium and corresponds to the junctional zone seen on MR imaging. The endometrial thickness measurements are optimally made on sagittal (long-axis) images of the uterus; this measurement should be performed on the thickest portion of the endometrium excluding the hypoechoic inner myometrium (Fig. 1). The endometrial thickness should be reported as the double thickness measurement [3]. If endometrial fluid is present, its diameter should be omitted; in such cases the endometrial thickness should be reported as the sum of the measurements obtained from the anterior and posterior endometrial walls. An endometrial thickness of 4 to 14 mm is normal in an adult premenopausal woman. Endometrial thickness and appearance vary with the phase of the menstrual cycle [4]. The position of the ovaries is variable but they are usually found in the posterior fold of the broad ligament, posterior and distal to the fallopian tubes. On sonography the ovaries can be localized anterior to the internal iliac vessels. The postpubertal ovary measures approximately 3 cm in length, 2 cm in width, and 1 cm in anteroposterior dimension. The upper limit for normal ovarian volume is highest in young adult women measuring approximately 9.8 to 14 mL and declines with increasing age [5]. Normal
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ler US in early pregnancy, the concept of as low as reasonably achievable is important [7] and the advantages of the Doppler US should outweigh the potentially harmful effects on the conceptus.
Normal first-trimester sonography Scanning in the first trimester may be performed either transabdominally or transvaginally. TVUS is preferred and is the community standard. The firsttrimester milestones are given in Tables 1 and 2. A gestational sac can be identified with TVUS at 5 weeks of gestational age, when it measures 5 mm. The yolk sac should always be seen by TVUS when a gestational sac measures greater than 10 mm and by transabdominal US when the mean sac diameter is greater than 20 mm [8,9]. An embryo with cardiac activity should be seen transvaginally when the gestational sac measures greater than 18 mm, and transabdominally when the gestational sac measures 2.5 cm. These discriminatory criteria should be used as guidelines. If the findings of the US examination are equivocal and the examination is technically difficult, a follow-up examination should be obtained. Gestational sac The blastocyst implants into the endometrium by approximately 23 days of menstrual age [10]. It measures 0.1 mm and is too small to be visualized on TVUS. Demonstration of peritrophoblastic flow by transvaginal color flow Doppler at this focal decidual thickening has improved the diagnostic sensitivity of intrauterine pregnancy (IUP) from 90% with TVUS alone to 99% using transvaginal color flow Doppler [11,12]. The peritrophoblastic flow has a characteristic high-velocity and low-impedance flow caused by shunting of blood from the spiral arteries into the intervillous spaces. According to Emerson et al [11], the peak systolic velocity of peritrophoblastic flow in a normal IUP ranges from 8 to 30 cm/second, before the visualization of the gestational sac. Yeh et al
Fig. 1. Sagittal TVUS of the uterus demonstrates a normal endometrial lining (arrowheads).
fallopian tubes cannot be visualized with current US imaging equipment
Scanning technique Ultrasound evaluation of the female pelvis is conducted with a real-time scanner, preferably using a sector or curvilinear transducer. The scanner is adjusted to operate at the highest clinically appropriate frequency, realizing that there is a trade-off between the resolution and beam penetration. Transabdominal pelvic US is performed with a full bladder using transducer frequencies of 3.5 MHz and above. Adequate distention of the bladder displaces the bowel from the field of view. Transabdominal US gives an initial overview of the uterus, adnexa, and any intra-abdominal free fluid. TVUS is performed with the patients bladder being empty, using a transducer frequency of 5 to 7.5 MHz. TVUS gives detailed information about the uterus and the adnexa. Higher-frequency transvaginal probes can be positioned closer to the pelvic organs resulting in improved spatial resolution and diagnostic accuracy. Currently available transducers of 10 MHz and above can identify the finer details of intrauterine gestation and have greatly contributed to the early diagnosis of abnormal gestation and to the management of firsttrimester bleeding. Color flow Doppler and pulsed Doppler may be added to the examination, as indicated by the gray-scale US findings. It is important to bear in mind that the energy output of Doppler US is substantially higher than that used for imaging and it may have potentially harmful effects on the conceptus [6]. Because of this risk, caution has been expressed over the routine use of Doppler US in early pregnancy evaluation. While performing Dopp-
Table 1 First-trimester scanning milestones Parameter Gestational sac Yolk sac Transabdominal US Transvaginal US Present at 5 wk (5 mm) Always present when GS > 10 mm GS > 18 mm
Always present if GS > 20 mm Cardiac activity GS > 2.5 cm
Abbreviations: GS, gestational sac; US, ultrasound.
R.M. Paspulati et al / Radiol Clin N Am 42 (2004) 297314 Table 2 Land marks of normal first-trimester pregnancy Gestational age 23 d 3.5 4 wk 4 4.5 wk 4.5 5 wk 5 5.5 wk Embryologic change Blastocyst implantation Decidual changes at implantation site Trophoblastic tissue Exocoelomic cavity of the blastocyst Secondary yolk sac Sonographic appearance Blastocyst measures 0.1 mm and is too small to visualize Focal echogenic decidual thickening at implantation site
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5 6 wk 5 6 wk
Embryo Embryonic cardiac activity
High-velocity and low-impedance trophoblastic flow at the implantation site on TVCFD Gestational sac (a sonographic term) is always seen when it measures > 5 mm and the serum b-hCG is between 1000 and 2000 mIU/mL (IRP) Yolk sac is seen as a thin-walled cystic structure within the gestational sac and should always be seen when the GS is > 10 mm; it is the first sign of a true gestational sac before the visualization of embryo Seen as a focal echogenic area adjacent to the yolk sac; should always be seen when the GS is > 18 mm Embryonic cardiac activity should always be seen when the embryo is > 5 mm; normal heart rate ranges from 100 115 beats/min between 5 6 wk of gestation
Abbreviations: CG, human chorionic goradotropin; GS, gestational sac; IRP, international reference preparation; TVCFD, transvaginal color flow Doppler.
[13] described a focal, eccentric, anechoic area in the endometrium caused by the embedded blastocyst as the intradecidual sign. They described this sign as early as 3.5 weeks of menstrual age on transabdominal US and reported a sensitivity rate of 92%, a specificity rate of 100%, and an accuracy rate of 93%. Laing et al [14] used TVUS to demonstrate this sign and found that the overall sensitivity, specificity, and accuracy for the intradecidual sign were only 48%, 66%, and 45%, respectively. With currently available high-frequency transvaginal probes, a gestational sac as small as 2 to 3 mm can be demonstrated at 4 weeks of gestational age [15 17]. On TVUS, the gestational sac is seen as a well-defined fluid-filled cavity with a surrounding hyperechoic rim, embedded eccentrically in the endometrial lining of the fundus or midbody of the uterus (Fig. 2). The sonographic term gestational sac represents the exocoelomic cavity of the blastocyst and the surrounding echogenic rim is caused by the developing chorionic villi and decidual tissue. The echogenic rim should have a minimum thickness of 2 mm and its echogenicity should exceed that of myometrium [1]. The double decidual sac sign of intrauterine gestation was first described in 1982 [18]. The double decidual sac sign consists of two concentric echogenic rings encasing a central anechoic focus that impress on the endometrial stripe. The inner echogenic rim represents the decidua capsularis and chorion laeve, whereas the outer echogenic rim represents the decidua parietalis; these echogenic rims are separated by a thin rim of fluid in the endometrial cavity (Fig. 3). This is a useful sign of IUP between 4 and 6 weeks of gestation. The crown-rump length (CRL)
of the embryo is a more accurate indicator of gestational age than the mean gestational sac diameter. The mean gestational sac diameter should be recorded, however, when an embryo is not identified. Because hCG production and gestational sac growth are related to trophoblastic function, there is excellent correlation of the serum hCG level, sac size, and the stage of pregnancy [19]. Kadar et al [20] first introduced the concept of a discriminatory level of the b subunit of hCG. The range of the serum b-hCG level at which an intrauterine gestational sac is visualized is the discriminatory zone. Although the discriminatory range of b-hCG varies from one laboratory to another, the widely accepted range is from
Fig. 2. Coronal TVUS of the uterus shows a gestational sac with hyperechoic margins (arrow) and endometrial cavity (curved arrow).
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Fig. 3. Double decidual sac sign. (A) Coronal TVUS of the uterus reveals an intrauterine gestational sac (straight arrow), decidua capsularis (curved arrow), decidua parietalis (arrowhead), and effaced endometrial cavity (asterisks). (B) Corresponding line diagram.
1000 to 2000 mIU/mL international reference preparation (IRP) for TVUS and 2400 to 3600 mIU/mL (IRP) for transabdominal US [10]. In normal pregnancy serum b-hCG should double or increase by at least 66% in 48 hours. Yolk sac The first structure to be seen within the gestational sac is the secondary yolk sac, which is a reliable indicator of a true IUP with a positive predictive value of 100%. The primary yolk sac is not seen by US because it shrinks at 4 weeks menstrual age and gradually disappears with the formation of the secondary yolk sac [21]. The secondary yolk sac is first seen on TVUS as a thin-walled cystic structure by the fifth gestational week and is virtually always seen by 5.5 weeks gestational age (Fig. 4) [22]. The yolk sac is round, measures less than 6 mm, and should be visualized by TVUS when a gestational sac measures more than 10 mm [10]. The yolk sac is involved in nutritive, metabolic, hemopoietic, and secretive functions during early embryonic development and organogenesis [23,24]. Abnormalities in its size and appearance are predictors of abnormal gestation [25]. Embryo The embryo should always be visualized by TVUS when the gestational sac measures greater than 18 mm, and transabdominally when the gestational sac measures 2.5 cm (Fig. 5). With the currently
available high-frequency transvaginal transducers, the embryonic disk is initially seen as a focal echogenic area of 1- to 2-mm thickness adjacent to the yolk sac between 5 and 6 weeks of gestational age [26 29]. Embryonic cardiac activity should always be seen when an embryo measures greater than 5 mm. Occasionally the heartbeat may be seen adjacent to the yolk sac even before the embryo is clearly visible.
Fig. 4. TVUS of the uterus demonstrates a yolk sac (thin arrow) outside the amniotic membrane (arrowhead), which has not yet fused with the chorion (curved arrow). Embryo (thick arrow) is seen within the amniotic sac.
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branes before 14 weeks of gestation is considered normal (see Figs. 4 and 5).
Spontaneous abortion Spontaneous abortion is defined as pregnancy terminating before the 20th completed week of gestation. Approximately 80% of spontaneous abortions occur in the first trimester. The causes of spontaneous abortions fall into two categories: genetic and environmental (maternal) as listed next:
Fig. 5. TVUS of the uterus shows a normal embryo and separate amniotic membrane (arrow) in close relation to the embryo. This should not be mistaken for nuchal translucency.
Levi et al [3] suggested a 4-mm CRL cutoff because their study demonstrated cardiac activity in all embryos with a CRL of 4 mm [30]. Other studies demonstrated 5 mm as the discriminatory CRL for detecting cardiac activity [31,32]. Although visualization of a living embryo does not ensure a viable pregnancy, the abortion rate decreases for living embryos as the gestational age increases, with a 0.5% demise rate for living embryos between 6 and 10 mm [33]. If the length of the embryo is less than 5 mm, follow-up US should be performed until the expected CRL exceeds the discriminatory value. Most of the studies reported a heart rate of 100 to 115 beats per minute between 5 and 6 weeks [34 36]. By 9 weeks of gestational age, the mean heart rate increases to about 140 beats per minute. The cardiac activity should be documented by M-mode. Amniotic sac The amniotic sac is formed in the fourth week of gestation between the ectoderm layer and the adjacent trophoblast. Before 6.5 weeks the amniotic membrane is so close to the embryo that the amniotic cavity around the embryo is not easily seen. The diameter of the amniotic cavity is nearly equal to the CRL. Between 5 and 7 weeks of gestational age the embryo is located between the amniotic and yolk sacs. On US, this amniotic sac embryo yolk sac complex appears as two small sacs and is called the double bleb sign [9]. The embryo and the inner amnion grow at a faster rate than the outer chorionic cavity with eventual fusion of the amniotic and chorionic membranes by 16 weeks of gestation [37]. Separation of the amniotic and chorionic mem-
Genetic or fetal causes Trisomy Polyploidy or aneuploidy Translocations Environmental or maternal causes Uterine Congenital uterine anomalies Leiomyoma Intrauterine adhesions or synechiae (Ashermans syndrome) Endocrine Progesterone deficiency (luteal phase defect) Hypothyroidism Diabetes mellitus (poorly controlled) Luteinizing hormone hypersecretion Immunologic Autoimmunity: antiphospholipid syndrome, systemic lupus erythematosus Infections Toxoplasma gondii, Listeria monocytogenes, Chlamydia trachomatis, Ureaplasma urealyticum, Mycoplasma hominis, herpes simplex, Treponema pallidum, Borrelia burgdorferi, Neisseria gonorrhoeae Genetic abnormalities are the most common cause of spontaneous abortions accounting for almost 50% to 60% of cases. Autosomal trisomy is the most frequently identified chromosomal abnormality resulting in first-trimester abortions. The incidence of abortions secondary to chromosomal abnormalities markedly increases after the maternal age of 35 years. The environmental or maternal causes account for a small percentage of spontaneous abortions. These include infection; anatomic defects (maternal mullerian defects); endocrine factors (failure of corpus luteum); immunologic factors (antiphospholipid antibody syndrome); and maternal systemic disease (diabetes mellitus, hypothyroidism). The algorithmic approach to first-trimester bleeding is summarized in Fig. 6.
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First Trimester Ultrasound

Embryo not visualized
MSD > 18MM
MSD < 18MM
YS present
YS absent
MSD < 10MM
MSD > 10MM
ED ED
F/U re: sac growth and embryo 1
B
Embryo visualized
Cardiac activity present
Cardiac activity absent
CRL > 5MM
CRL < 5MM
CRL > 5MM
CRL < 5MM
YS present
YS absent
YS normal
YS abnormal
MSD-CRL > 5MM
MSD-CRL < 5MM
HR N
HR AbN
? F/U 18 wks 1
F/U 2
F/U 2wks re: growth and cardiac activity 1
ED
F/U re: growth and cardiac activity 1
Fig. 6. (A, B) Proposed algorithms for evaluating women with first trimester bleeding. ED, embryonal demise; F/U, follow-up; HR ABN, heart rate abnormal; HR N, heart rate normal; YS, yolk sac. (From McGahan J, Goldberg B. Diagnostic ultrasound: a logical approach. Philadelphia: Lippincott, Williams & Wilkins; 1998; p. 142 3; with permission.)
The most common morphologic finding in early spontaneous abortions is an abnormality of development of the zygote, embryo, early fetus, or the placenta. Spontaneous abortion is clinically classified into threatened, inevitable, missed, incomplete, and complete abortions (Table 3).
Ultrasound findings in abortion The US findings depend on the developmental stage of the pregnancy at which the patient presents with symptoms. Familiarity with normal sonographic landmarks of first-trimester pregnancy is essential
R.M. Paspulati et al / Radiol Clin N Am 42 (2004) 297314 Table 3 Classification of spontaneous abortion Types Threatened abortion Clinical features Vaginal bleeding before 20 wk gestation without cervical dilatation Vaginal bleeding with partial expulsion of products of conception before 20 wk gestation and cervical dilatation Embryonic demise before 20 wk of gestation without expulsion of products of conception; may or may not have vaginal bleeding Vaginal bleeding and expulsion of all products of conception before 20 wk gestation Vaginal bleeding before 20 wk gestation with cervical dilatation US findings
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Incomplete abortion
Depending on the stage of pregnancy, US may show an empty uterus, intrauterine gestational sac with or without an embryo Thick, irregular endometrial lining caused by residual trophoblastic tissue and fluid Embryo without cardiac activity; small size of the embryo for the gestational age (see Fig. 10)
Missed abortion
Complete abortion
Empty uterus
Inevitable abortion
Variable depending on the degree of bleeding and expulsion of the products of conception
Abbreviations: US, ultrasound.
to diagnose a failing pregnancy. TVUS features of failing pregnancy are summarized in Table 4. The sonographic findings are to be correlated with serum b-hCG and menstrual age. In the pre-embryonic stage, the pregnancy outcome depends on the presence of the gestational sac and yolk sac and their morphologic features. Absent intrauterine gestational sac Failure to demonstrate intrauterine gestational sac by TVUS may be secondary to early IUP (b-hCG < 1000 mIU/mL) or secondary to ectopic pregnancy. When the serum b-hCG is more than 1000 mIU/mL (IRP) and there is no IUP, an ectopic pregnancy [19,20] must be excluded by careful evaluation of the adnexa. If there is no identifiable ectopic gestational sac, adnexal mass, or a large amount of adnexal fluid in the cul-de-sac, follow-up with b-hCG and TVUS is necessary until a definite diagnosis is made. When the endometrial lining is thick with echoes in the endometrial cavity and no intrauterine gestational sacs, an incomplete abortion with retained products of conception must be distinguished from decidual reaction of ectopic gestation. Transvaginal color flow Doppler of the endometrial contents is useful in differentiating trophoblastic tissue from blood clots and pseudogestational sac. Sparse flow on color Doppler with low peak systolic velocities (< 6 cm/second) and low to absent end diastolic flow suggests decidual reaction of an ectopic pregnancy (Fig. 7) [38,39]. With early IUP (< 5 weeks) multiple flashes of color with a peak systolic velocity of greater than 8 cm/second
and high diastolic component caused by trophoblastic arterial flow are noted [40]. Intrauterine gestational sac without an embryo A common and difficult problem arises when the gestational sac in the uterus lacks an embryo or yolk sac [41 43]. This can be caused by early normal IUP,
Table 4 TVUS features of pregnancy failure Ultrasound findings Absence of IUGS with serum b-hCG above the discriminatory level (1000 mIU/mL) IUGS > 10 mm without a yolk sac IUGS of >18 mm without an embryo Embryo of 5 mm and above without cardiac activity Embryo with bradycardia (< 100 beats/min) Subchorionic hematoma Comments Ectopic pregnancy has to be excluded
Follow-up with serum b-hCG and TVUS Anembryonic pregnancy Embryonic demise Poor prognosis and needs close follow-up with TVUS Correlation of pregnancy outcome with the size of hematoma is not well established and needs TVUS follow-up
Abbreviations: hCG, human chorionic gonadotropin; IUGS, intrauterine gestational sac; TVUS, transvaginal ultrasound.
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Fig. 7. Decidual reaction. (A) Sagittal TVUS shows thick echogenic endometrial lining without a gestational sac (arrowheads). This sonographic appearance can be seen in molar pregnancy; correlation with beta hCG is very important. (B) Sagittal TVUS with color Doppler did not demonstrate trophoblastic flow, confirming it to be decidual reaction (arrowheads). Patients beta hCG was 650 IU. On follow-up, the patient was shown to have a normal intrauterine pregnancy.
anembryonic gestation, or a pseudogestational sac of ectopic pregnancy. Anembryonic gestation is a form of failed pregnancy defined as a gestational sac in which the embryo failed to develop (Fig. 8A). A mean gestational sac diameter greater than 18 mm (TVUS) without a visualized embryo is unequivocal evidence of a failed, anembryonic pregnancy [44]. This also is referred to as an empty amnion sign (Fig. 8B) because of its sonographic appearance of a large well-defined amniotic sac without an embryo [45]. The growth rate of an anembryonic gestational sac is slower than that of a normal gestational sac, which increases by 1.13 mm/day. An abnormal gestational sac can be identified confidently when the rate of increase of the mean sac diameter is less than
0.6 mm/d on follow-up US [46]. Other minor criteria of an abnormal gestational sac include distorted sac shape and weakly echogenic or irregular choriodecidual reaction (Fig. 9). The presence of gestational sac in the lower uterine segment or cervix is usually seen in patients with abortion in progress (Fig. 10), but can also be seen secondary to low implantation. Demonstration of trophoblastic vascular flow on color Doppler is useful in differentiating low implantation from abortion. Yolk sac criteria of an abnormal gestation The absence of a yolk sac when the mean sac diameter of the gestational sac is more than 10 mm is
Fig. 8. Anembryonic pregnancy. (A) TVUS of uterus shows a large (> 18 mm) gestational sac (arrow) without an embryo. (B) An empty amnion sign of anembryonic gestation (arrow).
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the viability of the gestation. The most convincing evidence that a pregnancy has failed is to document absence of cardiac activity when CRL length is greater than 5 mm. In a missed abortion, the embryo may be small for the gestational age with a discrepancy between the mean sac diameter and the CRL (Fig. 11). Embryonic bradycardia is a poor prognosticator of pregnancy viability and requires follow-up [58]. Embryonic bradycardia is defined as a heart rate of less than 100 beats per minute before 6.2 weeks gestational age and less than 120 beats per minute between 6.3 and 7 weeks [59].
Fig. 9. Abnormal shape of the gestational sac. A 30-year-old woman with 5 weeks of amenorrhea presents with vaginal spotting. A TVUS of the uterus shows an intrauterine gestational sac of abnormal shape and lobulated contour. On follow-up patient had a spontaneous complete abortion.
Intrauterine growth restriction First-trimester growth restriction is a sign of a failing pregnancy. Growth restriction is detected by comparing the mean sac diameter with the CRL or by serial follow-up of these growth parameters. The average gestational sac diameters should be at least 5 mm larger than the CRL. A difference in size between mean sac diameter and CRL of less than 5 mm caries a high risk of subsequent embryonic demise [60]. When there is sac size and CRL discrepancy, a follow-up US examination is recommended because these fetuses have higher incidence of low birth weight and premature delivery [61,62]. Subchorionic hematoma Up to 20% of women with a threatened abortion have a subchorionic hematoma [44]. Perigestational
indicative of an abnormal gestation and is associated with spontaneous abortion [47 49]. A failing or failed pregnancy is also suggested when the yolk sac is abnormal in size and shape. Large (> 6 mm) irregular and calcified yolk sacs have been found to correlate with early pregnancy failure [50 52]. A large yolk sac is considered to be caused by an alteration of the metabolic functions of the yolk sac membrane with accumulation of secretions following embryonic death [53]. The association of a large yolk sac with aneuploidy has also been reported [50]. Although abnormal large yolk sac size is reported to be associated with subsequent pregnancy failure, another study with yolk sac diameter greater than the 95th percentile for gestational age reported normal pregnancy outcomes [54]. Because of this controversial issue, any patient with a large yolk sac should have a follow-up US because there is increased risk of spontaneous abortion. Apart from size, irregular, echogenic, calcified, or double yolk sacs (vitelline duct cyst) also are associated with early pregnancy failure [55,56]. Gestational sac with an embryo Although visualization of a living embryo does not ensure a viable pregnancy, the abortion rate decreases for living embryos as the gestational age increases, with a 0.5% demise rate for living embryos between 6 and 10 mm [29]. Because cardiac activity may not be demonstrated [57] in early normal embryos (CRL < 4 mm), follow-up US and correlation with the serum b-hCG level is useful in determining
Fig. 10. Abortion in progress. A TVUS of the uterus shows a low-lying gestational sac (arrow). Mixed hyperechoic and hypoechoic contents in the endometrial cavity of the fundus (arrowheads) represent decidual reaction and hemorrhage. The patient had a complete spontaneous abortion a few hours after the scan.
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with that in younger women (13.8% versus 7.3%, respectively), and was 2.3 times higher in women who presented with vaginal bleeding at 8 weeks gestational age or less compared with that in women who presented with bleeding at more than 8 weeks gestational age (13.7% versus 5.9%, respectively). Some investigators have calculated the volume of a subchorionic hematoma as a percentage of the gestational sac volume. When the volume of a hematoma is less than 40% of the gestational sac volume, the pregnancy outcome is favorable [64,66].
Fig. 11. Missed abortion. A 35-year-old woman with 10 weeks of amenorrhea presents with intermittent vaginal bleeding. TVUS shows a relatively small-sized embryo (arrow) compared with the gestational sac. No cardiac activity was demonstrated on pulsed Doppler.
Retained products of conception Retained products of conception typically consist of retained placental tissue. An echogenic mass in the uterine cavity is the most suggestive US finding. A heterogeneous mass or collection in the central cavity may represent a blood clot, or some combination of retained placenta, necrotic debris, and clot (Fig. 13). Color Doppler may help to differentiate vascularized trophoblastic tissue from nonvascularized blood clots. A normal-appearing endometrial stripe or punctate echogenic foci not associated with a discrete mass makes retained products of conception unlikely.
hemorrhage from chorionic frondosum is the most common source of vaginal bleeding in the first trimester of pregnancy. Subchorionic hemorrhage is secondary to abruption of the edge of the chorion frondosum decidua basalis complex or may be caused by marginal sinus rupture [63,64]. Although the hemorrhage usually abuts or elevates the edge of the chorion frondosum decidua basalis complex, the bulk of the hemorrhage is usually situated between the decidua capsularis, chorion laeve, and the decidua vera. Acute hemorrhage may be hyperechoic or isoechoic relative to the chorion, and it becomes isoechoic with the chorionic fluid in 1 to 2 weeks (Fig. 12). Several studies have correlated the pregnancy outcome in these patients with the size of the subchorionic hematoma, gestational age, and the maternal age. One of the largest studies [65] showed that the rate of pregnancy loss increases with hematoma size, advancing maternal age, and earlier gestational age. In this study, the size of the hematoma was graded according to the percentage of the chorionic sac circumference elevated by the hematoma. It was graded as small when it involved less than one third of the chorionic sac circumference, moderate when it involved one-third to one-half of the chorionic sac circumference, and large when two-thirds or greater of the chorionic sac circumference was involved. There was little difference in the rates of spontaneous abortion between pregnancies with small- and moderate-size hematomas (7.7% and 9.2%, respectively), but the rate doubled with large hematomas (18.8%). The spontaneous abortion rate was also twice as high in women 35 years of age or older compared
Gestational trophoblastic disease Gestational trophoblastic disease is a spectrum of pregnancy-related trophoblastic proliferative abnormalities that can present with first-trimester bleeding.
Fig. 12. Subchorionic hemorrhage. TVUS shows a gestational sac (curved arrow), chorion (straight thick arrow), and a subchorionic hemorrhage (straight thin arrow).
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Fig. 13. Retained products of conception with variable appearance. Sagittal (A) and coronal (B) TVUS in two different patients with persistent vaginal bleeding after spontaneous abortion show retained products of conception with increased echogenicity (arrowheads) in (A) and heterogeneous appearance in (B). This appearance is secondary to necrosis and blood clots. (C) Increased vascularity on color flow Doppler evaluation in a patient with retained products of conception.
Classification of gestational trophoblastic disease is as follows: Hydatidiform mole Complete mole Partial mole Gestational trophoblastic tumors Choriocarcinoma Invasive mole Placental site trophoblastic tumor
Hydatidiform mole (molar pregnancy) Molar pregnancy is a noninvasive process characterized by varying degrees of trophoblastic prolif-
eration and edema of villous stroma. Its incidence is 1 in every 1000 to 2000 pregnancies [67] and is estimated to be as high as 1 in 41 in patients with miscarriages [68]. Hydatidiform mole constitutes 80% of the cases of gestational trophoblastic disease with relatively high frequency of molar pregnancy at the beginning and end of the childbearing period. Mole recurrence is seen in about 1% to 2% of cases [69]. The absence or presence of fetus or embryonic elements is used to classify a molar pregnancy into complete or partial moles. Complete molar pregnancies are most often 46 XX, with the chromosomes completely of paternal origin and are referred to as androgenesis. The karyotype in partial mole is usually triploid (69 XXY) or even tetraploid (92 XXXY) with one maternal and two paternal haploid compo-
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nents. The fetus in partial mole is usually nonviable and exhibits features of triploidy, which include multiple congenital anomalies and growth restriction [70]. Histologically, the molar tissue has prominent villi with central acellular space corresponding to the macroscopic appearance of vesicles. In partial mole these changes are focal and less advanced. The clinical presentation of molar pregnancy, listed below, has changed appreciably over the last decades because of early diagnosis with TVUS and quantitative b-hCG estimation.
Uterine bleeding, which may vary from spotting
agnosis is made by markedly elevated serum b-hCG levels expected for the stage of gestation and by the characteristic sonographic appearance. Sonographic features of molar pregnancy Molar changes can be detected from 8 weeks of pregnancy by US. The uterine cavity is filled with multiple sonolucent areas of varying size and shape. This has been described as a snow storm appearance with low-frequency transabdominal scanning. With high-frequency transvaginal transducers, numerous discrete, anechoic (cystic) spaces are visualized corresponding to the hydropic villi (Fig. 14). These cystic spaces range from 1 to 30 mm in size and increase in size with gestational age. Large sonolucent areas or maternal lakes resulting from the stasis of maternal blood are seen between the vesicles. In partial mole, an intrauterine embryo is noted along with molar changes [71,72]. Because the trophoblastic changes develop at a slower rate in partial mole, it may present as enlarged placenta without macroscopic vesicular changes [73]. Women with a high b-hCG level for the gestational age without sonographic molar changes should have follow-up US to exclude partial mole. In missed abortion, impaired trophoblastic vascularity leads to hydropic degeneration of villi and can resemble a partial hydatidiform mole on US. The serum b-hCG is not elevated, however, and may be normal or at a lower level than for
to profuse hemorrhage
Uterine enlargement out of proportion to the
duration of pregnancy in 50% of cases

Absence of fetal parts or fetal heart sounds
despite an enlarged uterus

Pregnancy-induced hypertension before
24 weeks gestation
Hyperemesis Thyrotoxicosis, which is usually subclinical History of passage of grape-like vesicles trans-
vaginally Uterine bleeding is the most common presentation and it may vary from spotting to profuse bleeding. Occasionally patients may pass grape-like vesicles transvaginally. Clinically the uterine fundal height is more than is expected for the gestational period. Di-
Fig. 14. Complete hydatidiform mole. (A) Transabdominal sonogram of the uterus shows a complex mass with multiple welldefined anechoic cystic areas (arrows) corresponding to the vesicles of hydatidiform mole. There was no associated embryo. (B) Corresponding T1-weighted postgadolinium image of the uterus demonstrates intrauterine complex mass (arrowheads) with multiple well-defined hypointense lesions that are not enhancing and represent vesicles of hydatidiform mole (arrow).
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the expected gestational age. Rarely, a viable fetus may be associated with complete molar pregnancy [74] and is caused by the coexistence of a true mole and a normal fetus in dizygotic twin gestation. Demonstration of the typical trophoblastic flow is useful in differentiating the trophoblastic tissue of molar pregnancy from intrauterine blood clots in a patient with abortion. Theca-leutin ovarian cysts are seen in up to 25% to 60% of cases because of hyperstimulation of the ovaries by chorionic gonadotrophin secreted by the trophoblastic tissue [75]. In this condition, the ovaries are enlarged with multiple cysts having a soap bubble or spoke-wheel appearance. Treatment of hydatidiform mole consists of immediate evacuation of the mole and subsequent follow-up with serial measurement of serum b-hCG for detection of persistent trophoblastic proliferation or malignant change. TVUS is useful in monitoring patients following evacuation and chemotherapy [76 79]. If the b-hCG levels plateau or continue to rise, persistent trophoblastic tissue is diagnosed. Following evacuation of a hydatidiform mole, 18% to 29% with complete hydatidiform mole and 1% to 11% with partial mole develop a persistent trophoblastic tumor [80 83]. TVUS reveals nodules of residual echogenic trophoblastic tissue and central hypoechoic blood spaces. Doppler interrogation reveals typical low-resistance and high-peak systolic velocity vascular flow of trophoblastic tissue. Gestational trophoblastic tumors Gestational trophoblastic tumor refers to choriocarcinoma, invasive mole, and placental site trophoblastic tumor. It may follow a normal or a molar pregnancy, abortion, or ectopic pregnancy. Diagnosis is made primarily by persistent elevation of the serum b-hCG. Fifty percent of these tumors arise following hydatidiform mole, 25% following abortion, and 25% following normal or ectopic pregnancy [84]. Choriocarcinoma Choriocarcinoma is a malignant form of trophoblastic tumor that invades uterine myometrium and blood vessels resulting in distant metastasis. The absence of villous pattern is characteristic of choriocarcinoma, in contrast to hydatidiform mole and invasive mole. The most common sites of metastases are the lungs (over 75%) and the vagina (50%). Other sites of metastases include the vulva, liver, kidneys, brain, ovaries, and bowel [85]. The US appearance is indistinguishable from a complete mole, except in cases with myometrial and parametrial extension. TVUS reveals a heterogeneous intrauterine mass with
or without myometrial invasion. Doppler interrogation reveals typical trophoblastic flow and differentiates trophoblastic tissue from areas of hemorrhage and necrosis. Ovarian theca-leutin cysts are identified in more than a third of such cases. Cross-sectional imaging with CT and MR imaging is more accurate in demonstrating invasion of the myometrium and parametrium. Radiologic evaluation for distant metastases is mandatory in all cases of choriocarcinoma. Invasive mole This is defined as excessive trophoblastic overgrowth with invasion of the myometrium and occasional extension to the peritoneum or adjacent parametrium. Unlike choriocarcinoma there are no distant metastases. Invasive mole presents clinically as heavy vaginal bleeding after the evacuation of the molar pregnancy with persistent elevation of serum b-hCG. On TVUS it appears as focal areas of increased echogenicity within the myometrium [86]. Doppler color flow mapping of this area can evaluate the extent of this lesion and its subsequent response to chemotherapy (Fig. 15) [87 89]. Placental site trophoblastic tumor This is a very rare trophoblastic tumor, which arises from the placental implantation site following either a normal term pregnancy or abortion. These patients present with either abnormal bleeding or amenorrhea and might be presumed to be pregnant. Moreover, the b-hCG levels are not as high as in other forms of gestational trophoblastic disease [90,91]. They may invade the myometrium and in 15% to 20% cases behave in a malignant fashion with distant metastases. US features are indistinguishable from those of other gestational trophoblastic tumors [92,93].
Arteriovenous malformation of the uterus It is important to consider arteriovenous malformations in the differential diagnosis of first-trimester bleeding because of their sonographic resemblance to retained products of conception and gestational trophoblastic disease. Vascular malformations of the uterus are rare and potentially life-threatening lesions. They can be congenital or acquired following uterine trauma (surgery or curettage); use of intrauterine contraceptive devices; endometrial or cervical carcinoma; and previous treatment of gestational trophoblastic tumors [94]. Congenital arteriovenous malformations have multiple arteriovenous communications and may extend through the myometrium into the parametrium. Acquired lesions are arterio-
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Fig. 15. Invasive mole. (A) TVUS showing molar tissue invading the myometrial wall (arrowheads) of the fundus and endometrial cavity (arrow). (B) Color flow Doppler evaluation shows vascularity of the invaded myometrium. Endometrial cavity is shown by arrow. (C) Corresponding T2-weighted, sagittal image of the uterus demonstrates hyperintense myometrium (arrow) representing invasive molar tissue. Uninvolved endometrial lining is shown (arrowheads).
venous fistulas between a single artery and a vein. Vascular malformations persist following treatment in 10% to 15% of patients with gestational trophoblastic tumors. Gray-scale US shows multiple anechoic spaces with mosaic pattern of color signals within the cystic spaces on color Doppler US. Spectral analysis of the vessels shows high-velocity blood flow with a low resistive index [95,96], indistinguishable from a gestational trophoblastic disease (Fig. 16). These vessels can be distinguished from gestational trophoblastic disease because the serum b-hCG is normal.
Uterine arteriovenous malformations are one of the common causes of spontaneous abortions. Contrastenhanced CT, MR imaging, and angiography are other imaging modalities used to diagnose uterine arteriovenous malformations. The diagnosis of uterine arteriovenous malformations as the cause of vaginal bleeding is crucial because treatment is entirely different from that for retained products of conception or gestational trophoblastic disease, which can mimic arteriovenous malformations. The treatment of arteriovenous malformations is by embolization if the
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Fig. 16. Uterine arteriovenous malformation in a 35-year-old woman with history of spontaneous abortion presenting with vaginal bleeding. She was referred to exclude retained products of conception. (A) TVUS shows complex endometrial mass (arrowheads) with anechoic spaces (arrow). (B) Corresponding color flow Doppler demonstrates the mosaic pattern of flow within the mass (arrowheads). Arrow points to endometrial cavity. Pulsed Doppler (C) shows arterialized venous flow, diagnostic of arteriovenous malformation.
patient desires fertility and by hysterectomy if fertility is not an issue.
of early pregnancy failure can be made even before the embryo is visible.
Summary Vaginal bleeding is a leading cause of presentation for emergency care during the first trimester of the pregnancy. Clinical assessment of the pregnancy outcome at this stage is less reliable. US examination is crucial in establishing IUP and early pregnancy failure and to exclude other causes of bleeding, such as ectopic pregnancy and molar pregnancy. Diagnosis of a normal IUP at this stage not only assists the physician in an expectant management, but also gives a psychologic boost to the patient. With recent advances in US technology and the availability of highfrequency transvaginal transducers, reliable diagnosis
Acknowledgment The authors thank Bonnie Hami, MA, Department of Radiology, University Hospitals of Cleveland, Ohio, for her editorial assistance in the preparation of this article.
References
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Radiol Clin N Am 42 (2004) 315 327
The role of ultrasound in pregnancy-related emergencies

Noam Lazebnik, MD*, Roee S. Lazebnik, PhD
Department of Obstetrics and Gynecology, MacDonald Womens Hospital, University Hospitals of Cleveland, Case Western Reserve University School of Medicine, 11100 Euclid Avenue, Cleveland, OH 44106, USA
Although most births are uneventful, about 15% of all birthing women experience potentially lifethreatening complications, and at least 1% to 2% require major surgery. Although some complications can be prevented, and some predicted preemptively, most of the severe complications cannot be anticipated. To reduce mortality, a key component of maternal health care is the ability to diagnose, confirm, and treat women whose medical status is unstable in the antenatal, delivery, and postpartum periods. Sonography is the imaging modality of choice for diagnosing maternal-related abnormalities both during and following pregnancy and delivery. Pelvic ultrasound has long been the mainstay for evaluation of the female pelvis. It is widely used during pregnancy in countries where antenatal care is available. Most pregnant women are referred for ultrasound study to confirm gestational age and to rule out fetal malformations, abnormal placentation, and uterine and cervical abnormalities. At University Hospitals of Cleveland, Case Western Reserve University, a tertiary care medical facility, more than 12,000 obstetric ultrasound studies are performed yearly. About 13% of the total studies are performed in an emergency obstetric setup. This article describes the emergency conditions during pregnancy and the immediate postpartum period that might lead to a life-threatening situation for the pregnant patient or her fetus, and the spectrum of imaging findings associated with these conditions.
Ultrasound examinations in emergency situations are ordered to obtain specific, limited information when it is necessary or impossible to perform a complete fetal, placental, or pelvic organ survey. Limited examinations in antepartum and intrapartum emergency settings may include identification of fetal number, fetal presentation, presence or absence of fetal cardiac activity, localization of the placenta, assessment of amniotic fluid volume, and a biophysical profile. The relevant clinical information can be obtained by performing transabdominal study, transvaginal study, or combination of the two modalities. Occasionally, additional ultrasound studies are needed in cases of medical or surgical complications of the pregnant patient. Examples of such disorders include renal and gastrointestinal abnormalities and maternal vascular abnormalities.
Sonographic technique Modern ultrasound devices have variable-focus depths that allow the examiner to study structures in the near or far field as needed without changing transducers. A 2- to 5-MHz and 4- to 9-MHz transducer for transabdominal and transvaginal study, respectively, is very well suited. For a pelvic sonogram, performed transabdominally, the patients urinary bladder should be distended. A full bladder usually is unnecessary. The more advanced the pregnancy, the lesser the need for a full bladder. Whenever cervical and lower uterine segment or pelvic organs images are needed, endovaginal scanning is superior to transabdominal scanning. Improved visualization may be achieved using the vaginal approach, because the transducer is brought closer to
* Corresponding author. E-mail address: noam@cwru.edu (N. Lazebnik).
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the area being examined. It can be very helpful in studying the lower uterine segment and its relation to the placenta, evaluating the uterus, or measuring a cyst in an ovary in the early stage of pregnancy. The sonologist performing the study decides whether one or a combination of approaches is best for the particular case. There are no known contraindications to abdominal ultrasound study. Transvaginal studies are not recommended in case of premature rupture of the membranes. The use of this modality is controversial in cases of placenta previa, as discussed later. Careful judgment should always be applied in choosing to perform a transvaginal study because it might be contraindicated for maternal or fetal reasons. Furthermore, regardless of the indication for the study, one should always perform a transabdominal evaluation before considering vaginal scanning. The added views obtained by combining the two scanning modalities might be of significant help in establishing a correct diagnosis. It is highly advisable to follow a strict routine when one performs ultrasound study for an obstetric emergency. The first priority in a true obstetric emergency is to document a live in utero gestation, with a stable and normal heartbeat. Once this has been achieved one should document that there is no suspicion for a significant volume of free fluid or blood clots inside the gestational sac, the abdominal cavity, or the posterior cul-de-sac. The bladder and uterus should appear normal and intact, and no adnexal mass should be present.
Second- and third-trimester obstetric emergencies Pregnancy-induced hypertension Pregnancy-induced hypertension complicates 6% to 8% of pregnancies in the United States and accounts for 15% of maternal deaths. It ranks second only to embolic events as a cause of maternal mortality. It also is an important cause of perinatal morbidity and mortality. In pregnant women, two distinct hypertensive disorders are common: chronic hypertension and pregnancy-induced hypertension. Women with chronic underlying hypertension are at risk for pregnancy-induced hypertension, a multiorgan pathologic state with various subsets. One of the more severe forms of hypertensive disorder during pregnancy is HELLP syndrome. The HELLP syndrome in a pregnant woman is characterized by hemolytic anemia, elevated liver enzymes, and a low platelet count. Progressive nau-
sea and vomiting, upper right quadrant abdominal pain, and headache are usually the most common symptoms. During the physical examination, the physician notes impressive abdominal tenderness, especially in the right upper quadrant. The liver may be enlarged and liver function tests are abnormally elevated with evidence of hemolysis on a peripheral blood smear and the red blood cell and platelet counts may be low. When the disease is not treated early, up to 25% of affected women develop serious complications. Without treatment, approximately 1.1% to 3.5% of patients die from HELLP syndrome, usually because of liver rupture or other related maternal complications [1]. The pathophysiologic process of this condition begins with arteriolar vasospasm, which causes endothelial damage and fibrin deposition in the vessel lumen. This leads to the following events: (1) platelet deposition on the fibrin aggregates, reducing the number of circulating platelets (unlike disseminated intravascular coagulation, coagulation factors are not involved); (2) erythrocyte destruction by the fibrin aggregates (a microangiopathic hemolytic anemia), leading to abnormal cells in the peripheral smear (burr cells and schistocytes), an elevated indirect bilirubin level, and anemia; and (3) hepatocyte destruction caused by hepatic microemboli [2]. HELLP syndrome occurs in approximately 10% of pregnant women with preeclampsia or eclampsia. Preeclampsia may be mild or severe. Severe cases with high blood pressure and protein in the urine can progress to seizures (eclampsia). Severe cases are life-threatening to both the mother and fetus. Many women have a high blood pressure and are diagnosed with preeclampsia before they develop the HELLP syndrome. In some cases, however, HELLP symptoms are the first warning of preeclampsia and the condition is misdiagnosed as hepatitis, gallbladder disease, idiopathic thrombocytopenic purpura, hemolytic uremic syndrome, or thrombotic thrombocytopenic purpura. The fatality rate among neonates born to mothers with HELLP syndrome varies, depending on such factors as birth weight. The main treatment is delivery of the baby as soon as possible, because liver function in the mother rapidly deteriorates with this condition, a harmful state for both the mother and fetus. Sonographic findings Unlike the traditional role of sonography during pregnancy where the fetus, placenta, or the pelvic organs are the targets of the study, sonography plays a different role in HELLP syndrome; it can exclude biliary tract disease and identify altered hepatic and renal echo textures. Possible findings include
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patchy areas of increased echogenicity in the liver, diffusely increased renal echo texture and size, perirenal fluid, and hepatic subcapsular hematoma [3,4]. Uterine rupture One of the major causes of maternal and perinatal mortalities is rupture of the uterus. This obstetric hazard is also associated with short-term maternal morbidities, such as vesicovaginal fistula, rectovaginal fistula, bladder rupture, foot drop, psychologic trauma, and anemia [5]. In the long-term, because of the surgical intervention, the woman may become infertile as a result of indicated hysterectomy. Uterine rupture is defined as separation that requires operative intervention or is symptomatic. It involves the full thickness of the uterine wall. Uterine rupture may occur spontaneously but is more commonly associated with history of uterine surgery, such as dilation and curretage, classical cesarean or low transverse cesarean section, and myomectomy. Induction of labor using low- and high-dose regimens of prostaglandin E2 or with misoprostol might also result in uterine rupture. Prolonged deceleration (alone or proceeded by either severe late or variable decelerations) is the most reliable clinical finding occurring in 100% of cases when total fetal extrusion occurred [6]. The incidence of uterine rupture is 0.05% of all pregnancies [7], occurring between 1 in 140 and 1 in 300 of women with a pre-existing scar [8]. The risk of uterine rupture increases with the number of caesarean sections [9]. The perinatal mortality is 10 times that of the maternal mortality [7]. Leung et al [6] evaluated 78 cases of uterine rupture in a large tertiary care medical center and reported significant neonatal morbidity when 18 minutes or more elapsed between the onset of prolonged deceleration and birth. When the prolonged deceleration was preceded by severe late or variable decelerations, fetal asphyxia occurred as early as 10 minutes from the onset of prolonged deceleration. Sonographic findings The sonographic findings of uterine rupture during pregnancy include extrauterine blood collection, fetal parts outside the uterine cavity, intra-amniotic hemorrhage, and focal bulging of membranes through the site of dehiscence [10]. In a recently published study the authors raised numerous questions regarding the significance of cesarean scar defects and the ability of transvaginal ultrasound to predict the risk of uterine rupture in women choosing trial labor after cesarean section [11]. Transvaginal ultrasound demonstrated a cesarean scar as an echogenic line through
the myometrium near the level of the internal os, and a cesarean scar defect was present when there was an anechoic area (fluid) within the scar. Women who had prolonged labor before cesarean section were more likely to show a cesarean scar defect, and so were women who had multiple cesarean deliveries. The researcher reported that real-time transvaginal ultrasound was 87% sensitive and 100% specific for detecting cesarean scars [11]. Abnormal placentation Abnormal placentation in the form of placenta accreta, percreta, or increta is a rare but potentially life-threatening complication of pregnancy that is an increasingly frequent cause of maternal morbidity and mortality. The term refers to any placental implantation resulting in abnormal adherence to the uterine wall. Life-threatening hemorrhage can occur at delivery because of failure of placental separation from the uterine wall and occurs in about 40% of cases. It is associated with significant maternal morbidity and in rare cases maternal mortality [12]. Pathologically it occurs when the decidua basalis is partially or totally absent in conjunction with an imperfect development of Nitabuchs membrane, a fibrinoid layer that separates the decidua basalis from the placental villi [13]. The placental villi are in direct contact with the myometrium without intervening endometrial decidua. Clark et al [14] demonstrated the effect of previous cesarean section deliveries on the incidence of placenta accreta. They showed that the risk of placenta previa increases proportionately with the number of previous cesarean section deliveries (0.26% in an unscarred uterus, and up to 10% in women with four or more previous cesarean sections). Surgical intervention in the form of total abdominal hysterectomy is often indicated because of life-threatening hemorrhage at delivery, secondary to failure of placental separation from the uterine wall. Sonographic findings Placenta accreta can be diagnosed using grayscale and color Doppler sonography. Gray-scale findings include loss of the normally visible retroplacental hypoechoic rim corresponding to the decidua basalis and dilated venous vessels [12]. Progressive thinning of the retroplacental hypoechoic zone on serial examinations is an important clue (Fig. 1). Multiple placental lakes that may represent dilated vessels extending from the placenta through the myometrium form the so-called Swiss cheese appear-
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lakes with focal lacunar flow, hypervascularity linking the placenta to the bladder, dilated vascular channels with pulsatile venous flow over cervix, and poor vascularity at sites of loss of hypoechoic zone. Placenta previa Placenta previa occurs in approximately 1 in 200 to 250 pregnancies and is associated with potentially serious consequences from hemorrhage, abruption of the placenta, or emergency cesarean delivery. Abruption of the placenta occurs 14 times more frequently in pregnancies with placenta previa than in normal pregnancies, and cesarean delivery occurs four times more frequently because of the potentially serious consequences of persistent placenta previa at delivery. There are three types of placenta previa: (1) marginal previa where the edge of the placenta is less than 2 cm from the opening of the cervix, (2) partial placenta previa where the placenta partly covers the cervical opening, and (3) total previa where the placenta completely covers the cervical os (Fig. 2A). Marginal placenta previa is also known as lowlying placenta. The natural history of marginal placenta previa was studied by Rizos et al [19]. Placental localization by diagnostic ultrasound was performed at 16 to 18 weeks gestation in 1098 patients before amniocentesis for genetic indications. Marginal placenta previa was diagnosed in 58 patients, 47 of whom went on to delivery uncomplicated by placenta previa. There were five patients with placenta previa at delivery, four of whom had third-trimester bleeding. One patient was diagnosed as having a normal placental implantation at midtrimester but placenta previa was demonstrated at delivery. The incidence of placenta previa at 16 to 18 weeks was 5.3% and fell to 0.58% at delivery, indicating a 90% conversion rate. This conversion occurs secondary to rapid growth of lower uterine segment in the third trimester resulting in superior migration of placenta relative to the internal cervical os. Most cases of asymptomatic low-lying placenta convert to normal location of the placenta before delivery. The authors concluded that these patients should be observed with serial ultrasound studies at 6- to 8-week intervals until delivery or unequivocal conversion. They also recommended no restriction in activity unless the placenta previa persists beyond 30 weeks or becomes clinically manifest [19]. Traditionally, transabdominal study is used to document sagittal midline images of the lower uterine segment and cervix, preferably with a full bladder to document the presence of placental tissue extend-
Fig. 1. Placenta accreta. Longitudinal color Doppler image of placenta demonstrates thinning of the retroplacental hypoechoic zone (arrowheads). Color flow Doppler ultrasound highlights areas of increased turbulent flow that extend from the placenta into the surrounding uterine wall and cervix (arrows).
ance of the placenta [15]. Depending on the location of the implantation, the condition is referred to as placenta accreta, placenta increta, or placenta percreta. If the placental villi extend beyond the confines of the endometrium and attach to the superficial aspect of the myometrium, the term placenta accreta is used. Placenta increta refers to a situation in which the villi invade the myometrium, whereas the term placenta percreta is used if the villi advance into the serosa or parametria. Although this classification scheme is widely accepted, most published literature discusses these abnormalities collectively as placenta accreta [16]. Doppler ultrasound highlights areas of increased turbulent flow that may extend from the placenta into the surrounding uterine wall and cervix (see Fig. 1). Lerner et al [17] reported a sensitivity of 100% and a specificity of 94% for the prenatal detection of placenta accreta using color Doppler. This technique also allows turbulent flow to be visualized in cases of placenta percreta where placental vessels extend beyond the uterine serosa and may involve other pelvic organs, such as the bladder. Chou et al [18] have described the following findings associated with placenta accreta: dilated vascular channels with diffuse lacunar flow, irregular vascular
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Fig. 2. Placenta previa. (A) Transvaginal sonographic view at 10 weeks gestation reveals the placenta completely covering the internal cervical os. (B) Transabdominal view of the same case at 34 weeks gestation. The placenta covers the entire internal cervical os. The retroplacental hypoechoic zone is invisible in the lower uterine segment adjacent to the cervix also suggesting placenta accrete (arrows).
ing down to the region of the cervix (Fig. 2B). Because of concerns regarding the use of transvaginal study in patients with vaginal bleeding, possibly as a result of placenta previa, translabial (transperineal) study has been suggested as an alternative to transabdominal study [20]. Farine et al [21] compared the accuracy of the diagnosis of placenta previa using transvaginal sonography with that of the traditional transabdominal sonography. They concluded that transvaginal sonography was superior to transabdominal sonography in diagnosing placenta previa and invariably correct in ruling it out. Timor-Tritsch and Yunis [22] confirmed the safety of transvaginal sonography in patients suspected of placenta previa. They concluded that the angle between the cervix and vaginal probe is sufficient to prevent the probe from inadvertently slipping into the cervix and initiating or further aggravating vaginal bleeding. Placental abruption Third-trimester placental abruption complicates less than 1% of pregnancies but is associated with increased risk of preterm delivery and fetal death when it does occur [23]. The clinical diagnosis is usually based on bleeding, abdominal pain, and contractions, but sonography is often performed to visu-
alize the extent of subchorionic or retroplacental hematoma (Fig. 3). The diagnostic sensitivity for abruption has not improved despite significant improvements in ultrasound technology. Only one of every nine sonograms obtained to rule out placental abruption revealed evidence of a subchorionic or retroplacental hematoma [23]. Ultrasound study performed specifically to document placental abruption is usually unremarkable and is positive in only 25% of cases of placental abruption that are confirmed at delivery [24]. These researchers noted that there were no significant differences in clinical characteristics between women with positive or negative sonographic findings. They concluded that sonography is not sensitive for detecting abruption, but when a clot is visualized on sonography, the positive predictive value for abruption at delivery is high. They also noted that the shorter the scan-to-delivery interval, the greater the positive predictive value. When delivery occurred within 2 weeks of a positive sonographic finding, the diagnosis of placental abruption was confirmed in 100% of cases. Given that sonography is not a sensitive tool to diagnose placental abruption, sound clinical judgment suggests that even if the placenta appears grossly normal, a diagnosis of abruption should be considered when vaginal bleeding, abdominal pain, and uterine hypertonicity are present.
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Fig. 3. Placental abruption. (A) Retroplacental blood clot (arrows). (B) Large blood clot resulting from placental abruption occupying most of the fundal region of the uterus. Hyperechoic and hypoechoic irregular areas are seen within the clot (arrows). (C) A second blood clot is seen in the anterior lower uterine segment (arrows).
Vasa previa Despite dramatic improvements in diagnosis of maternal, fetal, and placental abnormalities vasa previa remains a true diagnostic challenge and continues to be a fatal condition for the fetus. For many years even following the introduction of ultrasound technology the diagnosis was made only after the membranes were ruptured and fetal exsanguination occurred. Vasa previa is a condition in which vessels run through the membranes below the presenting part, running over, or in close proximity to, the internal cervical os, unsupported by placenta or cord (Fig. 4) [25]. Spontaneous or artificial rupture of the membranes in labor often leads to fetal exsanguination, with mortality approaching 100%. With a high index
of suspicion, however, vasa previa can be diagnosed prenatally using ultrasound and color Doppler, allowing for elective delivery by cesarean section before membrane rupture with almost universal fetal survival [25]. Fung and Lau [26], Oyelese et al [27], and Lee et al [28] showed that a good outcome in vasa previa depended entirely on antenatal diagnosis of the condition by ultrasound. Screening all patients for vasa previa is time consuming and unnecessary because of low incidence. Documentation of placental cord insertion, however, should be part of any detailed obstetric sonographic examination. Recently Fung and Lau [26] and Oyelese et al [27] independently concluded that a low-lying placenta in the second trimester was the most important risk factor for vasa previa at term, whether or not the placenta subsequently remained low-lying at term. Other risk
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Fig. 4. Vasa previa. The placenta is posterior in location with marginal previa. The vessels (red and blue) communicate with an accessory placental lobe implanted on the left anterior lower uterine segment. Arrow points to the cervix.
factors for vasa previa include multiple pregnancies, pregnancies resulting from in vitro fertilization, and those with succenturiate lobe and bilobed placentae [25]. In all such pregnancies it is prudent to examine the region overlying the internal cervical os for evidence of vessels running over it. Postpartum hemorrhage Obstetric delivery has been associated with the potential for acute, massive blood loss to a degree unparalleled by other surgical procedures. Data from the Maternal Mortality Collaborative in 1988 indicate that hemorrhage was responsible for 11% of direct maternal deaths occurring in 1980 through 1985 [29]. No other condition in obstetrics, except perhaps shoulder dystocia, requires such rapid recognition and skillful response by the clinician to prevent loss of life. Sonographic findings The sonographic findings of retained placental tissue are often nonspecific because blood clots and retained products feature considerable overlap in sonographic appearance. In the first and early second trimester on transabdominal or transvaginal views of the endometrial cavity, thickened hyperechoic endometrial stripe greater than 5 mm, gestational sac (with or without a nonliving embryo), and round to ovoid fluid sac are suggestive of retained products. If the endometrial stripe is less than 5 mm,
especially if it is less than 2 mm, retained blood in the endometrial cavity is more likely than retained products of conception. Hertzberg and Bowie [30] reviewed the ultrasound images of 53 postpartum patients referred for possible retained products of conception and correlated specific ultrasound patterns with clinical and pathologic follow-up. The most common finding in patients with retained placental tissue was an echogenic mass in the uterine cavity, seen in 9 of 11 patients with pathologically proved retained placental tissue. In the remaining two patients with pathologically confirmed retained placenta, a heterogeneous mass was seen in the uterine cavity sometime during the course of serial sonography. Retained placental tissue was found unlikely when ultrasound demonstrated a normal uterine stripe endometrial fluid, or hyperechoic foci in the uterine cavity without an associated mass. The latter finding often was associated with recent uterine instrumentation. The sonographic appearance of retained placental tissue was shown to be variable, but detection of an echogenic mass in the uterus strongly supported the diagnosis. The authors concluded that solid echogenic masses in the lumen or uterine wall are the most specific findings for a retained placenta, whereas heterogeneous mass could be caused by retained placenta or from blood clots or infected or necrotic material in the absence of placental tissue [30]. The
Fig. 5. Retained products of conception. An echogenic area (calipers) representing placental tissue, debris, and blood is present in the endometrial cavity following manual removal of the placenta. Patient underwent dilation and curettage for continued uterine bleeding. The arrows point to retained products of conception still present subsequent to the dilation and curettage.
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authors suggested that sonographic evaluation for retained products of conception is best performed before uterine instrumentation to avoid confusion with iatrogenically introduced air. An example of retained products following term vaginal delivery is illustrated in Fig. 5. Di Salvo [10] noted anecdotally that low-resistance Doppler signals in these masses also can be predictive. When using Doppler sonography in this setting, however, it is important not to confuse lowresistance arterial signals that arise within the myometrium, which represent the placental implantation site, with similarly appearing Doppler signals arising from tissue within the endometrial cavity, which represent retained products [10].
Retained products of conception A spontaneous abortion is the loss of a fetus during pregnancy because of natural causes. The term miscarriage is the spontaneous termination of a pregnancy before fetal development has reached 20 weeks. The term spontaneous abortion refers to these naturally occurring events, not elective or therapeutic abortion procedures. More specific terms include missed abortion (a pregnancy demise where nothing is expelled); incomplete abortion (not all of the products of conception are expelled); complete abortion (all of the products of conception are expelled); threatened abortion (symptoms indicate a miscarriage is possible); inevitable abortion (the symptoms cannot be stopped and a miscarriage will happen); and infected abortion. Any one of these conditions might be associated with some degree of vaginal bleeding. The bleeding in incomplete abortion in which parts of the fetus or placental material are retained within the uterus might be associated with significant blood loss, however, and mandate surgical intervention in the form of uterine curettage to remove the remaining material from the uterus [31]. In the last decade with the introduction of mifepristone (RU 486) and oral or vaginal misoprostol to induce abortion in the first trimester, vaginal bleeding secondary to retained products of conception became more common [32]. Studies clearly establish misoprostol as an effective agent to empty the pregnant uterus in the first trimester [33]. Chia and Ogbo [32] showed medical evacuation of missed abortion with misoprostol to be an effective, safe, and cost-effective alternative to surgical evacuation of the uterus, and particularly suited for women not desiring hospital admission or a surgical procedure under general anesthesia [32]. Misoprostol is a synthetic prostaglan-
din E1 analogue. It was developed and marketed for prevention of peptic ulcer disease caused by prostaglandin synthetase inhibitors, but with its potent uterotonic and cervical ripening activity has found applications in the management of gynecologic and obstetric problems. In the United States it has been marketed as Cytotec, in 100- and 200-mg tablets. Similar effectiveness has been shown when it is given for a failed pregnancy or missed abortion [34,35]. Potential hypertonus as a result of drug accumulation has been associated with uterine rupture in the second or third trimester, and retained products of conception with significant bleeding [36]. Transvaginal sonography is a useful supplement to the clinical assessment in women who experience a spontaneous first-trimester abortion. Its use results in reduction of unnecessary general anesthesia and uterine curettage. Wong et al [37] showed that a first-trimester vaginal ultrasound study has a sensitivity and specificity of 100% and 80%, respectively, using a bilayer endometrial thickness of 8 mm or less. The ultrasound findings suggesting retained products of conception are a thickened endometrium of greater than 8 mm; complex hyperechogenic (blood and tissue debris) and hypoechogenic fluid material inside the endometrial cavity; a gestational saclike structure; or a space-occupying collection. Uterine fibroids Fibroid tumors are benign growths that develop in the muscular wall of the uterus. Although fibroids do not always cause symptoms, their size and location could lead to complications during pregnancy for some women including recurrent miscarriage, infertility, premature labor, fetal malpresentations, and complications of labor [38]. Lev-Toaff et al [39] reported their ultrasound findings of uterine fibroids during pregnancy. Fibroid size changes were analyzed on the basis of trimesters. In the second trimester, smaller fibroids increased in size, whereas larger fibroids decreased in size. In the third trimester, a decrease in size was documented regardless of initial size. The most common patterns of echotexture were hypoechoic, heterogeneous, and echogenic rim. The development of a heterogeneous pattern or anechoiccystic spaces on a follow-up study was accompanied by severe abdominal pain. The development of these patterns apparently indicates significant degeneration of the fibroid (Fig. 6). Fibroids located in the lower uterine segment were accompanied by a higher frequency of cesarean section and retained placenta. Fibroids located in the uterine corpus were
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Fig. 6. Color flow Doppler of uterus demonstrates a posterior lower uterine segment degenerating fibroid. The heterogeneous pattern with anechoic-cystic spaces suggests degeneration process within the fibroid. A feeding vessel can be seen between the myometrium and the fibroid (arrow).
create loss of heart rate variability, presumably by anesthetizing the brainstem center that modulates intrinsic cardiac automaticity. In addition, vasoactive agents cross the placenta and produce predictable changes to fetal heart rate and further influence the interpretation of the fetal tracing, rendering fetal heart rate monitoring through the use of standard external Doppler probes useless. In many similar challenging cases, the use of real-time ultrasound and color Doppler adds valuable data to assess the fetal status. Intermittent abdominal real-time ultrasound assessment of the fetus and placenta can be used for abdominal procedures that do not permit the use of standard external Doppler probes by covering the ultrasound transducer with a sterile sleeve. Abrupt changes in heart rate, baseline rates outside the acceptable range of 120 to 160 beats per minutes, and abnormal Doppler readings of the fetus or the placental vasculature should prompt the anesthesiologist to look for obvious causes of uteroplacental insufficiency.
more frequently associated with early abortions. Multiple fibroids were accompanied by a higher frequency of malpresentation and premature contractions compared with cases with one or two fibroids (Fig. 7) [39]. Abdominal surgery and trauma during pregnancy Emergency surgery is indicated during pregnancy for the management of trauma, malignancy, or acute medical illness. Women in the childbearing years are among the population at greatest risk for trauma. Trauma occurs in 5% to 10% of pregnancies and is responsible for 36 maternal deaths per 100,000 pregnancies, which is considerably higher than pregnancy-related mortality [40]. Penetrating abdominal injury from gunshot and knife wounds or associated with motor vehicle accidents results in 5% maternal mortality. A much higher perinatal death rate in the range of 41% to 71% is reported [41]. Fetal death can be the result of maternal instability, placental abruption, direct fetal injury and hemorrhage, or as a consequence of premature delivery. The fetal status must be assessed carefully for evidence of developing compromise. Monitoring fetal heart rate is an important aspect of these procedures, and is technically feasible after the 16th week for nonabdominal surgery. The surgeon and obstetrician alike must be aware that fetal heart rate monitoring helps guide the management of maternal cardiorespiratory parameters, and is useful even if it does not influence a decision to deliver the fetus [42]. Anesthetic drugs
Maternal nonobstetric emergencies during pregnancy Venous thromboembolism Venous thromboembolism occurs infrequently during pregnancy. It is a leading cause of illness and death during pregnancy and the puerperium and
Fig. 7. Gray-scale ultrasound longitudinal view shows a posterior lower uterine segment fibroid undergoing degeneration. The patient experienced premature uterine contractions starting at 29 weeks and delivered prematurely at 31 weeks by cesarean section secondary to lower uterine segment obstruction from the fibroid. Arrowhead points to the internal cervical os and calipers depict the whole length of the cervix.
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remains a diagnostic and therapeutic challenge [43]. In the general population the incidence of pregnancyassociated venous thromboembolism has been estimated to vary from 1 in 1000 to 1 in 2000 deliveries [43]. The risk of venous thromboembolism is five times higher in a pregnant woman than in a nonpregnant woman of similar age. Postpartum venous thromboembolism is more common than antepartum venous thromboembolism [43]. Women with congenital thrombophilic abnormalities, such as mutations within factor II or V of the coagulation factors, mutations leading to deficiency of protein S, or protein Cor persistent presence of antiphospholipid antibodies have an increased risk of venous thromboembolism during pregnancy and the puerperium. In individuals with well-defined hereditary thrombosis risk factors, such as the factor V:R506Q mutation, the factor II:G20210A mutation, antithrombin deficiency, or protein C deficiency, a relative risk of pregnancyassociated venous thromboembolism between 3.4 and 15.2 has been found [43]. Women with previous venous thromboembolism have an approximately 3.5-fold increased risk of recurrent venous thromboembolism during pregnancy compared with nonpregnant periods [43]. Pelvic thrombophlebitis Pelvic thrombophlebitis is considered to be a rare disorder of the puerperium with an incidence of 0.05% to 0.18% [44]. The ovarian veins are the most frequently involved veins in puerperal pelvic venous thrombosis. The clinical manifestations of the condition range from asymptomatic or dull abdominal pain to sepsis, pulmonary embolism, and even death. Unremitting fever and lower-quadrant or flank pain usually occurs within the first 1 to 2 days after delivery [45]. An abdominal mass is palpable in about half of the patients, which may lead to the suspicion of acute appendicitis. Torsion of the ovarian pedicle, broad ligament hematoma, and pelvic abscess may also occur. This condition is usually managed conservatively, with intravenous heparin and antibiotics, and rarely surgically. Imaging modalities used in the diagnosis include sonography, CT, and MR imaging [44]. Gallbladder disease Gallbladder disease is four times as common in women as in men, and pregnancy seems to contribute to the development of gallstones [46]. The symptoms of gallbladder disease during pregnancy do not differ from those reported for the nonpregnant population
and include steady, severe pain in the upper abdomen that increases rapidly and lasts from 30 minutes to several hours, pain in the back between the shoulder blades, pain under the right shoulder, nausea or vomiting, abdominal bloating, recurring intolerance of fatty foods, belching, and indigestion. Ultrasound scans are highly sensitive to the detection of gallstones. Sonographic findings with biliary disease include gallstones, sludge, wall thickening, the sonographic Murphys sign, biliary dilatation, and ductal stones [47]. In a study done in Dublin, Ireland, realtime ultrasound scanning was used to examine the pelvic area and the upper part of the abdomen in a prospective study of 512 healthy, pregnant women to determine the prevalence of gallstones [47]. Twentythree women (4.5%) had gallstones. Fourteen (60.9%) of the pregnant women were unaware of the presence of gallstones. Ultrasound technique was shown as the modality of choice to diagnose gallbladder disease in the parous and nonparous state including acute gallbladder disease [46] Acute renal disorders Acute renal failure has become a rare complication of pregnancy [48]. This is the result of the significant decline of septic abortion and its related complications; the improvement of prenatal care; the prevention of volume contraction, which is mainly caused by uterine hemorrhage; early diagnosis; and the treatment of other classic maternal complications, such as preeclampsia and acute pyelonephritis [48]. The incidence of bilateral renal cortical necrosis has also been declining during the last decade. Acute fatty liver, a potentially fatal disease, often is complicated by acute renal failure [48]. Ultrasound often is the first imaging technique to be used in patients with renal failure, hematuria, or proteinuria. Gray-scale ultrasound evaluation, color flow Doppler, and resistive indices provide adequate renal evaluation. In the initial clinical stages of renal parenchymal diseases, the kidneys may present normal ultrasound appearance and normal resistive indices values. Different renal parenchymal diseases may reveal similar appearance on ultrasound and Doppler ultrasound evaluation [48]. Percutaneous renal biopsy is often necessary to reach definite diagnosis. Renal vasculitides and tubular-interstitial nephropathies are identified more frequently by gray-scale ultrasound and Doppler ultrasound than glomerular nephropathies, because glomerular component accounts only for 8% of the renal parenchyma, whereas the highest percentage is occupied by vascular and tubulointerstitial component [48].
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Follow-up of acute renal failure, during and after medical treatment, is the most useful field of use of gray-scale ultrasound and Doppler ultrasound techniques, because a progressive lowering of resistive indices is correlated to a progressive recovery of renal function [48]. Hydronephrosis in pregnancy occurs in more than 80% of pregnancies and begins as early as 11 to 15 weeks [49]. The dilatation of the ureters in the early months of pregnancy is probably caused by atony of the neuromuscular apparatus, but what underlies this is not clear. The cause of the later dilatation of the abdominal segment of the right ureter and renal pelvis is a somewhat controversial subject. It is believed to be caused by pressure on the right ureter at the pelvic brim by the natural inclination to the right of the enlarged uterus, whereas the left ureter is protected by the rectosigmoid. Urolithiasis during pregnancy is a difficult clinical problem in which carefully selected radiologic studies play an essential role. It has been shown that sonography, particularly Doppler sonography, plays a major role in the diagnosis of urolithiasis in pregnancy [49]. Studies evaluating the intrarenal resistive index in asymptomatic pregnant patients have shown that both right and left kidneys have similar resistive indices, and there is no change in resistive indices during pregnancy [50]. In the absence of underlying renal disease, however, a difference of greater than 0.1 in resistive indices should prompt further sonographic confirmation of mechanical ureteral obstruction. This includes unilateral absence of a distal ureteral jet or direct visualization of a stone either at the ureterovesical or ureteropelvic junction [10]. Unilateral absence of a ureteral jet with the patient supine should always be confirmed by re-evaluation with the patient in the contralateral decubitus position, because the cause of the absent jet may merely be compression of the ureter by the uterus rather than an obstructing calculus [51]. Splenic artery aneurysm Splenic artery aneurysm occurs predominantly in women and most of the aneurysms are asymptomatic until rupture [52]. Over half of those that rupture occur during pregnancy or in women who have had children. Rupture during pregnancy is associated with a very high maternal and fetal mortality rate [52]. Although this condition is uncommon, good maternal-fetal outcome can only be achieved by early diagnosis and prompt treatment. Ordinarily, in suspected unruptured splenic artery aneurysm the gold standard for diagnosis is arteriography [53]. Ultraso-
nography and pulsed Doppler, however, are preferable in pregnancy [54]. Gray-scale sonography might fail to detect the unruptured splenic artery aneurysm if marked calcification of the aneurysmal wall is present [54]. Pulsed Doppler sonography has been used to document turbulent pulsatile flow along the aneurysmal wall. When patients with ruptured splenic artery aneurysm present with acute abdominal pain, an emergency ultrasound scan may reveal free fluid in the upper abdomen and the diagnosis is subsequently confirmed at laparotomy [54].
Summary Most complications of pregnancy allow time for transfer to specialized obstetric ultrasound units, but many women present to the emergency room or the labor and delivery unit with signs and symptoms suggesting genuine acute medical emergencies, where successful outcome depends on prompt diagnosis of the disorder and rapid appropriate medical management. The use of ultrasound technology in obstetric emergencies is well established. Ultrasonography plays a major role in such cases as the most important tool clinicians are using to identify the correct etiology and diagnosis, whereas in other cases it helps limit the differential diagnosis. One of the goals of any advanced training program in obstetrics and gynecology and radiology is to allow the skilled physician to perform the proper ultrasound study in case of an obstetric emergency to facilitate the proper diagnosis, enabling the medical team to provide the best possible care.
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[53]
[54]
is characterization feasible with ultrasound? Eur Radiol 2002;12:2006 20. Boridy IC, Maklad N, Sandler CM. Suspected urolithiasis in pregnant women: imaging algorithm and literature review. AJR Am J Roentgenol 1996;167: 869 75. Nazarian GK, Platt JF, Rubin JM, et al. Renal duplex Doppler sonography in asymptomatic women during pregnancy. J Ultrasound Med 1993;12:441 4. Wachsberg RH. Unilateral absence of ureteral jets in the third trimester of pregnancy: pitfall in color Doppler US diagnosis of urinary obstruction. Radiology 1998;209:279 81. Selo-Ojeme DO, Welch CC. Spontaneous rupture of splenic artery aneurysm in pregnancy. Eur J Obstet Gynecol Reprod Biol 2003;109:124 7. Wagner WH, Allins AD, Treiman RL, et al. Ruptured visceral artery aneurysms. Ann Vasc Surg 1997;11: 342 7. Lang W, Strobel D, Beinder E, et al. Surgery of a splenic aneurysm during pregnancy. Eur J Obstet Gynecol 2002;102:215 6.
Radiol Clin N Am 42 (2004) 329 348
Adnexal mass with pelvic pain

Emily M. Webb, MD, Gretchen E. Green, MD, Leslie M. Scoutt, MD*
Department of Diagnostic Radiology, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06520, USA
The routine use of ultrasound (US) in the evaluation of pregnant patients has resulted in more frequent detection of adnexal masses, which occur in approximately 2% of pregnancies. This estimation includes masses with a wide variety of appearances and etiologies that range from asymptomatic ovarian cysts to surgical emergencies, including ovarian torsion, ectopic pregnancy, and tubo-ovarian abscess [1]. Although many adnexal masses are detected incidentally, this article focuses on the evaluation of pregnant women who present with an adnexal mass in the setting of acute pelvic pain. Clinical diagnosis in pregnancy is a challenge because the differential diagnosis for an adnexal mass that presents with pelvic pain is broad and includes pregnancy-related and unrelated causes. The clinical presentation and natural history of abdominal and pelvic disease may be altered in pregnancy. US is an ideal tool for evaluating a pregnant patient. It is excellent in defining pelvic anatomy and pathology without the risks of ionizing radiation inherent to many imaging techniques.
and unnecessary surgery can be avoided, to the benefit of mother and fetus.
Follicular cysts and corpus luteal cysts Most adnexal masses identified during pregnancy are non-neoplastic, physiologic cysts, including corpus luteal cysts and follicular cysts. These cysts can be seen in early pregnancy but usually involute by midterm [1]. Follicular cysts vary in size from 3 to 8 cm in diameter. They result from failure in ovulation, most likely secondary to changes in the release of pituitary gonadotropins. The fluid contained within the immature follicle is not completely reabsorbed, which produces an enlarged follicular cyst [2]. On US examination, a follicular cyst should appear as a thin-walled, anechoic, round, or oval structure that demonstrates increased through transmission (Fig. 1). After ovulation has occurred from a mature follicle, the granulosa cells, which line the follicle, become luteinized. Blood accumulates in the central cavity during vascularization and then resorbs to form the corpus luteum [2]. The corpus luteum is described as a cyst when it reaches more than 2.5 to 3 cm [2]. Corpus luteal cysts are typically thin-walled, unilocular cysts that can range in diameter from approximately 3 to 11 cm [2]. The corpus luteum can have a wide range of appearances on US in the first trimester of pregnancy, however. The most common appearance is that of a round, thin-walled hypoechoic structure that demonstrates diffuse, homogenous, lowlevel echoes (Fig. 2) [3]. Other reported gray scale appearances in order of decreasing frequency include a cyst with a thick wall and anechoic center (Fig. 3), a cyst that contains scattered internal echoes, or a thinwalled simple cyst that is similar in appearance to a follicular cyst [3]. In most cases, color Doppler
Pregnancy-related disease Several disease processes, either specific to pregnancy or with an increased incidence in pregnant patients, can cause acute pelvic pain and an associated adnexal mass. These disease processes vary from benign, often asymptomatic entities to diseases that require emergent treatment. Differentiation is critical so that appropriate treatment can be provided
* Corresponding author. E-mail address: scoutt@biomed.med.yale.edu (L.M. Scoutt).
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Fig. 1. Simple ovarian or follicular cysts. These two ovarian cysts are completely anechoic, with thin, nearly imperceptible walls (arrow), and they demonstrate increased through transmission (arrowheads). Fig. 3. Atypical corpus luteal cyst. This exophytic cyst has an anechoic center with a thick, relatively hypoechoic wall (arrow) with a thin rim of vascularity. Although it may be difficult to differentiate such a structure from an ectopic pregnancy, in general the wall of an ectopic pregnancy is more echogenic and usually not so thick.
evaluation of the corpus luteum demonstrates a circumferential ring of fire of vascularity with a low resistance waveform pattern. In a study by Durfee and Frates [3], 92% of corpus luteal cysts demonstrated this pattern of blood flow with a mean resistance index of 0.49 and mean peak systolic velocity of 17 cm/second. Acute pelvic pain in pregnancy is commonly caused by hemorrhage into a follicular or corpus luteal cyst. Cyst rupture or leakage also may cause severe pelvic pain and hemorrhage, sometimes requiring laparoscopy or laparotomy [2,4]. The US appearance of hemorrhagic ovarian cysts varies because the US characteristics of hemorrhage change over time [4 7]. Initially a hemorrhagic cyst demonstrates a diffuse, homogeneous pattern of low-
level echoes. The wall may be vascular but should be thin and regular. In a study by Baltarowich et al [6], most hemorrhagic cysts (92%) demonstrated increased through transmission. Over time as the clot forms, a lace-like, reticular pattern of internal echoes develops because of the presence of fine fibrous
Fig. 2. Corpus luteal cyst. This exophytic corpus luteal cyst contains low-level internal echoes. The cyst wall is markedly vascular on color Doppler evaluation, which demonstrates ring of fire (arrows).
Fig. 4. Hemorrhagic cyst. Note lace-like or spider web pattern of internal echoes. The cyst wall is smooth and regular. Increased through transmission is present. Doppler interrogation reveals no evidence of internal blood flow, and the appearance changes over time as the blood clot continues to resorb.
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Fig. 5. Hemorrhagic cyst. Clot within a hemorrhagic cyst often adheres to the cyst wall and is lenticular in shape (arrow). Doppler examination does not demonstrate internal vascularity within adherent clot but may do so in a neoplastic mural nodule. Despite the absence of vascularity on this color Doppler image, follow-up imaging in 6 weeks is recommended to ensure that the clot continues to resolve. Occasionally Doppler interrogation does not demonstrate vascularity in tumor nodules because of low velocity, low volume flow, or sampling error.
septae (fish net) (Fig. 4). The clot may appear as an echogenic mass either mobile or adherent to the cyst wall but without evidence of vascularity. Typically, the clot retracts over time and adheres to the cyst wall in a lenticular shape (Fig. 5). Lysis of red blood cells may result in layering fluid or debris. Follow-up examination at a 6- to 8-week interval should demonstrate that a hemorrhagic cyst changes in appearance and decreases in size [7]. In patients with rupture or leakage of fluid from the corpus luteal cyst, the cyst may have an angular or crenated appearance, and free fluid that contains low-level echoes or frank clots may be observed in the culde-sac or surrounding the ovary [2,7].
risk factors include presence of an intrauterine device, exposure to diethylstilbestrol, adhesions from prior surgery, and previous ectopic pregnancy (Box 1). The reported increased incidence of ectopic pregnancy is also likely in part accounted for by an apparent increase because of early US evaluation of symptomatic pregnant patients. Endovaginal US almost certainly documents some early ectopic pregnancies that otherwise would have resolved without coming to medical attention. Endovaginal US, combined with quantitative b-human chorionic gonadotropin (b-HCG) analysis, is an excellent tool for identifying ectopic pregnancy and differentiating from other causes of adnexal mass in the pregnant patient with pelvic pain. The first goal of endovaginal US in the patient suspected of harboring an ectopic pregnancy is to assess for an intrauterine pregnancy because ectopic pregnancy can be reasonably excluded when an intrauterine pregnancy is identified [9]. Only rarely does an ectopic pregnancy occur synchronously with an intrauterine gestation. Heterotopic pregnancy is estimated to occur in only 1 in 2600 to 1 in 30,000 pregnancies in the general population [10], but it likely occurs in up to 1 in 100 in patients with multiple risk factors who are undergoing infertility treatment [11]. An intrauterine gestational sac should be seen on endovaginal US when the b-HCG is more than 2000 mIU/mL (approximately 4 6 weeks gestation). The earliest positive sign of an intrauterine pregnancy is the intradecidual sign, which is defined as a fluid collection with an echogenic rim located eccentrically within either the anterior or posterior layer of the endometrium adjacent to the echogenic line that represents the endometrium [12,13]. The intradecidual sign should be visible at 4.5 weeks gestation, but it can be confused with a pseudosac or decidual cyst. A study reported by Laing et al [12] demonstrated a low enough sensitivity and specificity to warrant a recommendation to document the development of a yolk sac or fetal pole on follow-up examination to
Ectopic pregnancy The incidence of ectopic pregnancy has increased over the past three decades, and it recently reached a plateau at a reported rate of 19.7 per 1000 pregnancies [8]. Ectopic pregnancy remains the leading cause of maternal death in the first trimester and the second leading cause of maternal mortality overall [8]. Improved treatments for infertility and pelvic inflammatory disease and an increase in the size of the patient population at risk for ectopic pregnancy in large part account for the increased incidence. Other Box 1. Conditions that predispose to ectopic pregnancy

Prior pelvic inflammatory disease Presence of an intrauterine device Treatment of infertility Tubal surgery Previous ectopic pregnancy Diethylstillbestrol exposure
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confirm an intrauterine pregnancy. The double decidual sac sign is formed when the gestational sac is surrounded, at least in part, by two echogenic layersdecidual capsulans (inner) and decidual parietalis (outer)and is separated by the hypoechoic endometrial cavity [9]. It should be seen when the mean sac diameter is more than 10 mm. Because endovaginal US (when using a high-frequency transducer) typically demonstrates a yolk sac with an intrauterine pregnancy by the time the mean sac diameter (MSD) is more than 8 mm, the double decidual sign is of limited use in the evaluation of patients with suspected ectopic pregnancy. The presence of trophoblastic flow (high velocity, low impedance) around an endometrial fluid collection further supports the diagnosis of an intrauterine pregnancy, although pulsed Doppler should be used with caution because of concerns regarding heat deposition in the developing fetus. A pseudosac, an intrauterine fluid collection formed in response to hormonal influences on the endometrium as the result of the presence of an ectopic pregnancy, can be distinguished from an intrauterine pregnancy by its central location in the endometrial cavity, oval shape, poorly defined margins, absence of decidual reaction, single decidual layer, and absence of trophoblastic flow. Ectopic pregnancy most commonly (95%) occurs in the ampullary or isthmic portions of the fallopian tube. An ectopic pregnancy can be diagnosed with confidence when an adnexal mass that contains a yolk sac or viable embryo is identified (Fig. 6) [14]. In the absence of a visualized yolk sac or fetal pole, the so-called echogenic adnexal (or tubal) ring sign
Fig. 7. Ectopic pregnancy. Note echogenic tubal ring (arrow) medial to the right ovary (cursors). Amorphous hypoechoic material between ovary and ectopic pregnancy likely represents hemorrhage.
Fig. 6. Ectopic pregnancy. A yolk sac (arrow) and fetal pole (arrowhead) are present within this echogenic tubal ring (curved arrow) located in the cul de sac. U, uterus. Note that the wall or ring of this ectopic pregnancy is much more echogenic than the wall of the corpus luteal cyst in Fig. 3.
is the next most specific US finding for ectopic pregnancy (Fig. 7) [15]. Adnexal rings are usually located between the ovary and uterus. In 14% to 33% of cases, the adnexal ring is contralateral to the corpus luteum [16]. The echogenic adnexal ring typically has a relatively anechoic center and vascular wall (sometimes only focally). It may be difficult to differentiate the tubal ring of an ectopic pregnancy from an exophytic corpus luteal cyst. An anechoic structure with an echogenic, vascular rim truly located within the ovary is statistically much more likely to be a corpus luteal cyst, because true intraovarian ectopic pregnancies are rare. Frates et al [17] reported that the wall of the adnexal ring is more echogenic compared with the ovarian stroma in 88% of ectopic pregnancies, whereas the wall of the corpus luteal cyst was usually relatively hypoechoic. Corpus luteal cysts and ectopic pregnancy demonstrate low-resistance arterial flow on Doppler examination [18]. Color Doppler is helpful primarily for increasing conspicuity. Differentiation between an ectopic pregnancy and an exophtic corpus luteal cyst can be aided by gently tapping on the ovary with the transducer. Independent movement of the ovary indicates an extraovarian location of the adnexal ring, which confirms ectopic pregnancy. A hemorrhagic ovarian cyst occasionally can produce an adnexal ring sign, and when associated with significant hemoperitoneum, it may mimic ectopic pregnancy [19]. Evaluation of the cul-de-sac and Morrisons pouch is important to detect echogenic fluid that could represent blood (Fig. 8) [20]. Transabdominal US is particularly helpful for evaluation of these areas and visualization of the patients point of maximal tenderness if not imaged on endovaginal US. Blood need
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Fig. 8. Hemoperitoneum from a ruptured ectopic pregnancy. Note echogenic free fluid (arrow) outlining loops of bowel.
neither be echogenic nor the consequence of tubal rupture, however; hemoperitoneum may be anechoic (albeit rarely) and can occur secondary to leakage from the fimbriated end of the fallopian tube or even from a ruptured hemorrhagic corpus luteal cyst. Endovaginal US has replaced culdocentesis as the method of choice for detecting hemoperitoneum [21]. Brown and Doubilet [14] reported that demonstration on US of an extrauterine gestational sac that contains a yolk sac or embryo or a tubal ring has high specificity rate (99.5% 100%) and high positive predictive value (97.8% 100%) for the diagnosis of ectopic pregnancy. Sensitivity rate was, however, found to be low (20.1% 64.6%). When the most nonspecific finding that suggests ectopic pregnancy the presence of any adnexal mass other than a simple cystwas used as the sole diagnostic criterion, sensitivity rate was improved (84.4%) with only slightly diminished specificity rate (98.9%) and positive predictive value (96.3%) [14]. The sonographer should remember that in up to 26% of ectopic pregnancies, no intrauterine pregnancy or adnexal abnormality may be detectable by endovaginal sonography [22]. Clinical correlation and close follow-up are of paramount importance. Although the terms are occasionally used interchangeably, the term cornual pregnancy should be reserved for an intrauterine pregnancy implanted in one horn of a bicornuate or septate uterus, whereas an interstitial ectopic pregnancy (approximately 2% 4% of all ectopic pregnancies) occurs in the interstitial (or intramyometrial) portion of the fallopian tube. An interstitial ectopic pregnancy typically develops much longer before becoming symptomatic, and it often presents late in the first trimester or early in the
second trimester. A ruptured interstitial pregnancy poses a significantly increased risk of severe, lifethreatening hemorrhage. On US examination, the sac is eccentrically located within the uterine wall, and the surrounding myometrium is thinned (<5 mm) or even absent laterally. The interstitial line sign describes an echogenic line that reflects the two opposing layers of endometrium seen adjacent to the gestational sac but not surrounding it. This sign has been reported to be 80% sensitive and 99% specific for diagnosing interstitial ectopic pregnancy, compared with 40% sensitive and 62% specific for eccentric location or 40% sensitive and 74% specific for myometrial thinning [23]. Even more convincing is visualization of myometrial tissue interposed between the gestational sac and echogenic line (endometrial cavity). It may be difficult to distinguish interstitial and cornual pregnancies. Braxton Hicks contractions or fibroids occasionally can cause a normal intrauterine pregnancy to be eccentrically placed. If there is doubt about the diagnosis, follow-up may be helpful. Cervical pregnancies are rare but are important to diagnose accurately because routine dilation and curettage may cause life-threatening hemorrhage. Cervical ectopic pregnancies may be difficult to differentiate from pregnancies implanted in the lower uterine segment or miscarriages. An hourglass appearance of the uterus, a gestational sac seen within the cervical canal or in an eccentric location, invasion of the cervical stroma or the presence of trophoblastic flow, and visualization between the external and internal cervical os may be helpful in differentiating a cervical pregnancy from an impending miscarriage, although trophoblastic flow occasionally can be noted during miscarriage. Abdominal pregnancy, defined as an ectopic pregnancy located in the peritoneal cavity, occurs in 1 in 10,000 pregnancies. It is a medical emergency because of high associated maternal and fetal morbidity and mortality. Surgery is indicated as soon as the diagnosis is made. In rare cases of undetected advanced abdominal pregnancy with fetal demise, lithopedion formation (fetal calcification) can occur. This is usually found incidentally and can appear on US as a large echogenic mass. Treatment for ectopic pregnancy increasingly includes medical and even expectant management, in addition to laparoscopic surgery. Close interval follow-up with endovaginal US, monitoring serial b-HCG levels, and reassessment of the patients clinical stability are crucial elements of expectant therapy [24]. Methotrexate is a folic acid antagonist that inhibits the synthesis of purines and pyrimidines, which
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prevents DNA synthesis and cell multiplication. It acts primarily on the rapidly dividing trophoblastic cells of the embryo [87]. Although exact eligibility criteria continue to change with increasing experience and vary somewhat among institutions, medical management with methotrexate is most effective when an ectopic pregnancy is small (<3 4 cm), b-HCG is low (<15,000 20,000 IU/mL International Reference Preparation [IRP]), and cardiac activity is absent. Medical management of ectopic pregnancy may, however, be attempted despite one or more of these criteria not being met. These patients have a higher incidence of failure of treatment and may require multiple doses of methotrexate [88]. Absolute contraindications to medical therapy include pain, hemodynamic instability, or evidence of large hemoperitoneum. Eligibility criteria and absolute contraindications of methotrexate treatment are further discussed in Boxes 2 and 3 [87,88]. In the 2 to 4 weeks after methotrexate administration, an ectopic pregnancy can demonstrate persistent vascularity and can increase in size secondary to infarction and hemorrhage. These findings are normal, and, in an asymptomatic patient, do not represent failure of treatment. To avoid confusion, sonographic follow-up is sometimes avoided during this time as long as the patient remains asymptomatic. If a patient develops pain, US follow-up is necessary to evaluate for signs of tubal rupture, such as a dramatic increase in the size of the ectopic pregnancy or large hemoperitoneum. Pain can develop during the normal course of methotrexate therapy, 4 to 5 days after administration, because of the infarction of trophoblastic tissue. The development of pain does not necessarily indicate failure of treatment or tubal rupture. Pain secondary to trophoblastic tissue infarction should resolve within 12 to 24 hours. Baseline b-HCG levels are recorded before methotrexate administration. The b-HCG begins to fall gradually after 4 days. If there is
Box 3. Medical contraindications to methotrexate therapy

Abnormal liver function tests (LFTs)
(elevated transaminases) Immunodeficiency Any type of blood dyscrasia Leukocyte count of <2000 Platelet count of >100,000 Peptic ulcer disease Active pulmonary disease Renal disease Known sensitivity to methotrexate
more than a 15% fall in b-HCG from the baseline, a second injection of methotrexate is not required [88].
Theca lutein cysts Theca lutein cysts are caused by elevated levels of chorionic gonadotropin and are seen in patients with hydatidiform mole or choriocarcinoma and in the setting of exogenous chorionic gonadotropin administration for treatment of infertility [2]. The cysts are lined by theca cells, which may or may not be luteinized [2]. Cysts are usually multiple and bilateral and typically range in diameter from 3 to 20 cm [25]. Symptoms are usually mild, including pelvic fullness and dull pelvic pain. Acute pain can occur in the setting of cyst rupture or hemorrhage [2]. The cysts resolve spontaneously after treatment of gestational trophoblastic disease or cessation of fertility therapy. Theca lutein cysts may persist for long periods, however, despite relatively low levels of b-HCG [25]. US examination demonstrates multiple simple cysts in both ovaries (Fig. 9).
Box 2. Eligibility criteria for methotrexate therapy

Ovarian hyperstimulation syndrome Ovarian hyperstimulation syndrome (OHSS) is a potentially dangerous iatrogenic complication of pharmacologic ovulation induction for the treatment of infertility [26]. It occurs in the setting of abnormally high levels of b-HCG and less frequently has been reported in spontaneous singleton and multiple pregnancies, sex hormone producing tumors, and choriocarcinoma [26 28]. Although the precise pathophysiology remains unknown, b-HCG seems to trigger an increase in vascular permeability that
Hemodynamically stable Absence of large hemoperitoneum Absence of pain Ectopic size <3.5 4 cm C-HCG levels with peak values >15,000 20,000 mIU/mL (IRP) F Cardiac activity in gestational sac Absence of any contraindications
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Fig. 9. Theca lutein cysts. Note multiple simple bilateral ovarian cysts in this patient with a hydatidiform mole. A pocket of free fluid is present between the two ovaries (arrow).
results in ovarian enlargement, cyst formation, and third spacing of fluid. The renin-angiotensin system, vascular endothelial growth factor, and cytokines are believed to be chemical mediators in this process [29,30]. Whelan and Vlahos [31] emphasize risk stratification as the key to preventing OHSS or minimizing its severity. Generally accepted risk factors include young age, presence of theca lutein cysts, and elevated estradiol levels. Known polycystic ovarian syndrome or the presence of multiple peripheral ovarian follicles (the necklace sign) on US in a patient with a clinical presentation that suggests polycystic ovarian syndrome is also a risk factor for OHSS [32]. Women who undergo ovulation induction therapy whose ovaries contain several small or intermediate-sized follicles are at greater risk for developing OHSS than women with large (>15 mm) follicles, especially when seen in conjunction with high levels of estradiol (>3000 pg/mL) [33]. Higher baseline ovarian volume of more than 10 mL also has been shown by Danninger et al [34] to predict subsequent development of OHSS and may become a more important predictor with the widespread availability of US units capable of providing three-dimensional images with highly accurate, reproducible measurements of ovarian volume. A patient at higher risk for OHSS may require more intensive monitoring (including US) or undergo an alternative pharmacologic ovulation induction technique. It is estimated that mild OHSS may occur in as many as 65% of women who undergo ovulation induction. The incidence of clinically important (moderate to severe) OHSS ranges from 1% to 10% of exogenously induced
ovulation cycles, but only a small percentage of these cases are severe (0.5% to 5%) [35,36]. OHSS is more severe in patients who become pregnant after ovulation induction. The spectrum of clinical presentation ranges from nausea, vomiting, and abdominal pain to massive ascites, acute respiratory distress syndrome, and hypotension, classified according to severity by Golan et al [30]. Pain may be caused by rupture of or hemorrhage into the enlarged cysts or ovarian torsion. Approximately 20% of patients who receive gonadotropin therapy develop mild to moderate ovarian enlargement [37]. Ovarian diameter more than 5 cm is a criterion for diagnosis of mild OHSS, although the ovaries are frequently more than 10 cm in diameter. US is the most exact method of detecting ovarian enlargement. It is also preferable to bimanual examination because of the risk of ovarian rupture [30]. On US, multiple large, thin-walled cysts are identified. Pulsed Doppler may demonstrate increased intra-ovarian arterial diastolic flow or nonphasic venous flow, which indicates decreased venous return [38]. Acute pain may be caused by hemorrhage into a cyst, cyst rupture, or ovarian torsion. Debris or low-level echoes within the cysts may be seen when hemorrhage occurs. Cyst rupture can result in an irregularly shaped cyst with adjacent free fluid or fluid in the cul-de-sac (Fig. 10). Because ovarian enlargement predisposes to ovarian torsion, documentation of ovarian blood flow is important in patients who present with acute pain (see next section). In severe cases of OHSS, US can be used to detect and monitor complications. US examination may demonstrate ascites or pleural fluid, criteria used in determining whether hospitalization is necessary [31]. Oliguria may prompt a request for renal US evaluation, although in the setting of OHSS this is usually secondary to impaired venous return from the kidneys secondary to extrinsic compression by ascites. Patients with OHSS are at increased risk of thromboembolism caused by hemoconcentration and may benefit further from US examination for various complications, such as deep venous thrombosis. Thoracic complications, such as pulmonary embolism (1.9%), acute respiratory distress syndrome (2.4%), infection (3.8%), atelectasis (20%), and pleural effusion (29%; usually right-sided), may occur [39]. Unilateral pleural effusion has been reported as an isolated finding in OHSS [40,41]. A large pleural effusion often predicts hemodynamic instability. Treatment is supportive: hemodynamics, hematocrit, electrolytes, liver and kidney function (including urine output), and coagulation parameters are monitored. Some authors have advocated an outpatient treatment approach, facilitated in part by
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Fig. 10. Ovarian hyperstimulation syndrome. (A) Note marked enlargement of the right ovary within calipers. Numerous cysts are seen, several of which contain internal echoes. There is a small amount of free fluid adjacent to the enlarged ovary. (B) Pulse Doppler interrogation reveals high-velocity systolic and diastolic flow, which excludes the diagnosis of ovarian torsion. The patients pain is likely caused by hemorrhage into these cysts or rupture of these hemorrhagic cysts.
US-guided follicular aspiration [42]. Navot et al [32] reported US-guided paracentesis as the treatment of choice when medical therapy is insufficient; alternatives include transvaginal aspiration of ascites or follicular cysts. OHSS typically resolves in 7 to 10 days unless pregnancy ensues, in which case recovery is more prolonged.
Ovarian torsion Ovarian or adnexal (ovary and fallopian tube) torsion is a surgical emergency that requires prompt diagnosis and treatment. There is increased risk
during pregnancy, and ovarian torsion occurs in approximately 1 in 1800 pregnancies [1,43]. Approximately 25% of adnexal torsions occur in pregnant patients [1]. Adnexal torsion most commonly occurs between 6 and 14 weeks gestation and in the immediate puerperium [1,44]. Ovarian torsion is the result of partial or complete rotation of the ovarian pedicle on its axis, which results initially in impaired lymphatic and venous drainage and eventual loss of arterial perfusion [43,45]. It occurs more commonly on the right side [44]. Torsion can be difficult to diagnose clinically because the presenting symptoms, including pain, nausea, and vomiting, are nonspecific and similar to many causes of acute abdomen [43,45].
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Because ovarian enlargement of more than 6 cm predisposes to ovarian torsion [46,47], women who undergo ovulation induction have the highest incidence because of the development of numerous theca lutein cysts, which can massively enlarge the ovaries [2,30]. Mashiach et al [47] reported that torsion was more common in women with OHSS who subsequently became pregnant, compared with women with OHSS alone. Enlargement of the ovary secondary to a corpus luteal cyst or incidental benign ovarian neoplasm, most commonly a mature mature cystic teratomas or cystademoma, also can predispose to ovarian torsion [44]. Ovarian torsion rarely occurs in the presence of ovarian carcinoma or endometriosis because of fixation of the ovaries to adjacent structures by adhesions. The US appearance of ovarian torsion varies depending on the degree of ischemia and infarction and the time course [44]. The ovary is typically enlarged. Numerous small follicles are often seen at the periphery of the ovary [43,45,48]. The central ovarian stroma becomes heterogeneous with areas of increased echogenicity, which represent hemorrhage, and more hypoechoic areas, which represent edema
(Fig. 11A) [44]. With frank infarction, cystic, clotted areas may be observed. Free fluid within the pelvis or adjacent to the ovary also can be seen [44,50]. Although the range of gray scale features varies, the ovary rarely has a completely normal appearance. Classically, Doppler interrogation demonstrates absence of arterial flow (Fig. 11B). It is important, however, to remember that early in the process there may be obstruction of lymphatic and venous flow with preservation of arterial perfusion [49 51]. Occasionally only diastolic or venous flow is lost early on. Because the ovary has dual arterial supply, in early torsion only one may be occluded [51]. In a patient who presents with acute pain and an ovary that demonstrates real-time findings consistent with ovarian torsion, the diagnosis should be suggested even in the presence of documented arterial blood flow (Fig. 12) [48 51]. When color Doppler imaging and pulsed Doppler sampling do not demonstrate arterial flow within the ovarian parenchyma, the diagnosis is more easily made. All Doppler parameters must be set carefully to maximize detection of slow flow to avoid a false-positive diagnosis caused by technical factors. Sampling error also may cause
Fig. 11. Ovarian torsion. (A) The ovary is enlarged with several small peripherally located cysts (arrows). The central ovarian stroma is heterogeneous, with echogenic areas representing hemorrhage and hypoechoic areas representing edema. No flow is detected with color Doppler. (B) Because pulse Doppler is more sensitive to low-velocity, low-volume flow, meticulous sampling with pulse Doppler should be performed. No flow could be demonstrated in this case.
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and masses spontaneously resolve several months after delivery [53]. The diagnosis should be entertained to avoid unnecessary oophorectomy. In case reports, the lesions have been described on US as solid ovarian masses. Cystic components may be present secondary to necrosis [53].
Disease unrelated to pregnancy Diagnoses such as ectopic pregnancy and ovarian torsion are likely to be at the top of the differential list in a pregnant patient who presents with acute pelvic pain and an adnexal mass. There are, however, many gynecologic and nongynecologic causes of acute pelvic pain and pelvic mass that are unrelated to pregnancy and may still occur in this population.
Fig. 12. Early ovarian torsion. Note classic gray scale features of torsion: ovarian enlargement, central amorphous, heterogeneous stroma, and small peripheral cysts. Pulse Doppler interrogation revealed some arterial flow in this woman, who presented less than 2 hours after the acute onset of severe pelvic pain.
Pelvic inflammatory disease and tubo-ovarian abscess false-positive diagnoses. Fleischer et al [52] reported that the preservation of parenchymal venous flow is a useful indicator of ovarian viability. The twisted vascular pedicle also can be seen on color Doppler sonography. Demonstration of flow within the twisted vascular pedicle may be a useful marker of ovarian viability (Box 4). Adnexal torsion that is diagnosed before tissue infarction is managed with laparoscopic detorsion surgery followed by progesterone replacement if the corpus luteum is removed. If tissue infarction and necrosis have occurred, then laparotomy with salpingo-oophorectomy is usually required to prevent peritonitis. Pelvic inflammatory disease (PID) is most commonly caused by sexually transmitted infection by Chlamydia species or Neisseria gonorrhea. Uterine instrumentation and the placement of intrauterine contraceptive devices also are risk factors [44]. Less frequently, PID may be caused by direct extension
Box 4. Sonographic findings of ovarian torsion Gray scale findings
Luteoma of pregnancy Luteoma of pregnancy is a rare entity, with fewer than 200 cases reported in the literature [53]. Luteomas consist of non-neoplastic tumor-like masses of lutein cells and are often multifocal and bilateral [2,53]. The luteoma range up to 20 cm in diameter, but most are in the 5- to 10-cm range [2]. Luteomas are usually clinically occult, only coming to attention when visualized during cesarean section or postpartum tubal ligation [2]. Occasionally, luteomas can have androgenic effects that result in fetal hirsutism and virilization. As is the case with any large adnexal mass, however, luteomas may precipitate ovarian torsion that results in acute pelvic pain. Although their morphologic appearance can be ominous and suggest malignancy, biopsy is adequate for diagnosis,
Ovarian enlargement Peripherally located follicles Heterogeneous central ovarian stroma

Internal hemorrhage (echogenic) Internal edema (hypoechoic)
Cystic necrosis of the ovary Free fluid F Underlying precipitating mass Range of color/pulsed Doppler findings Normal Loss of venous flow Loss of diastolic flow Absence of flow Twisted vascular pedicle
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of infection from appendicular or diverticular abscesses, and in these instances disease tends to be unilateral [44,46]. Fortunately, acute PID is a rare entity in the pregnant patient. The cause of PID in pregnancy is uncertain, but recurrence of old inflammatory disease is considered the most common cause [54]. PID is typically an ascending infection that begins as a cervicitis, progresses to endometritis, and ultimately involves fallopian tubes or ovaries (tubo-ovarian complex). Only approximately 5% of patients with PID progress to abscess formation. PID can be difficult to diagnosis secondary to vague or confusing symptoms. It should be suspected in the setting of fever, pelvic discomfort, and purulent vaginal discharge. Many patients do not demonstrate these classic symptoms, however, and US imaging often plays a crucial role in diagnosis and patient management [4]. Pelvic US is frequently normal in the early stages of PID [44,46]. As disease worsens or becomes more chronic, several appearances can be identified on US imaging. US may reveal dilatation of one or both fallopian tubes. Hydrosalpinx is characterized by its tubular shape or folded configuration [55]. A well-defined echogenic wall and linear echoes that protrude into the anechoic tubal lumen are also characteristic [55]. Hydrosalpinx can be differentiated from fluid-filled bowel loops by the absence of peristalsis [55]. Dilated fallopian tubes also may contain diffuse, low-level echoes that represent debris or hemorrhage (Fig. 13) or appear as a complex cystic adnexal mass that demonstrates multiple fluid levels and septations [4,44]. Once the disease has progressed to abscess formation (Fig. 14), a complex adnexal mass is observed on US examination. The ovary may not be identifiable separate from the mass but actually may be engulfed by the infection,
Fig. 14. Tubovarian abscess. Note complex fluid collection engulfing right ovary (arrow).
although relative sparing of the ovary has been reported. The ovary is sometimes enlarged with indistinct margins secondary to peri-ovarian inflammation, termed the tubo-ovarian complex [4]. Pressure from the transducer often causes pain during the examination, and the pelvic organs may appear fixed to the surrounding tissues. The serosal contour of the uterus may be indistinct because of surrounding inflammatory exudate. Pus may be seen within the cul-de-sac or around the liver with an appearance of free fluid containing low-level echoes [4,44,46]. A US that demonstrates findings that suggest PID (ie, a thick-walled, fluid-filled tubular adnexal mass with or without free intrapelvic fluid) has been reported to have a sensitivity rate of 85% and a specificity rate of 100% for the diagnosis [56]. Any complex multilocular adnexal mass in an appropriate clinical setting can represent PID, however. Hydrosalpinx is not always present. Abscess drainage or conservative surgical procedures with antibiotic therapy are often recommended in managing PID complicated by tubo-ovarian abscess during pregnancy. There is no true consensus on management in this population, however [54].
Endometrioma Endometriosis is a common cause of abdominal pain. In younger women, endometriosis is defined as the presence of functional endometrial tissue outside of the uterus [43]. The classic triad of clinical symptoms includes pelvic pain, dysmenorrhea, and infertility [43,57]. Endometriosis has an estimated prevalence of 1% in reproductive age women [57]; however, the incidence of endometriosis in women with infertility is closer to 40% [43]. Overall, endo-
Fig. 13. Pyosalpinx. Note layering debris or pus (curved arrow) in the dilated fallopian tube.
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Fig. 15. Endometrioma. The cystic lesion medial to the right ovary contains diffuse low-level echoes (arrow) and demonstrates increased through transmission. The wall is thin and regular.
metriomas account for approximately 4% of adnexal masses diagnosed during pregnancy [1]. Endometriomas can have a diverse range of appearances on US, from anechoic cysts to complex cystic masses that contain multiple septations to heterogeneous echogenicity. Classically endometriomas appear on US as thin-walled unilocular cystic masses that contain diffuse, low-level echoes (Fig. 15) [43,57 59]. Patel et al [59] reported that hyperechoic wall foci and multilocularity, in the absence of malignant features, highly suggest endometrioma. Layering or anechoic foci within a background of homogeneous low-level echoes also have been described. Margins may be indistinct and angulated secondary to associated adhesions. The appearance on US may be similar to
that of a hemorrhagic cyst [60]. The pattern of internal echoes within a hemorrhagic cyst is more often lace-like, however, as opposed to the homogeneous hypoechoic internal echoes characteristic of endometrioma, and hemorrhagic cysts more often present with acute pain [43]. Endometriomas are more frequently multiple, and their appearance is more stable over time when compared with hemorrhagic cysts. Hemorrhagic cysts and endometriomas may have vascular walls on color Doppler interrogation [61]. An increased likelihood of mural vascularity in endometriomas has been reported in patients with acute pelvic pain and may serve as a relative marker of disease activity, although this is somewhat controversial [62]. Endometriomas can be bizarre looking and cannot always be distinguished readily from malignancy. The presence of irregular walls or vascular nodularity should raise concern, because clear cell or endometroid carcinomas rarely may develop within endometriomas (<1%). MR imaging may be useful to document the presence of hemorrhage within an ovarian mass when US examination is equivocal.
Leiomyomata Leiomyomata are the most common benign uterine neoplasms and are composed of smooth muscle cells with varying amounts of fibrous connective tissue and collagen. Leiomyomata are most commonly diagnosed in premenopausal women, with an incidence of 20% to 30% in women over the age of 30 [43]. Some studies have indicated that careful
Fig. 16. Acute hemorrhagic infarction of a fibroid in a patient who presented with acute pelvic pain 4 days postpartum. (A) Sagittal US image of the uterus (U) reveals an echogenic subserosal fibroid (arrow) with a small amount of adjacent free fluid. (B) Follow-up CT scan demonstrates lack of enhancement of the uterine mass (arrow), which is consistent with acute hemorrhagic infarction.
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Fig. 17. Pedunculated leiomyoma. Note large left leiomyoma connected to the uterus by a thin pedicle (arrowhead).
pathologic evaluation can demonstrate leiomyomas in up to 80% of women of reproductive age [1]. Uterine leiomyomata are diagnosed in 0.3% to 4% of pregnancies, usually because a pedunculated subserosal leiomyoma simulates an ovarian neoplasm [1,45]. Pedunculated leiomyomata may undergo torsion and necrosis, which results in acute pelvic pain [45]. Fibroids are hormonally dependent and can rapidly increase in size during pregnancy, which results in hemorrhagic infarction, which may cause acute, severe pelvic pain (Fig. 16). Leiomyomata have variable appearance on US. They most frequently appear as round, homogeneous solid, wellcircumscribed masses that are usually hypoechoic or isoehoic to the myometrium and more rarely relatively echogenic. Areas of decreased echogenicity secondary to degeneration and necrosis may be seen, especially in lesions larger than 5 cm. Distal acoustic shadowing, often in a striated pattern, is commonly noted. Calcification is most common in older women [63]. It may be difficult to identify the site of myometrial attachment of a pedunculated leiomyoma on gray scale imaging. Both ovaries should be identifiable separate from the mass, however (Fig. 17), and color Doppler imaging may help to identify a vascular pedicle. When sonographic evaluation of an adnexal lesion is indeterminate in differentiating a pedunculated leiomyoma from a solid ovarian neoplasm, MR imaging can be useful in further characterization [64].
cystadenomas [1]. Mature cystic teratomas are benign neoplasms that usually contain tissue derived from all three germ cell layers [2,43]. Occurring most commonly in the active reproductive years [43], dermoids account for 40% to 50% of benign ovarian neoplasms and are bilateral in 10% to 15% of cases [43]. Malignant transformation is rare (<2% of cases) and is most common in older women [47]. Dermoids are usually asymptomatic unless torsion or rupture occurs [43]. US appearance of mature cystic teratomas ranges from that of a solid homogeneously echogenic mass with posterior attenuation (Fig. 18) to a completely anechoic structure that mimics an ovarian cyst. Several US features, however, have been described as specific to mature cystic teratomas. A predominately cystic mass with an echogenic mural nodule is a characteristic appearance. The mural nodule, or dermoid plug, may contain hair, teeth, or fat [65]. If calcium is present, distal acoustic shadowing is observed. [43,66]. Linear echogenic foci that represent hair fibers, an echogenic hair ball floating at a fluidfluid interface (Fig. 19), and fat-fluid levels are also specific features [43,67,68]. A study by Patel et al [66] found that the positive predictive value was 100% when an ovarian mass had two or more US features considered specific for mature cystic teratomas. In this study, the sensitivity of US for detection of dermoids was reported as 85% [66]. Diffusely echogenic mature cystic teratomas can escape detection by US because they appear similar to bowel [43]. When a palpable adnexal mass can be diagnosed confidently as a mature cystic teratoma, surgery can be delayed safely until after delivery. If US is nondiagnostic but suspicious, CT or MR imaging may
Benign and malignant neoplasms Ovarian neoplasms are most often asymptomatic unless they precipitate ovarian torsion, although such lesions may present with vague abdominal or pelvic pain and urinary frequency. Most ovarian neoplasms detected during pregnancy are benign. The most common of these are mature cystic teratomas and
Fig. 18. Mature cystic teratoma of the ovary. Note large echogenic mass on the left (arrowheads).
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Fig. 19. Mature cystic teratoma of the ovary. Note echogenic hairball floating (arrow) at the fat/fluid interface. The liquid fatty layer contains low-level echoes. Becuase the fat is lighter than the serous fluid, the more echogenic layer is more anterior in this supine patient.
document the presence of fat within dermoids, thereby confirming the diagnosis. Serous and mucinous cystadenomas are benign neoplasms that most commonly occur in reproductive age women [43]. They can be difficult to differentiate sonographically from malignant cystadenocarcinomas because of the wide spectrum of appearances on US. Serous cystadenomas typically are large, unilocular, thin-walled cystic lesions that may demonstrate thin septations or papillary projections (Fig. 20). They are bilateral in 20% of cases [43]. Mucinous cystadenomas are typically larger, measure up to 30 cm, and may contain internal low-level echoes secondary to mucin content. Septations are common. Papillary projections are less common and the mass usually unilateral [43]. Malignant neoplasms comprise approximately 3% of adnexal masses diagnosed in pregnancy [1]. The most common malignant neoplasms that come to attention during pregnancy include germ cell tumors, low-grade ovarian cancers, and invasive epithelial ovarian cancers. Most women diagnosed with ovarian cancer during pregnancy present with stage 1 disease [1]. In many cases the US appearance of complex cystic adnexal masses is indeterminate and the differential diagnosis of cystadenoma or cystadenocarcinoma must be considered. The presence of thick vascular septations (>3 mm), mural nodularity, papillary processes, thick, irregular walls, solid areas, invasion or fixation of adjacent structures, and associated findings, such as ascites or serosal implants,
increase the likelihood of malignancy (Figs. 21, 22) [68,69]. The likelihood of malignancy also increases with age, elevation of serum CA-125 level, and positive family history [70]. It is not possible to differentiate benign solid lesions (eg, fibromas or thecomas) from malignant germ cell or stromal tumors [69]. The presence of a purely solid tumor indicates a higher probability of metastatic carcinoma than primary ovarian cancer (Fig. 23) [71]. Numerous authors have reported that ovarian malignancies tend to have increased peak systolic flow (peak systolic velocity >35 cm/second) and low resistance perfusion (resistive index <0.4 or perfusion index <1) [68,70,72,73]. There is significant overlap in the distribution of peak systolic velocity, resistive index, and perfusion index values between benign and malignant lesions, however, and no discriminatory value is accepted [68,70,72,73]. Lack of detectable flow by means of color Doppler US does not exclude ovarian malignancy [72]. The management of an ovarian mass during pregnancy is controversial. Surgery in the first trimester is associated with pregnancy loss, and surgery in the third trimester can result in premature labor [1]. Although US is excellent at detecting adnexal masses, it is not always accurate in differentiating benign from malignant lesions. Although the previously described morphologic characteristics and internal vascularity with high peak systolic velocity and low resistive index suggest malignancy, these features are nonspecific, with a positive predictive value of approximately 50% [73]. The real value of US lies in the high negative predictive value (nearly 99%) of US features considered to be benign [73]. In a pregnant patient with a palpable adnexal mass and US features diagnostic of a benign entity, such as a serous or hemorrhagic cyst, dermoid or pedunculated fibroid, surgery may be postponed safely until after delivery or avoided
Fig. 20. Serous cystadenoma. Note thin, regular septations (arrow) in this cystic adnexal mass.
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Fig. 21. Stage 1 serous cystadenocarcinoma. This 28-year-old patient presented at 12 weeks gestation with a palpable right adnexal mass. (A) US reveals mural irregularity (arrow), which represents small papillary projections. (B) These papillary projections (arrow) are seen on corresponding MR image. Gravid uterus (U) is anterior.
altogether. Masses with multiple malignant features require prompt surgery. Masses that appear more benign are often followed by serial examinations until the second trimester, which is the optimal time for surgery in terms of maternal and fetal safety. In equivocal cases, MR imaging may be useful in further characterizing an adnexal mass.
Perforated appendicitis Appendicitis is the most common cause of nongynecologic acute pelvic pain in women and the most common diagnosis that requires emergent surgical intervention during pregnancy [4,74]. The inci-
dence of gestational appendicitis has been reported as 0.05% to 0.14% [45,74]. Although the incidence of acute appendicitis is not increased in pregnancy, appendiceal rupture occurs two to three times more frequently and occurs in up to 25% of cases, secondary to delay in diagnosis and surgery [1,45]. Patients with appendicitis typically present with fever, leukocytosis, nausea, vomiting, and peri-umbilical pain, which gradually moves to the right lower quadrant. These symptoms may be altered, muted, or absent in pregnancy, however, which contributes to delays in
Fig. 22. Serous cystadenocarcinoma. Note large complex adnexal mass on color Doppler with a vascular solid component (arrow).
Fig. 23. Krukenberg tumor (metastasis from gastric carcinoma). This 27-year-old woman presented at 32 weeks gestation with acute abdominal pain, bilateral solid ovarian masses, and ascites (only one mass is shown here). Although the differential diagnosis would include benign lesions, such as fibroma and fibrothecoma, the pronounced vascularity and ascites are worrisome for malignancy.
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diagnosis and the increased incidence of perforation and associated morbidity and mortality in this population [1,45,74 76]. In pregnancy, the most common presenting symptom is right-sided abdominal pain, regardless of the gestational age [76]. The position of the appendix is elevated above McBurneys point after the first trimester, however, and pain may be more localized to the right upper quadrant than the right lower quadrant and is often confused with cholecystitis [45]. Although CT is the imaging modality of choice in evaluating patients with suspected appendicitis, it is to be avoided in pregnant patients because of the risks of ionizing radiation to the fetus. US examination is often the first-line imaging modality in this patient population. US is a specific, although relatively insensitive, test for the diagnosis of acute appendicitis. Prospective studies have reported US specificity rates of 86% to 100% and sensitivity rates as high as 75% to 90% in patients with clinically suspected appendicitis [4]. In most clinical practices, however, the appendix is infrequently visualized, which limits the sensitivity and negative predictive value of the examination. In one study, on-call residents were only able to detect the appendix by US in 13% of cases in which appendicitis was clinically suspected [77]. Sensitivity for detection of appendicitis was 50% on US compared with 100% on CT [77].
The examination is performed with a linear array transducer. The cecum and psoas muscle can be used as landmarks to help localize the appendix. Graded compression is used to displace overlying bowel at the point of maximum tenderness [4,78]. An abnormal appendix appears as a blind-ending, aperistaltic loop of bowel that does not compress [4,79]. Transversely, the loop should be more than 6 mm in diameter (outer wall to outer wall) (Fig. 24) [4, 80 82]. This measurement criterion provides high sensitivity but limited specificity, because the normal appendix has been reported to have a diameter of up to 13 mm secondary to intraluminal contents [81,82]. The combined wall thickness should not exceed 6 mm in a normal appendix [4,82]. Increased vascularity may be noted on Doppler interrogation. In some cases, a shadowing appendicolith is seen [4]. The surrounding area also should be evaluated carefully to exclude loculated periappendiceal fluid or gas, which suggests abscess formation [4,78]. Recent reports suggest that MR imaging may be beneficial in evaluating patients for suspected appendicitis when US is nondiagnostic [83,84]. Appendicitis in pregnancy requires prompt surgery. Maternal mortality from appendicitis has diminished to approximately 0.1% but still exceeds 4% when perforation occurs [1]. Fetal mortality is less than 2% but is more than 30% in the case of perforation [1].
Diverticulitis Diverticulitis is uncommon in pregnant women. Patients present with lower quadrant (usually left) pain, fever, and leukocytosis [4]. Whereas CT is the gold standard in evaluation of suspected diverticulitis, US is a preferred modality in the pregnant patient, and a small body of literature has indicated that US can be used to make this diagnosis accurately. Pradel et al [85] reported that CT and US had an accuracy rate of 84% in diagnosing diverticulitis. US and CT findings were not statistically significantly different in terms of sensitivity rates (85% and 91%, respectively) and specificity rates (84% and 77%, respectively) [85]. Although transabdominal US scanning seems less sensitive in identifying diverticular abscess compared with CT, endovaginal US scanning is just as sensitive if the area is within reach of the vaginal probe [4]. US may identify an abnormal loop of bowel in the region of the patients pain with an irregular lumen and outpouchings beyond the bowel wall. The colonic wall may appear thickened but less concentrically so than in primary colitis. An adjacent walled
Fig. 24. Acute appendicitis. Transverse view demonstrates a thick-walled (arrow), noncompressible appendix with a surrounding fluid collection (F).
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off fluid collection or extraluminal shadowing air suggests perforation and abscess formation [4]. These results are operator dependent; however, US should not be overlooked as a viable alternative imaging modality for diagnosing diverticulitis in the pregnant patient.
Epiploic appendigitis Epiploic appendigitis is an uncommon entity. It is caused by torsion or ischemic infarction of one of the epiploic appendages of the colon, which incites a subsequent inflammatory reaction [4,86]. Epiploic appendages are rudimentary in children and reach their full size in adulthood. Most of them measure 2 to 5 cm in length and are 1 to 2 cm thick [4,86]. The largest appendages are found in the descending colon and cecum, which are the most common locations for torsion to occur [86]. Epiploic appendages are enlarged in obese patients, which increases their risk for torsion [86]. Patients most commonly present with acute or subacute left lower quadrant pain and leukocytosis. When cecal epiploic appendages are involved, the clinical picture may mimic appendicitis. Fever is usually absent [4,86]. Normal epiploic appendages are not visible on US unless the colon is surrounded by extraluminal fluid. In epiploic appendigitis, US demonstrates an ovoid, hyperechoic, solid, noncompressible mass at the point of maximum tenderness. The mass is often surrounded by a thin hypoechoic rim, believed to represent thickening of the serosa of the appendage and the adjacent parietal peritoneum [4,86]. The lesions are typically located between the anterior abdominal wall and the colon, from which they arise. The mass often adheres to the adjacent peritoneum, which can be observed on real-time sonography during inspiration and expiration [86]. Color Doppler signal is typically absent within the echogenic mass. Minimal blood flow is sometimes identified immediately external to the hypoechoic rim, however. This lack of vascularity is in contrast to the prominent color flow that is seen in secondary inflammation of the epiploic appendages in persons with diverticulitis [86].
with an adnexal mass can occur in pregnant patients, however. Some causes are benign and others require urgent management and treatment. Clinical presentation and physical examination can be misleading in pregnancy. The location of pain may be atypical for the pathologic entity, the pain may be muted, and in the case of infection, fever and leukocytosis can be absent. US examination is a safe and effective method for evaluating these patients. Sonographic characterization of adnexal masses may make a definitive diagnosis or focus the differential, which allows for prompt and appropriate treatment of patients.
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Radiol Clin N Am 42 (2004) 349 363
Acute painful scrotum

Vikram Dogra, MD*, Shweta Bhatt, DMRD, DMRE
Department of Radiology, Case Western Reserve University, University Hospitals, 11100 Euclid Avenue, Cleveland, OH 44106, USA
High-frequency transducer sonography using gray scale along with pulsed and color Doppler is the imaging modality of choice for evaluating patients who present with acute scrotal pain. Disease processes such as testicular torsion, epididymo-orchitis, and intratesticular tumors have the common symptom of pain at presentation, and sonographic evaluation helps in differentiating patients who require surgical from patients for whom conservative management is sufficient. Sonography with a highfrequency transducer helps to characterize better the testicular flow and, in many instances, suggests more specific diagnoses. This article is organized on the basis of the pathophysiology of the disease process with emphasis on color Doppler when applicable. This article is intended to familiarize the reader with new technology and provide new insights into the sonographic diagnosis of painful scrotum.
Imaging anatomy A normal adult testis has medium-level echoes and measures 532 cm [1]. The tunica albuginea is the fibrous sheath that covers the testicle. The tunica albuginea is covered by the tunica vaginalis. Septae extend from the tunica albuginea into the testicle and divide the testes into lobules (Fig. 1). The posterior surface of the tunica albuginea is reflected into the interior of the gland, which forms the incomplete septum known as the mediastinum of the testis. Sonographically, the mediastinum of the testis is an echogenic band (Fig. 2) of variable thickness that extends
* Corresponding author. E-mail address: Dogra@uhrad.com (V. Dogra).
across the testis in the craniocaudal direction. If imaged at an angle, it may resemble a testicular tumor. Each lobule is composed of many seminiferous tubules that open via tubuli recti into dilated spaces called the rete testes within the mediastinum. The normal rete testis can be identified at high-frequency ultrasound (US) in 18% of patients as a hypoechoic area with a striated configuration adjacent to the mediastinum testis [1]. These in turn communicate via efferent ductules with the epididymal head. The epididymis is composed of a head, body, and tail, the ducts of which continue as the vas deferens in the spermatic cord. The epididymis is seen as a 5- to 12-mm pyramidal structure lying atop the superior pole of the testes. The head of the epididymis is usually isoechoic to the testis, and its echotexture may be coarser than that of the testicle [2,3]. High-frequency transducer sonography permits visualization of the body of epididymis, which measures 2 to 4 mm. The right and left testicular arteriesbranches of the abdominal aortaprovide the vascular supply to the testis. A transmediastinal artery branch of the testicular artery occurs in approximately one half of normal testes (Fig. 3) [4]. It courses through the mediastinum to supply the capsular arteries and is usually accompanied by a large vein. The deferential artery, a branch of the superior vesicle artery, and the cremasteric artery, a branch of the inferior epigastric artery, supply the epididymis, vas deferens, and peritesticular tissue [5]. Branches of the pudendal artery supply the scrotal wall [6]. Venous drainage is via the pampiniform plexus. Four testicular appendages have been described: the appendix testis, the appendix epididymis, the vas aberrans, and the paradidymis. They are remnants of embryologic ducts [7]. The appendix testis and the appendix epididymis are usually seen on scrotal so-
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Fig. 1. Diagrammatic transverse representation of the anatomy of the testis illustrates the relationships of the tunica albuginea to the mediastinum testis and the mediastinum testis to the rete testis. (Courtesy of Vikram Dogra, MD.)
nography. The appendix testis is attached to the upper pole of the testis in the groove between the testis and the epididymis (Fig. 4A). The appendix epididymis, another appendage (Fig. 4B), is attached to the head of the epididymis and is encountered unilaterally in 34% and bilaterally in 12% of postmortem series. Presence of minimal fluid facilitates their visualization on sonography.
Scanning technique Scrotal sonography is performed with the patient lying in a supine position and the scrotum supported by a towel placed between the thighs. Optimal results
are obtained with 7- to 14-MHz high-frequency linear-array transducers. The testes are studied in two planes (ie, along the long and transverse axes). The size and echogenicity of each testicle and the epididymis are compared with those on the opposite side. In patients being evaluated for an acute scrotum, the asymptomatic side should be scanned initially to set the gray scale and color Doppler gains to allow comparison with the affected side. Color Doppler and pulsed Doppler are optimized to display low-flow velocities, and blood flow in the testis and surrounding scrotal structures is documented, including the spectral Doppler recording of the intratesticular arterial flow in both testes. Transverse images with portions of each testis on the same image should be recorded in gray scale and color Doppler. Power Doppler also may be used to
Fig. 2. Longitudinal view of a normal testis demonstrates the mediastinum testis (arrow) as an echogenic band.
Fig. 3. Transverse oblique view of the testis demonstrates the transmediastinal artery as a linear hypo-echoic band (arrow).
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Fig. 4. (A) Appendix testis (arrow) directly attached to the testis (T). Presence of fluid (asterisk) facilitates its visualization. (B) The appendix of the epididymis (cystic appearance) (arrow) is seen attached to the head of the epididymis (E).
visualize intratesticular flow in patients with an acute scrotum. Additional techniques, such as the Valsalvas maneuver or upright positioning, can be used as needed for venous evaluation.
Inflammatory causes Fourniers gangrene Fourniers gangrene constitutes a urologic emergency that demands early recognition because of its high mortality rate, which is reportedly as great as 75% [8]. The diagnosis of Fourniers gangrene is based primarily on clinical examination rather than on imaging studies. When clinical findings are ambiguous, however, diagnostic imaging is useful [1]. Fourniers gangrene is a synergistic polymicrobial necrotizing fasciitis of the perineum or perirectal or genital area that predominantly affects the scrotum in men and frequently extends to involve the lower abdominal wall. Predisposing conditions include diabetes mellitus, alcoholism, advanced age, and immunodeficiency syndrome [9]. Fourniers gangrene is characterized by obliterative endarteritis, which results in a cutaneous and subcutaneous vascular necrosis. The most common pathogens isolated in patients with this syndrome are Klebsiella, Proteus, Streptococcus, Staphylococcus, Peptostreptococcus, Escherichia coli, and Clostridium perfringens [8,10,11]. It
was first described in 1883 as an idiopathic condition of the scrotum. The disease currently differs from the original description in that it includes women and is known to be secondary to a defined source of infection in 95% of the cases. Conventional radiography, CT, and sonography can aid in determining the location and cause of gas in the scrotum. Crepitus (gas in the tissue) has been reported in 18% to 62% of cases and can be detected by US, CT, and conventional radiography. Subcutaneous gas within the scrotal wall is the sonographic hallmark of Fourniers gangrene [12]. Sonographically, the gas appears as numerous discrete hyperechoic foci with reverberation artifacts (Fig. 5A, B) [12,13]. Other sonographic findings include scrotal wall thickening while the echotexture of the testis and epididymis remains normal. Inguinoscrotal hernia can present with gas on sonographic examination and can be differentiated from Fourniers gangrene by the presence of gas within the protruding bowel lumen and away from the scrotal wall [1]. Epididymo-orchitis Acute epididymo-orchitis or epididymitis is the most common cause of acute scrotum in adolescent boys and adults. Sexually transmitted Chlamydia trachomatis and Neisseria gonorrhea are common pathogens in men younger than 35 years. In prepubertal boys and men over 35 years of age, the dis-
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Fig. 5. (A) Surgically confirmed case of Fournier gangrene. Longitudinal US of the testis (T) shows sparing of the testis. Both sonograms show air (arrowhead) parallel to the transducer face with reverberation artifact (arrow). (B) Axial CT in another patient with proven Fournier gangrene, which shows subcutaneous air (arrowhead) dissecting the fascial planes.
ease is most frequently caused by E coli and Proteus mirabilis [14]. Prehn [15] described the clinical differentiation of scrotal pain associated with epididymitis and acute torsion. Pain associated with acute epididymo-orchitis is usually relieved when the testicles are elevated over the symphysis pubis; however, the scrotal pain associated with testicular torsion is not lessened with this maneuver (Prehns sign). Other causes, such as sarcoidosis, brucellosis, tuberculosis, cryptococcus, and mumps, also may cause epididymitis and orchitis. Drugs, such as amiodarone, also may cause epididymitis (chemical epididymitis) [16]. Complications of acute epididymitis include chronic pain, infarction, abscess, gangrene, infertility, atrophy, and pyocele. Epididymitis first affects the tail of the epididymis and then spreads to involve the body and head of the
Fig. 6. Clinically proven epididymo-orchitis. Transverse US of the testis (T) shows a markedly enlarged epididymis (arrows) with variable echotexture.
epididymis. Orchitis develops in 20% to 40% of cases of epididymo-orchitis by direct spread of infection. On gray scale, the epididymis is enlarged and usually appears hypoechoic or hyperechoic (secondary to hemorrhage) (Fig. 6) [17]. Other signs of inflammation, such as reactive hydrocele or pyocele with scrotal wall thickening, are present in most cases. Diffuse testicular involvement is confirmed by testicular enlargement and an inhomogeneous testicular echotexture. Gray scale sonographic findings are nonspecific, but acute epididymo-orchitis is the most common disorder with this combination of findings. In one study that involved 20 cases of epididymoorchitis, 11 of 20 cases had enlarged and heterogeneous appearance of the epididymis or testis [18]. In orchitis there is edema of the testis contained within an unyielding tunica albuginea, which results in various scales of reflectivity, seen as heterogeneity on sonography [16,19]. This variable reflectivity may be seen as a diffuse process or focal involvement, the latter manifested as multiple hypoechoic lesions within the testicular parenchyma. It is difficult to differentiate focal areas of heterogeneity from neoplastic lesions. A heterogeneous echo pattern does not always signify orchitis. The increased blood flow to the epididymis and testis on color Doppler examination is a well-established criterion for the diagnosis of epididymo-orchitis (Fig. 7) [20]. Normally, epididymal arterial flow is of a low-resistance, high-flow state. With the US machines currently in use, blood flow can be seen in a normal epididymis on color Doppler sonography. In one study it was seen in 100% of the cases [21]. The mere presence of color flow in epididymis is not equivalent to epididymitis; therefore, it is important to compare the vascularity in both epididymii.
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mumps-related epididymo-orchitis, 9 of 11 cases were unilateral, and all 11 cases had an enlarged testis and increased testicular vascularity. Testicular echogenicity was uniformly decreased in all 11 cases [26]. Hyperemia and heterogeneity isolated to the testis can be seen in cases of orchitis, tumor, infarction, and especially transient torsion of the testis. Because intratesticular venous flow is difficult to detect in normal testes, increased and easily detected venous flow in the testes greatly suggests orchitis [20].
Cellulitis
Fig. 7. Clinically proven epididymo-orchitis. Color Doppler of the testis (T) shows marked hyperemia of the epididymis (arrow).
Increase of vascularity in acute epididymitis is secondary to the increased number and concentration of identifiable vessels with hyperemia, which results in a high-flow/low-resistance pattern [22 24]. Analysis of the spectral waveform also can provide useful information, because inflammation of epididymis and testis is associated with decreased vascular resistance to that seen in normal individuals. In the testes of a normal healthy volunteer, the resistive index (RI) is rarely less than 0.5, but more than half the patients with epididymo-orchitis have an RI of less than 0.5 (Fig. 8) [22,24,25]. In normal testes, intratesticular venous flow is difficult to detect. Easy detectability and increased venous flow in the testes greatly suggest orchitis. The absence of venous flow in the presence of arterial signal in orchitis is abnormal and suggests venous occlusion, which may be secondary to impending infarction or underlying coagulopathic disorder. Reversal of the spectral Doppler diastolic plateau in acute epididymo-orchitis suggests venous infarction. In all cases of testicular inhomogeneity diagnosed as epididymo-orchitis, if there is no demonstrable improvement with antibiotic treatment, the diagnosis should be reconsidered. Tumor markers, a hypercoagulation profile, or repeat US may reveal a different diagnosis, such as testicular tumor or thrombosis.
Scrotal wall cellulitis is common in patients who are obese or immunocompromised or have diabetes. The sonographic signs are an increase in scrotal wall thickness and the presence of hypoechoic areas with increased blood flow shown on color Doppler. Scrotal wall cellulitis may lead to scrotal abscess. Such abscesses are usually well loculated, with irregular walls and low-level internal echoes [1].
Intratesticular abscess This condition is usually secondary to epididymoorchitis, but other causes include mumps, trauma, and testicular infarction (Fig. 9). The sonographic features include shaggy irregular walls, an intratesticular lo-
Primary orchitis Mumps is the commonest cause of orchitis without accompanying epididymitis and is bilateral in 14% to 35% of cases [1]. Sonographically, the testes appear enlarged with decreased echogenicity. In one study of
Fig. 8. Duplex Doppler evaluation of the testis demonstrates an RI of 0.44 and increased vascularity of the testis in a patient with epididymo-orchitis.
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Fig. 9. Surgically confirmed testicular abscess. Transverse US of the testis (T) shows fluid-debris level (arrow) consistent with intratesticular abscess that developed secondary to epididymo-orchitis.
cation, low-level internal echoes, and occasional hypervascular margins [27].
Vascular Testicular torsion Testicular torsion and epididymo-orchitis commonly present with pain. The main role of US is to differentiate acute testicular torsion, which is a surgical emergency, from epididymo-orchitis. Clinical differentiation of these conditions is difficult, with a nearly 50% false-positive rate for diagnoses of testicular torsion based solely on clinical findings, which often results in unnecessary surgical exploration [28]. Hunter described the first case of testicular torsion [15]. Torsion of the spermatic cord occurs most commonly from 12 to 18 years of age but can occur at any age. The chance of torsion of the testis or its appendage developing by age 25 is approximately 1 in 160 [29], with 2% of testicular torsions being bilateral [30]. Patients with acute torsion present after a sudden onset of pain followed by nausea, vomiting, and a low-grade fever. Physical examination reveals a swollen, tender, and inflamed hemiscrotum. The cremasteric reflex is usually absent [31], and the pain cannot be relieved by elevation of the scrotum [15]. Testicular torsion causes venous engorgement that results in edema, hemorrhage, and subsequent arterial
compromise, which results in testicular ischemia. The extent of testicular ischemia depends on the degree of torsion, which ranges from 180 to 720 or more. Experimental studies indicate that 720 torsion is required to occlude the testicular artery [32]. When torsion is 180 or less, diminished flow is seen. The testicular salvage rate depends on the degree of torsion and the duration of ischemia. A nearly 100% salvage rate exists within the first 6 hours after the onset of symptoms, a 70% rate in 6 to 12 hours, and a 20% rate in 12 to 24 hours [33]. Intravaginal torsion occurs within the tunica vaginalis. In patients with Bell-Clapper deformity (Fig. 10), tunica vaginalis completely encircles the epididymis, distal spermatic cord, and the testis rather than attaches to the posterolateral aspect of the testis [1,34]. This leaves the testis free to swing and rotate within the tunica vaginalis, much like a clapper inside a bell. Bell-Clapper deformity is bilateral in 80% of patients. Testicular perfusion can be evaluated by color Doppler, power Doppler, or spectral Doppler sonography. Color Doppler sonography can demonstrate intratesticular flow reliably [17,24,35]. Power Doppler sonography uses the integrated power of the Doppler signal to depict the presence of blood flow. Higher power gains are more likely with power Doppler sonography than with standard color Doppler sonography, which results in increased sensitivity for detecting blood flow. Power Doppler sonography is valuable in scrotal sonography because of its increased sensitivity to low-flow states and its independence from the Doppler angle correction [36,37]. Pulsed Doppler sonography is a useful method to identify flow in the testis using the time-velocity spectrum to quantify blood flow [38]. The spectral waveform of the intratesticular arteries characteristically has a low-resistance pattern [35], with a mean RI of 0.62 (range, 0.48 0.75) [17]. This is not true for testicular volumes less than 4 cm3, however, which
Fig. 10. Diagram represents abnormal (Bell-Clapper deformity) and normal insertion of the tunica vaginalis. (From Dogra V, Ledwidge ME, Winter III TC, et al. Bell-Clapper deformity. AJR Am J Roentgenol 2003;180:1176 7; with permission.)
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Fig. 11. Surgically confirmed testicular torsion. (A) Color Doppler US of the testis (T) demonstrates the absence of intratesticular blood flow with peripheral hyperemia (arrows). (B) Involvement of the epididymis in testicular torsion. There is no blood flow within the testis (T) or epididymis (E). Peripheral hyperemia is seen (arrow).
are often found in prepubertal boys, in whom diastolic arterial flow may not be detectable [39]. The role of color Doppler and power Doppler sonography in the diagnosis of acute testicular torsion is well established [24,40]. Using the presence or absence of identifiable intratesticular flow as the only criterion for detecting testicular torsion, color Doppler was 86% sensitive, 100% specific, and 97% accurate in the diagnosis of torsion and ischemia in painful scrotum (Fig. 11A, B) [23]. The high degree of accuracy is attributable to the improved depiction of power Doppler sonography over color Doppler sonography in normal prepubertal and postpubertal testes [41]. Sonographic findings vary with the duration and degree of rotation of the spermatic cord.
Gray scale images are nonspecific for detecting testicular torsion [22] and often appear normal if the torsion has just occurred. Testicular swelling and decreased echogenicity are the most commonly encountered findings 4 to 6 hours after the onset of torsion. Twenty-four hours after the onset, the testis has a heterogeneous echotexture secondary to vascular congestion, hemorrhage, and infarction, which is referred to as late or missed torsion. An enlarged and hypoechoic epididymal head may be visible because the deferential artery that supplies the epididymis is often involved in the torsion (Fig. 12A, B). In the setting of testicular torsion, normal testicular echogenicity is a strong predictor of the testicular viability [42]. Gray scale findings of testicular torsion are sum-
Fig. 12. Surgically confirmed testicular torsion. Gray scale US of the testis (A) shows an enlarged testis with a hypoechoic appearance. (B) Epididymal involvement in testicular torsion in another patient. The epididymis (E) is enlarged and appears hypoechoic. There was no blood flow in the testis or epididymis on color Doppler examination (not shown).
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Table 1 Gray scale findings of testicular torsion Testicular torsion Acute torsion with viable testis Acute torsion with infarction Gray scale patterns Normal
Hypoechoic pattern that may be total or partial in case of a partial infarct Acute torsion with Hyperechoic and heterogeneous hemorrhagic infarction echo patterns Chronic torsion Hypoechoic with small testis
enlarged, heterogeneous testis, ipsilateral hydrocele, skin thickening, and no color flow Doppler signal in the testis or the spermatic cord [51]. In children, power Doppler US is more sensitive than color Doppler US for detection of intratesticular blood flow. In one study, power Doppler US demonstrated intratesticular blood flow in 66 (97%) testes, whereas color Doppler US demonstrated intratesticular blood flow in 60 (88%) testes. Combined techniques depicted blood flow in all 68 (100%) testes [52].
Appendiceal torsion marized in (Table 1). Other indicators include the presence of scrotal wall thickening and reactive hydrocele. Because gray scale findings are often normal in the early phases of torsion, the Doppler component of the examination is essential. The absence of testicular flow on color and power Doppler sonography is considered diagnostic of ischemia provided that the US scanner is optimized to detect slow flow, is limited to the use of a small color-sampling box, and is adjusted for the lowest repetition frequency and the lowest possible threshold setting [43]. The threshold should be set just above the detection of color noise. The absence of color flow Doppler on US examination is not synonymous with testicular torsion, because other conditions, such as testicular polyarteritis nodosa, can mimic torsion [44]. The color flow Doppler and spectral Doppler waveform findings in testicular torsion are summarized in Box 1. Torsion may be complete, incomplete, or transient. Cases that show partial or transient torsion present a diagnostic challenge. The ability of color Doppler imaging to diagnose incomplete torsion accurately remains undetermined. The role of spectral Doppler analysis is not well established for diagnosing partial torsion, but the findings may be useful (Fig. 13A, B) [45]. No studies are available to validate the role of spectral Doppler in partial torsion; however, sporadic case reports exist to suggest its usefulness [46,47]. Asymmetry in the testicular RIs with decreased diastolic flow or diastolic flow reversal may be seen. The presence of a color or power Doppler signal in a patient with the clinical presentation of torsion does not exclude torsion [47]. Extravaginal testicular torsion occurs exclusively in newborns. Torsion occurs outside the tunica vaginalis when the testis and gubernaculums are not fixed and are free to rotate [48]. The affected neonate presents with swelling, discoloration of the scrotum on the affected side, and a firm painless mass in the scrotum [49,50]. The testis is typically infarcted and necrotic at birth. Sonographic findings include an The normal appendix testis appears as an ovoid structure 5 mm in length in the groove between the testis and the epididymis. The appendix testis is isoechoic to the testis and occasionally may be cystic. The appendix epididymis is of the same approximate dimensions as the appendix testis but is more often pedunculated [53]. These appendages may become twisted. Torsion of either appendage produces pain similar to that experienced with testicular torsion, but the onset is more gradual. The classic finding on physical examination is a small, firm nodule that is palpable on the superior aspect of the testis and exhibits a bluish discoloration through the overlying skin; this is called the blue dot sign [54]. The cremasteric reflex still can be elicited, although it is usually absent in testicular torsion. Approximately 91% to 95% of twisted testicular appendices involve the appendix testis and occur most often in boys aged 7 to 14 years. Sonographic evaluation of torsion of the appendages of the testes usually reveals a circular mass with variable echogenicity adjacent to the testis or epididymis (Fig. 14) [55,56]. Reactive hydrocele and skin thickening are common in these cases. Increased peripheral flow may be seen around the torsed testicu-
Box 1. Testicular torsion: color flow Doppler patterns 1. Absent arterial and venous flow 2. Increased RI on affected side (diminished or reversed diastolic flow) 3. Decreased flow velocity difficult to measure because of small vessels/ angle correction but may be subjectively inferred by relative difficulty in finding small, low-amplitude flow on symptomatic side
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Fig. 13. Surgically confirmed partial torsion. (A) The left testis shows normal intratesticular arterial spectral waveform. (B) In the same patient, the right testis demonstrates diastolic flow below the baseline, which indicates loss of tissue perfusion. This waveform pattern is abnormal and suggests partial testicular torsion. (From Dogra VS, Sessions A, Mevorach A, et al. Reversal of diastolic plateau in partial testicular torsion. J Clin Ultrasound 2001;29:105 8; with permission.)
lar appendage on color Doppler US [14,23,24]. These cases are managed conservatively with attention given to pain management. The pain usually resolves in 2 to 3 days with atrophy of the appendix that may calcify. The role of sonographic examination in torsion of the testicular appendages is to exclude testicular torsion and acute epididymo-orchitis.
Varicocele Idiopathic varicocele Venous drainage of the scrotum is via the pampiniform plexus of draining veins; it is formed around the upper half of the epididymis in a variable fashion and continues as the testicular vein through the deep inguinal ring. The right testicular vein empties into
Fig. 14. Clinically proven case of appendiceal torsion. Longitudinal view of the testis (T) shows a predominantly hypoechoic area (arrow) adjacent to the epididymis (E).
the inferior vena cava and the left testicular vein into the left renal vein. Abnormal dilatation of the veins of the pampiniform plexus results in varicocele, which is usually caused by incompetent valves in the internal spermatic vein. This results in impaired drainage of blood into the spermatic cord veins when the patient assumes an upright position or during a Valsalvas maneuver. Varicoceles have been noted in approximately 15% of the general population and in up to 40% of men with infertility [57]. Patients with idiopathic varicoceles usually present between the ages of 15 and 25 years. The veins of the pampiniform plexus normally range from 0.5 to 1.5 mm in diameter, with the main draining vein as large as 2 mm in diameter. Varicoceles are more common on the left side for the following reasons: (1) the left testicular vein is longer, (2) the left testicular vein enters the left renal vein at a right angle, (3) in some men, the left testicular artery arches over the left renal vein, thereby compressing it, (4) the descending colon distended with feces may compress the left testicular vein [58], and (5) a nutcracker effect of compression of the left renal vein may occur between the superior mesenteric artery and the abdominal aorta [59]. Varicocele is a clinical diagnosis, and palpation reveals a scrotal mass that may feel like a bag of worms with or without a palpable thrill. In one study, all patients with palpable varicoceles had a spermatic vein diameter of 5 to 6 mm [60]. The clinical gradation of varicoceles is given in Table 2. Sonography should be performed in supine and upright positions. The sonographic appearance of
358 Table 2 Grade I Grade II Grade III
Secondary varicoceles
Not visible but palpable on Valsalvas maneuver. Less visible but palpable without Valsalvas maneuver Always visually identifiable and palpable without Valsalvas maneuver.
varicocele consists of multiple, serpigenous, tubular structures of varying sizes larger than 2 mm in diameter, which are usually best visualized superior or lateral to the testis. When large, they can extend posterior and inferior to the testis. Occasionally, lowlevel internal echoes can be detected in these dilated veins secondary to slow flow. Color flow and duplex Doppler sonography optimized for low-flow velocities confirms the venous flow pattern with phasic variation and retrograde filling with Valsalvas maneuver. The sensitivity and specificity rates of varicocele detection approach 100% with color Doppler sonography. The relationship between nonpalpable (subclinical) varicocele and infertility remains controversial. After treatment, however, these patients partners have a 40% pregnancy rate [61]. Approximately one third of men who undergo evaluation for infertility present with varicocele; however, not all patients with infertility have a palpable varicocele. In a study of 1372 infertile men, varicocele was found in 29% by sonography; however, only 60% had a palpable varicocele [62]. Diagnosis of subclinical varicocele is important because treatment improves sperm quality in as much as 53% of these cases.
Secondary varicoceles result from increased pressure on the spermatic vein produced by disease processes, such as hydronephrosis, cirrhosis, or abdominal neoplasm. Neoplasm is the most likely cause of nondecompressible varicocele in men over 40 years of age. It is classically from a left renal malignancy invading the renal vein [3]. Nondecompressible varicoceles on the left or right should prompt evaluation of the retroperitoneum to exclude retroperitoneal masses and thrombus or tumor extension to the left renal vein. An abdominal mass always should be suspected when an older man presents with a new varicocele.
Intratesticular varicocele An intratesticular varicocele can occur in association with an extratesticular varicocele, but intratesticular varicoceles are more commonly found alone [63]. Clinical implications and the pathogenesis of the newly defined condition, intratesticular varicocele, are not yet well established. Patients with intratesticular varicocele may have pain related to passive congestion of the testis, which eventually stretches the tunica albuginea. The sonographic findings of intratesticular varicocele are similar to those of pampiniform plexus varicocele [58]. Sonographic features include multiple anechoic, serpigenous, tubular structures of varying sizes within the testis. Color flow and duplex Doppler sonography demonstrate the venous flow pattern with a characteristic venous spectral wave form, which increases
Fig. 15. Intratesticular varicocele. (A) Longitudinal view of the testis (T) shows tortuous anechoic, tubular areas (arrow) within the testis. (B) Corresponding spectral Doppler waveform demonstrates characteristic venous flow with positive Valsalvas maneuver.
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with Valsalvas maneuver (Fig. 15A, B) [58]. The main differential considerations are cyst, hematoma, epidermoid cyst (echogenic rim), and tubular ectasia. Use of color flow and duplex Doppler affords easy differentiation. In every longstanding case of varicocele that presents with pain, this entity should be considered and sought [58].
Intratesticular arteriovenous malformation Intratesticular arteriovenous malformation is a rare, benign entity. Its pathogenesis may be congenital or posttraumatic. The characteristic arterialized venous spectral waveform is universal to all arteriovenous malformations [64], and the main differential consideration is intratesticular hemangioma [65].
Testicular trauma Testicular trauma typically results from athletic injury, a motor vehicle accident, a direct blow, straddle injury, or penetrating gunshot trauma. Blunt trauma accounts for approximately 85% of these cases, and penetrating trauma comprises the remaining 15%. A direct blow to the testis with impingement against the symphysis pubis or ischial ramus is the most common mechanism of injury from blunt trauma. Approximately 50 kg of pressure is necessary to rupture the tunica albuginea during blunt trauma. Testicular rupture is a surgical emergency, and more than 80% of
Fig. 17. Surgically confirmed testicular fracture secondary to trauma. Color Doppler US of the testis demonstrates a linear hypoechoic area (arrow) that runs obliquely across the testis and represents the testicular fracture line.
Fig. 16. Surgically confirmed tunica albuginea rupture. In this case of testicular trauma, color Doppler US shows a contour abnormality (arrow) that represents extruded testicular contents through the ruptured tunica albuginea. The asterisk represents accompanying hematocele.
ruptured testes can be saved if surgery is performed within 72 hours after injury [66,67]. Trauma can result in contusion, hematoma, fracture, or rupture of the testis [1]. Scrotal US with color flow Doppler is helpful in determining the nature and extent of the injury. The scrotal sonography has 100% sensitivity for testicular injuries and 80% specificity for tunica albuginea fractures [68]. Approximately 20% of patients who seek medical attention after testicular trauma have testicular rupture [69]. Sonographic findings in testicular rupture include interruption of the tunica albuginea, contour abnormality (Fig. 16), a heterogeneous testis with irregular, poorly defined borders, scrotal wall thickening, and a large hematocele [70,71]. Color and power Doppler sonography are helpful because either can detect disruption of the normal capsular blood flow of the tunica vasculosa. Heterogeneous intratesticular lesions are caused by hemorrhage or infarction. Direct visualization of a fracture line is rare and is seen only in 17% of cases (Fig. 17) [71]. Sonographic findings in testicular trauma are summarized in Box 2. Hematocele is a blood collection within the tunica vaginalis. On sonography, acute hematoceles are echogenic, whereas older hematoceles appear as fluid collections with low-level echogenicity, fluidfluid levels, or septations. Hematoceles may be caused by extratesticular or intratesticular bleeding, although there is no definite US evidence of testicular rupture. The presence of associated hyperechoic or hypoechoic changes in the testicular parenchyma suggests testicular rupture.
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Box 2. Sonographic findings in testicular trauma 1. Contour abnormality of the testis 2. Disruption of the tunica albuginea (evidenced by interruption of tunica vasculosa) 3. Direct visualization of a fracture line 4. Presence of hematocele 5. Intra- or extratesticular hematoma 6. Heterogeneous appearance of the testis 7. Hyperemia of the epididymis Note that any of the above mentioned findings may be seen in isolation or in any combination.
Hematomas can involve the testis, epididymis, or scrotal wall. Their sonographic appearance varies with time. Acute hematomas appear hyperechoic and subsequently become complex with cystic components. Hematoma appears avascular on color Doppler sonography [14,40]. Color Doppler sonography in posttrauma patients may reveal focal or diffuse hyperemia of epididymis, which is called traumatic epididymitis [72]. Patients with intratesticular hematomas fare poorly without exploration, and 40% of the hematomas result in testicular infection or necrosis, which often requires orchiectomy. Scrotal exploration is warranted if there is compelling evidence of testicular fracture or rupture on scrotal sonography or physical examination. The presence of a large hematocele is another indication for exploration. Small hematoceles, epididymal hematomas, or contusions of the testis generally pose little risk to the patient and do not require surgical exploration [73]. In posttrauma patients with sonographic testicular abnormality, if surgical exploration is not immediate, their progress should be followed to demonstrate sonographic resolution of the lesion, because 10% to 15% of testicular tumors first present after an episode of scrotal trauma [6]. Complications of testicular trauma include testicular atrophy, infection, infarction, and infertility.
Hernias occur because of persistent patency of the process vaginalis with protrusion of the peritoneal contents, such as omentum or bowel, through it into the tunica vaginalis [32]. US is helpful for patients with equivocal physical findings and patients who present with acute inguinoscrotal swelling. Herniation of the abdominal or pelvic contents in the groin region may be divided into two main categories: inguinal and femoral. Inguinal hernias are the most common and can be subdivided into direct and indirect types. Direct inguinal hernias travel through the Hassalbachs triangle, a weakness in the anterior abdominal wall. The borders of this triangle are formed by the lateral border of the rectus sheath medially, the inferior epigastric artery laterally, and the inguinal ligament inferiorly [74]. Indirect hernias travel lateral to the inferior epigastric artery and through the inguinal canal; they constitute 80% of all hernias. A femoral hernia occurs within the femoral canal that lies medial to the femoral vein. Because of the narrowness of the femoral ring (the opening that forms the neck of a femoral hernia), it is more likely than an inguinal hernia to become incarcerated [75]. Femoral hernia is common in women, with the right side more frequently affected.
Miscellaneous conditions Inguinal hernia A hernia may present acutely as a nonpainful mass or as a painful swelling with incarcerated bowel.
Fig. 18. Surgically confirmed case of inguinal hernia. Gray scale US of the testis (T) shows the presence of air (arrowhead) in a loop of bowel away from the skin surface with reverberation artifact (arrow). (Compare with Fig. 5A.)
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Sonographic appearance depends on the hernial sac contents. Most commonly it contains bowel; the next most common content is omentum. Other rare contents include Meckels diverticulum and urinary bladder. Gray scale findings are a fluid- or air-filled loop of bowel in the scrotum (Fig. 18). Finding realtime peristalsis indicates the presence of bowel. Occasionally, because contraction of the dartos also can mimic peristalsis on real-time sonography; the examiner should be aware of this possibility to avoid misdiagnosis [1]. If the omentum has herniated, areas of high echogenicity are present, which correspond to omental fat. Bowel strangulation is more common with indirect than direct inguinal hernia. An akinetic dilated loop of bowel observed sonographically in the hernial sac is reported to have high sensitivity (90%) and specificity (93%) rates for the recognition of bowel strangulation [76]. Hyperemia of the scrotal soft tissue and bowel wall suggests strangulation [17]. Patients with Richters hernia, a strangulated hernia in which only a portion of the circumference of the bowel is obstructed [77], usually present with gastroenteritis. Such cases can present a diagnostic challenge because of the hernias small size and the eccentric bowel wall involvement with limited luminal compromise. This hernia commonly occurs at a femoral site. It is important to recognize this condition because preoperative delays in diagnosis and high postoperative morbidity are common compared with other types of strangulated hernias [78]. Testicular tumors Testicular tumors sometimes can present with acute pain. This presentation is usually secondary to epididymo-orchitis or hemorrhage within the tumor. Ten percent of testicular tumors are brought to attention secondary to epididymo-orchitis [1]. Seminoma is the most common tumor to masquerade as acute orchitis. It is presumed to infiltrate and obstruct the seminiferous tubules, and it results in orchitis [1]. Leukemia and lymphoma can have a similar presentation. Gray scale findings of intratesticular tumors are nonspecific and usually hypoechoic in appearance. Hyperemia also can be seen in testicular tumors. Acute epididymo-orchitis and intratesticular tumors larger than 1.5 cm may have increased blood flow on color Doppler examination. Hypervascularity seen with tumors is sonographically indistinguishable from inflammatory hypervascularity [2]. There are no reliable sonographic criteria to distinguish malignant from focal benign intratesticular lesions, such as
infarction, hemorrhage, infection, or non germ-cell tumor [79]. The presence of epididymal involvement strongly suggests a nonneoplastic process. All patients with a heterogeneous echo pattern of testis should be followed to demonstrate their sonographic resolution so that tumors with epididymoorchitis presentation are not missed.
Summary The ability of US to diagnose the pathogenesis of the acute scrotum is unsurpassed by any other imaging modality. It is the first imaging performed in patients with acute scrotum. Knowledge of the normal and pathologic sonographic appearance of the scrotum and proper sonographic technique is essential for accurate diagnosis of acute scrotum. High-frequency transducer sonography combined with color flow Doppler sonography provides the information essential to reach a specific diagnosis in patients with testicular torsion, epididymo-orchitis, and testicular trauma.
Acknowledgments The authors would like to acknowledge Bonnie Hami, MA, for her assistance in the preparation of the manuscript and Joseph Molter for his assistance in preparation of photographs.
References
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Radiol Clin N Am 42 (2004) 365 381
Ultrasound evaluation of abdominal aortic and iliac aneurysms and mesenteric ischemia
Kathryn Hermsen, MD*, Wui K. Chong, MB, FRCR
Department of Radiology, CB #7510, University of North Carolina, 101 Manning Drive, Chapel Hill, NC 27599, USA
Ultrasound (US) has been used routinely since the mid 1980s to evaluate the abdominal aorta. Color Doppler imaging allows characterization of flow patterns [1]. It is the preferred method for diagnosis and surveillance of abdominal aortic aneurysms (AAAs) because of its accuracy, ease of use, and cost effectiveness [1,2]. US has been used to characterize aortic diseases, such as mycotic aneurysm, posttraumatic pseudoaneurysm, dissection, and detection of mural thrombus and AAA rupture [3,4]. Other applications of sonography include characterization of iliac arterial disease and postoperative evaluation of endovascular AAA repair. US plays a role in noninvasive diagnosis of mesenteric vascular occlusive disease in patients with suspected chronic intestinal ischemia.
Anatomy and histology The aorta enters the abdomen at the aortic hiatus at the T12 level. It descends anterior to the lumbar vertebrae immediately left of midline and tapers distally [5]. The normal luminal diameter of the infrarenal abdominal aorta varies according to age and gender. In young patients without vascular disease, it measures 2.3 cm in men and 1.9 cm in women [6]. It increases in size with age. In one study, average luminal diameter in men without aneurysm with a mean age 70.4 years was 2.8 cm [2]. The aorta is an elastic artery composed of three layers: the tunica intima, tunica media, and tunica adventitia. The aortic intima is thick and is composed
* Corresponding author. E-mail address: khermsen@unch.unc.edu (K. Hermsen).
of an endothelial lining, a connective tissue layer, and an internal elastic membrane. The endothelium consists of squamous cells oriented parallel to the direction of blood flow and connected by tight junctions. The tunica media is composed of smooth muscle and connective tissue. The tunica adventitia of the aorta is thin and consists of connective tissue fibers, fibroblasts, and macrophages. It also contains the innervation of the aorta and its blood supply (vasa vasorum) [7]. The aorta bifurcates to form the common iliac arteries near the level of the umbilicus (approximately L4). The common iliac arteries proceed anterolaterally in association with the common iliac veins and bifurcate into the internal and external iliac arteries [5]. Major branches of the abdominal aorta routinely visualized by US include the celiac axis, superior mesenteric artery (SMA), and renal arteries. The celiac axis is the first major division of the abdominal aorta. It generally gives rise to the left gastric, hepatic, and splenic arteries, although anatomic variants are frequent [3]. The left gastric artery is seldom visualized by US [8]. The SMA arises anterior to the L1 vertebra and posterior to the body of the pancreas [9]. It travels with the superior mesenteric vein anterior to the duodenum and inferiorly to divide within the mesentery 5 to 6 cm from its origin. The normal inferior mesenteric artery is infrequently visualized by US. In disease states it may hypertrophy and become visible [8]. The renal arteries arise from the lateral wall of the aorta within 1.5 cm of the SMA [3]. Supernumerary renal arteries are frequent [3]. Branches of the aorta and the iliac arteries are classified as muscular arteries. When compared with the elastic arteries, such as the aorta, their intima are thinner and have less subendothelial connective
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tissue. Likewise, the tunica media contains less elastic material. The tunica adventitia is thicker and has greater collagen content [7].
Flow characteristics As characterized by color Doppler, the aorta is a high-resistance vessel. Velocity climbs rapidly in early systole and falls rapidly in early diastole [3]. The proximal aorta demonstrates biphasic waveforms with reversal of flow in early diastole. The distal aorta demonstrates triphasic waveforms (small component of forward flow in late diastole). Normal blood flow is laminar (Fig. 1) [1]. The celiac axis demonstrates high-resistance flow at its origin with rapid systolic upstroke and rapid decline (Fig. 2). Hepatic and splenic arteries are lowresistance vessels with substantial forward flow throughout diastole [3]. The SMA is a high-resistance vessel in the fasting state. In the fasting patient, flow is triphasic, with rapid systolic upstroke and reversal of flow in early diastole. In the postprandial state, spectral Doppler waveform of the SMA changes to a low-resistance, high-flow pattern secondary to decrease in splanchnic vascular resistance. Peak systolic velocity (PSV) increases and forward flow is seen throughout diastole (Fig. 3) [8]. Moneta et al [10] described the effects of meal content on mesenteric vascular resistance. Test subjects were imaged after ingesting varying amounts of fat, proteins, and carbohydrates. Control meals consisted of water or mannitol. In the
SMA, PSV, end diastolic velocity (EDV), and mean velocity increased with all except water. The greatest changes were demonstrated in end diastolic flow [10]. The neurohumoral mechanisms behind this response are incompletely understood. Hormones released in the presence of fat, carbohydrates, and proteins, including cholecystekinin, vasoactive intestinal peptide, gastrin, secretin, and kinins, are released into the bowel wall and act as vasodilators. Decreased oxygen concentration that results from increased consumption associated with active transport of nutrients may act as a vasodilatory stimulus [11]. Postprandial changes in vascular resistance are considerably less pronounced in the celiac axis (CA), which indicates that this is a low-resistance circuit regardless of feeding [8]. In the study by Moneta et al, minimal changes were observed in the CA with feeding [10].
Imaging techniques The primary limitations in imaging the abdominal aorta are patient body habitus and the presence of bowel gas. Thinner patients are more easily imaged. No bowel preparations have proved effective in limiting the effect of interposed bowel gas. In imaging of the abdominal aorta, patients are usually scanned after an 8- to 10-hour fast. The presence of barium within the bowel attenuates US transmission, and imaging should be postponed after gastrointestinal procedures. The patient is initially scanned in the supine position using linear 4-, 3.5-, or 2.5-MHz transducers; curved 5- or 3.5-MHz transducers are also used, depending
Fig. 1. (A) Normal aorta with normal triphasic waveform. Note rapid systolic peak followed by rapid decline and brief reversal of flow characteristic of a high resistance vessel. (B) Normal aortic transverse diameter measurement.
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Fig. 4. (A, B) Importance of obtaining measurement perpendicular to plane of vessel. Oblique measurements may overestimate lumen diameter. Fig. 2. Normal celiac axis origin and bifurcation. The left gastric artery is seldom seen.
on patient body habitus [1]. The aorta is imaged in sagittal and transverse planes at its proximal, mid, and distal portions. In the presence of a tortuous aorta, it is important to obtain measurements perpendicular to the long axis of the vessel. Oblique measurements
Fig. 3. (A) Fasting SMA. Note rapid systolic upstroke and low diastolic flow. (B) Postprandial SMA. Note increased diastolic forward flow.
may overestimate the lumen diameter (Fig. 4) [12]. The anteroposterior and transverse diameters are measured from outer wall to outer wall. The common iliac arteries are imaged at the level of the bifurcation in anteroposterior and transverse diameter. In the upper abdomen, a good acoustic window is often found in the midline between the rectus abdominus muscles. The lateral aspect of the rectus muscles also may provide a good window, especially for visualizing the iliac vessels [3]. A left lateral decubitus or oblique approach is often helpful in patients with excessive bowel gas and for visualizing the mid and lower abdominal aorta. Use of slow graded compression with the transducer may displace bowel loops. Color Doppler may aid in identifying the aorta [1]. Flow characteristics (laminar versus turbulent) and measurements, including PSV and EDV, are documented. Flow within the renal arteries is demonstrated, and each kidney is observed in long axis. The aorta is visualized similarly after endovascular stenting using 2.5- and 3.75-MHz curved transducers. Duplex and color flow Doppler analysis is obtained at the level superior to the stent, at its proximal attachment, including right and left iliac attachments. Flow within the SMA and renal arteries is documented. The maximum transverse diameters of the graft lumen and aneurysm sac are measured in the anteroposterior and transverse planes. The clot within the aneurysm sac is observed with color Doppler in the transverse and longitudinal planes to evaluate for leak around the stent or flow within the sac. Detectable flow is considered an indication of leak [13]. Another indicator of graft compromise is enlargement of the aneurysm sac or failure of the aneurysm sac to regress. Multiple types of endoleaks have been described. In 1997, White first described endoleaks (Box 1) [14,15]. Cursory evaluation of the mesenteric arterial vasculature is undertaken in routine imaging of the
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Box 1. White classification of endoleaks[15] Type I: Direct communication between the graft and aneurysm sac via an ineffective seal at the graft ends or attachment sites. Type II: Retrograde flow through lumbar arterials, the inferior mesenteric artery (IMA), or accessory renal arteries feeds into the aneurysm sac. Type III: Seen in modular, multisegmental grafts. Leak occurs through deficiency in graft fabric and may be a result of altered hemodynamics secondary to aneurysm sac shrinkage. Type IV: On contrast, CT appears as a blush of contrast outside the graft from contrast diffusion through the naturally porous graft fabric or through small defects in the fabric at the site of sutures or struts. May require angiography to distinguish from Type III graft.
Doppler angle of 60 or less while obtaining velocity measurements [8,18 20].
Abdominal aortic pathology Aneurysm An aneurysm is an abnormal expansion of a vessel. Aneurysms are classified as false or true. True aneurysms include all three layers of the vessel wall. Multiple configurations of true aneurysms are described. Most AAAs are true aneurysms and are fusiform; 97% are infrarenal. Only 2% to 7% extend to the juxtarenal or suprarenal aorta [21]. Aneurysms that occur proximal to the renal arteries are more likely to be mycotic or posttraumatic. AAA is a common condition, with a prevalence of 1% to 4% in people aged 50 or older [1]. Most of these aneurysms are idiopathic. The strongest association with AAA is atherosclerotic disease. Other risk factors for development of AAAs include male gender, smoking, chronic obstructive pulmonary disease, age, and family history. Most patients with AAA are asymptomatic. Some patients may present with abdominal or lower extremity pain [3]. The most common physical examination finding is a pulsatile abdominal mass. The physical examination, however, has poor predictive value in the detection of AAA [22]. Sonography is the primary imaging study for detection of aortic aneurysms. The accuracy of US in the diagnosis of AAA approaches 100% [3,27]. The typical US appearance of AAA is of a dilated vessel with an irregular lumen. Ulceration or cystic changes may be seen as focal hypoechoic regions within the vessel wall [3]. Echogenic mural thrombus is present in most large lesions and may be circumferential or eccentric (Figs. 5, 6). Juxtarenal AAAs may appear to involve the renal arteries at US because of apparent overlap of the aneurysm wall with the renal ostia. Careful evaluation of the course of the renal arteries and aorta in multiple planes may clarify the relationship of the aneurysm to the renal arteries. Multidetector CT with coronal reconstruction or aortography is usually required to evaluate renal artery involvement in juxtarenal aneurysms, however [1]. Flow within AAAs may be laminar or turbulent. Turbulent flow is associated with formation of mural thrombus (Fig. 7). It has been proposed that thrombus imparts tensile strength to the aneurysm wall by absorbing forces generated by flow. Mower used computer-generated models of AAA that ranged in size from 2 to 4 cm to study the effects of thrombus size and composition on wall stress [23]. In this
abdominal aorta. More detailed examination to assess for mesenteric occlusive disease faces several technical challenges. Bowel gas, respiratory motion, and vessel depth confound identification of the mesenteric vessels [8]. Various methods have been used to reduce interference by gas, including cathartic bowel preparation the night before, oral simethicone 15 minutes before examination, liquid diet the evening before followed by 8- to 12-hour fast, and fasting alone [16,17]. The CA is scanned from its origin to its bifurcation. The SMA is examined from its origin and followed 5 to 6 cm distally. In the fasting state, the normal SMA waveform is triphasic. Should a biphasic waveform be observed, the sonographer searches for a replaced hepatic artery. This anatomic variant occurs in approximately 20% of the population. It arises from the lateral SMA and travels cephalad and right to supply the liver. The presence of a replaced hepatic artery results in biphasic SMA flow [16,17]. The position of the CA and SMA in the upper abdomen often requires high Doppler angles of insonation. Unfortunately, this introduces error in determining flow velocities, which usually results in falsely elevated values [8]. Care must be taken to maintain a
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Fig. 7. Turbulent flow within AAA. Note the hypoechoic thrombus (arrow).
Fig. 5. (A) Transverse view of AAA with mural thrombus (arrow). (B) Color Doppler demonstrates turbulent flow within lumen outlining thrombus.
Fig. 6. Pitfalls in measuring AAA. (A) This echogenic line (solid arrow) is easily mistaken for the aortic wall. It actually represents the surface of the thrombus that lines the wall of a large AAA. Open arrow demarcates the true aortic wall. (B) On the transverse view, the large mural thrombus is better seen. (Open arrows mark the true vessel wall.)
study, the larger the mural thrombus, the greater the reduction in wall stress. Organized mural thrombi imparted greater tensile strength than more pliant ones. The authors speculated that the tendency of eccentric mural thrombi to collect along the ventral wall may explain the rarity of ventral rupture [23]. The presence of mural thrombus also may help to restore laminar flow. The most catastrophic complication of abdominal aortic aneurysm is rupture. Rupture carries a high mortality rate. Fifty percent of patients do not reach the hospital alive. The overall mortality rate is 80% to 94% [1]. Signs and symptoms associated with rupture include severe abdominal and back pain, nausea and vomiting, and hypotension [1]. Aneurysm size and rate of enlargement are the most important factors in predicting potential rupture. In a 15-year study, Brown et al [24] followed 476 patients with AAA larger than 5 cm who were deemed unfit surgical candidates. The risk of rupture in male patients with AAA of 5 to 5.9 cm was 1% per year; in male patients with AAA 6 cm or larger, the risk was 14.1%. Gender differences also were noted in this study. Women with aneurysms of similar size were at fourfold higher risk for rupture [24]. Aneurysms are generally expected to enlarge 2 to 4 mm per year. Aneurysms that enlarge by 5.5 to 6 mm per year are regarded as high risk for rupture [12]. Sharp et al [25] identified 32 patients with aneurysms less than 5.5 cm per year that had enlarged 5 mm or more in the past 6 months. Over a period of 50 patient years, none ruptured. Thus, the risk of rupture was calculated to be 0 to 6 per 100 patient years [25]. CT is the imaging modality of choice in the setting of rupture because it is not subject to technical factors, such as interposed bowel gas, and grants a greater perspective on the extent of bleeding
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[3]. The US appearance of rupture is that of a large, usually hypoechoic retroperitoneal fluid collection. Other complications of AAA include embolization of mural thrombus, occlusion of the renal and splanchnic arteries, obstructive uropathy (usually on the left), and arteriovenous fistula (usually with the inferior vena cava [IVC], or left renal vein) (Fig. 8) [2,3]. A less common complication is duodenal obstruction, which results from compression of the duodenum (SMA syndrome) between an enlarging AAA and the SMA [26]. US is ideal for monitoring AAAs because it is inexpensive, does not require the use of contrast material or radiation, and is highly accurate. CT is often used in AAA evaluation, but it faces some technical limitations. Because the aneurysmal aorta is frequently ectatic, slices obtained in the axial plane only may be obtained with a degree of obliquity, which potentially overestimates the size of the aneurysm. Because changes in measurements of only a few millimeters may influence management greatly, potential effects of measurement variability between CT and US are an important consideration.
Fig. 8. Left ureteral obstruction by AAA. (A) Distal AAA. Lumen diameter is normal proximally and expands distally. (B) Mild left hydronephrosis secondary to compression by AAA.
Wanhainen et al [2] evaluated differences in observer measurements between CT and US in 475 patients. Thirty-three were found to have AAAs (defined as diameter larger than 3 cm). In patients with normal aortas (<3 cm), US overestimated the diameter by 2.8 mm in anteroposterior diameter and 3.8 in transverse diameter. The difference in aneurysmal aortas was greater, with a variability of 8 mm or less in anteroposterior and 10.6 mm in transverse measurements. The authors found the variability in transverse measurements to be unacceptably high and preferred using anteroposterior diameters in assessing aneurysm size [2]. There is no true gold standard modality in the measurement of AAA. Lanne et al [12] reported greater reliability for US using an automated echo tracking device for measurement of the aortic lumen. Frequent indications for aortic US are the finding of a pulsatile abdominal mass on physical examination and evaluation of an AAA incidentally discovered on a CT performed for another purpose. Unfortunately, however, many AAAs are not discovered until rupture. Given the dismal prognosis of rupture and the relatively low mortality rate for repair (2% 5%), is screening for AAA in high-risk patients a viable option? Lee et al [27] examined the cost effectiveness of conducting a quick screen (ie, abbreviated US) evaluation of the abdominal aorta in atrisk populations. The examination was limited to less than 5 minutes and was performed at reduced cost. The sensitivities and specificities for the quick screen and standard duplex US were 100%. The emphasis was on screening patients with known risk factors, such as male gender, smoking, hypertension, hyperlipidemia, other peripheral vascular disease, and coronary artery disease. They found screening in at-risk populations to be cost effective and recommend screening in men over age 60 [27]. Although most AAAs are idiopathic, certain connective tissue disorders carry an increased risk of AAA. Ehler-Danlos syndrome is a group of disorders associated with abnormal collagen synthesis. Type IV Ehler-Danlos syndrome is associated with vascular abnormalities, including aneurysms of the elastic arteries and their major branches. Catastrophic complications have been reported with angiography in patients with Type IV Ehlers-Danlos syndrome, and it is generally avoided [28]. Pseudo or false aneurysms are generally the result of a defect in the intima through which blood flows. Blood escapes through a defect in the arterial wall and is contained by the surrounding soft tissue. Blood flows into the aneurysm during systole and out during diastole, which produces a characteristic appearance on color Doppler imaging that has been likened to the
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changes [30]. They most frequently occur in the iliacs, followed by the aorta. On sonography, the aneurysm wall is thickened with surrounding hypoechoic fibrotic tissue. US and CT have proved the most useful modalities in diagnosing inflammatory aneurysms [31]. Inflammatory AAAs may be seen in the setting of retroperitoneal fibrosis. In this setting, the fibrotic tissue may extend laterally into the retroperitoneum, and the ureters may become obstructed [32]. Inflammatory aneurysms carry a higher rate of morbidity and mortality than idiopathic AAAs and are more likely to present with pain in the absence of rupture [30]. Erythrocyte sedimentation rate is usually elevated. Pennell et al [33] described a triad of chronic abdominal pain, weight loss, and elevated erythrocyte sedimentation rate in a patient with AAA as highly suggesting inflammatory AAA. Dissection Aortic dissection occurs when a defect in the aortic wall allows the entry of blood, which separates the intima from the media [34]. Two lumens are created: a false lumen, which consists of blood within the vessel wall, and the true vessel lumen. Although the vessel does enlarge, dilatation is considerably less pronounced than with true aneurysms. Most often, dissection occurs along a segment of varying length and ends with re-entry of the blood column into the true lumen via a second intimal defect. This serves to decompress the hematoma and delay rupture [35]. Isolated abdominal aortic dissection is exceedingly rare in the absence of blunt abdominal trauma [36]. Most aortic dissections originate in the thoracic aorta, usually the ascending aorta. Several classifications exist; the most commonly used are the DeBakey and Stanford classifications. Two thirds of dissections involve the ascending aorta, usually within a few centimeters of the aortic valve. In DeBakey types 1 and 3, the dissection plane may extend into the abdominal aorta [37]. The pathogenesis behind dissection remains controversial. Dissection in the absence of a clear intimal tear has been documented, which suggests that dissection occurs through a defect in the media created by intramural hemorrhage. The importance of abnormalities of the media has been a topic of interest in the pathogenesis of dissection. Increased incidence of dissection in patients with Turners, Ehlers-Danlos, or Marfan syndrome, all of which have underlying abnormalities of the media, suggests that a primary defect of the media underlies dissection. To date, no specific histologic abnormalities have been demonstrated [38]. Sonesson et al [39] used US to show that
Fig. 9. Classic color Doppler Yin-Yang appearance of pseudoaneurysm. Blood enters the false aneurysm (red), strikes the back wall, and reverses direction (blue).
Yin-Yang sign (Fig. 9). False aneurysms caused by penetrating trauma show to and fro flow in the neck, with blood leaving the artery during systole and re-entering during diastole. Aortic pseudoaneurysms are most frequently posttraumatic or mycotic [3,28]. Mycotic aneurysms refer to aneurysms of any type that have become infected. They are more frequent in patients younger than 50 years, unlike idiopathic AAAs, which are more frequent in patients over age 60. Two broad categories of mycotic aneurysms have been described: those that form secondary to aortic wall factors (atherosclerosis or stents) and those that are seeded from a distant source. The second group is divided according to source of infection: intravascular (frequently in the form a septic emboli) and extravascular (usually formed by contiguous spread from a nearby infected site). The most frequent causative organisms are staphylococci and salmonella. An important feature of mycotic aneurysms is their tendency to enlarge rapidly and their propensity for rupture [4,29]. Few specific US findings are reported. Naganuma et al [4] described the presence of gas echoes in the wall of a mycotic aneurysm with sonography. Inflammatory aneurysms are a relatively uncommon type of true aneurysm that constitutes approximately 4% of AAA. They are characterized by fibrotic thickening of the adventitia and chronic inflammatory
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patients with Marfan syndrome had abnormal compliance of the aorta. Most dissections occur in patients without connective tissue disorders, however. In these cases, by far the strongest association with dissection is the presence of hypertension [37]. CT and MR imaging are the imaging modalities of choice in dissection that involves the abdominal aorta. Dissection may be an incidental finding in US evaluation of the aorta, however. The intimal flap created between the true and false lumen is best visualized with US in the transverse plane [38]. The flap moves with arterial pulsation if flow through the false lumen is preserved. (This may not be seen if the flap is thickened.) Doppler waveforms in both lumens may appear bizarre, with spectral broadening and reversed flow. Velocity tends to be slower in the false lumen (Fig. 10). A true AAA with organizing thrombus may look like a dissection on sonography. The outer layer of thrombus can appear echogenic and be mistaken for an intimal flap, whereas deeper thrombus appears anechoic and can mimic the false lumen [40]. Color Doppler increases the specificity of US in evaluating dissection. Flow in the false lumen may be too slow for detection with Doppler. Thrombosis within the false lumen frequently occurs and is a significant
pitfall in the use of US for characterization of dissection. Nguyen [41] described a case of pseudodissection in which an intimal flap with flow on either side was described with sonography. This was shown on CT to be an AAA with mural thrombus. The perception of flow within the false lumen was attributed to mirror image artifact caused by a calcified thrombus surface layer or incorrect color flow assignment in the anechoic portion of the thrombus [41]. US is not the primary imaging modality for aortic dissection because most dissections involve the thoracic aorta.
Ultrasound and aortic endografting In the early 1990s, Parodi [42] first reported the endoluminal repair of abdominal aortic aneurysm. Given the relatively high operative morbidity and mortality rates associated with open repair (3% 10% mortality and 15% 40% perioperative morbidity) [43], AAA repair using stent grafts offers a less invasive alternative to open repair, with reduced morbidity and mortality rates. The most frequent complication of endografting is the development of leak-
Fig. 10. (A, B) Abdominal aortic dissection with intimal flap (arrow). (C) Turbulent flow within dissection.
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age into the aneurysm sac excluded by the graft. This may occur via direct communication with the graft lumen at its attachment site or back flow from collateral arteries communicating with the aneurysm sac. Leaks are frequent, with cited incidences as high as 40% [13]. Lifelong monitoring is required. Although the gold standard for postoperative monitoring is CT, US has been used with varying success. It offers several potential advantages, including avoidance of potentially nephrotoxic contrast agents and radiation exposure [3,44,45]. Initial studies that compared CT and US demonstrated promising results for US. In 1998, Kronzon et al [43] studied 17 patients after stent repair of AAA with color Doppler imaging (CDI) and CT. US was successful in demonstrating flow within the excluded aneurysm lumen using color Doppler and in measuring aneurysm size (Figs. 11, 12). Sato et al [44] reported a sensitivity rate of 97%, specificity rate of 74%, and accuracy rate of 82% for US in detecting endoleak. With the advent of improved helical scanning techniques, including thinner collimation and delayed imaging, Golzarian et al [45] demonstrated improved reliability of CT compared with US. US detected clinically significant leaks within the stent graft and iliac limbs; however, it frequently missed small perigraft leaks. Using CT as the standard for evaluating US performance, US detected endoleak with a sensitivity rate of 77% and specificity rate of 90% [45]. After this, Pages et al [13] demonstrated a poorer sensitivity and specificity in endoleak detection of 48% and 93%, respectively. Although CDI did detect some endoleaks not detected on CT, the use of delayed postcontrast CT imaging could detect these leaks. CDI performed better in monitoring aneurysm size, with a sensitivity rate of 88% and specificity rate of 76% in demonstrating no change in AAA size. As with unrepaired AAA, US
and CT demonstrated some discrepancy in measurements. If a preoperative US is available as a baseline, however, US can be effective in monitoring aneurysm size [13]. Some authors suggest using both CT and US when following endografts [13,45]. In a recent study, Greenfield et al [46] found that US was more accurate than CT for characterizing endoleaks. In a study of seven endoleaks classified as type II by CT, US demonstrated two of these to be type I leaks. Type I leaks generally require immediate repair, whereas type II are often managed conservatively because they tend to resolve without treatment. These findings dramatically altered care. US findings in proximal limb type I leaks were high velocity flow at the site of the proximal attachment. Distal limb attachment site leaks demonstrated flow in the sac opposite the direction of that in the lumen. IMA flow was antegrade in type I leaks. Type II leaks were characterized by slower flow within the aneurysm sac and retrograde flow in the IMA. These finding suggest an adjunct role for US in characterizing endoleaks detected by CT [46].
Mesenteric vascular ultrasound Chronic intestinal ischemia Chronic intestinal ischemia (CII) is caused by inadequate blood supply to meet the metabolic demands of the enteric tract after feeding. In the postprandial state, intestinal motility increases, as does oxygen demand from active transport of nutrients. Clinically, this presents as postprandial pain. The clinical diagnosis is one of exclusion. It is a relatively rare entity with no pathognomonic findings. CII occurs most commonly in elderly women (75%) [8,20]. Patients typically present with colicky
Fig. 11. (A) Longitudinal image of AAA shows stent (arrow) and wall of aneurysm (thick arrow). (B) Application of color Doppler demonstrates flow within the graft lumen and hypoechoic clot (arrow) in the excluded aneurysm sac.
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Fig. 12. Type 2 endoleak. (A, B) Color Doppler demonstrates flow outside the graft lumen (arrow). (C) CT correlate: blush of contrast outside the limbs of the stent (arrow).
postprandial epigastric pain, occasionally with radiation to the back. Symptoms begin 15 to 30 minutes after eating and persist 1 to 3 hours. Patients associate feeding with pain and frequently develop food phobia, with anorexia and marked weight loss. Changes in bowel habits are also frequent [16]. The abdominal examination is usually nonspecific, with no localizing or peritoneal signs. An abdominal bruit is often present, but this finding is too nonspecific to make the diagnosis of CII to make the diagnosis of CII. Laboratory data are neither sensitive nor specific. Malabsorption of various nutrients has been described in the setting of CII. Villous atrophy and
epithelial flattening has been shown in biopsy series. These findings are unreliable and nonspecific, however [8,16,20,47]. Atherosclerotic narrowing at the origin of the mesenteric vessels is the most common factor that predisposes to CII. Other processes, such as vasculitis, extrinsic or intrinsic compression, and drug reactions, also may produce symptoms (Box 2). Although CII is relatively rare, atherosclerotic narrowing of the mesenteric vasculature is common. In one autopsy series, 6% to 10% of patients had stenosis of 50% or more. High-grade CA stenosis is also frequently well tolerated. In high-grade CA stenosis or occlusion, the
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Box 2. Associations with chronic intestinal ischemia Atherosclerotic disease Inflammatory vasculitis Radiation Polyarteritis nodosa (PAN) Connective tissue disease 1. Bergers 2. Systemic lupus erythematosus (SLE) 3. Rheumatoid arthritis (RA) Extrinsic compression 1. Neurofibromatosis 2. Median arcuate ligament syndrome Drug reactions Cocaine
gastro- and pancreaticoduodenal arteries form an important collateral pathway. In SMA stenosis or occlusion, flow may be reconstituted via the hepatic artery and pancreaticoduodenal arteries. In highgrade stenosis or occlusion of the SMA and CA, the IMA may form sufficient collaterals via the middle colic artery and pancreaticoduodenals (the arch of Riolan) to supply the foregut. IMA stenosis is most frequently asymptomatic [8]. Because the splanchnic vessels are able to form extensive collateral pathways, significant stenosis or occlusion of two of the three mesenteric vessels is generally required to produce symptomatic ischemia, although high-grade stenosis of the SMA alone may produce symptoms. Collateralization also makes prediction of CII difficult. The presence of two-vessel disease or complete SMA occlusion does not imply the presence of CII in the absence of symptoms [8]. The diagnosis of CII frequently is delayed because of its tendency to mimic more common disorders, such as symptomatic gallstones, cholecystitis, pancreatic cancer, and peptic ulcer disease. The average time from onset of symptoms to diagnosis is 18 months [16]. Traditionally, CII has been diagnosed via angiography. There is reluctance to perform angiograms for nonspecific clinical findings because of
its invasiveness, cost, and potential complications in elderly patients. Noninvasive screening tests in symptomatic patients are needed to evaluate the mesenteric vasculature. The successful application of Doppler sonography for diagnosis of mesenteric ischemia was first described by Jager in 1984 [47]. High PSVs were found at the origins of the SMA and celiac arteries. PSV in the SMA was more than 300 cm/second. Spectral broadening and monophasic waveforms with loss of reversed diastolic flow also were noted [47]. In a subsequent validation study, Moneta [19] sought to establish specific US criteria for high-grade SMA and CA stenosis. One hundred patients underwent mesenteric duplex scanning followed by arteriography. In this study, a PSV of 275 cm/second or more predicted 70% stenosis, with a sensitivity rate of 92% and specificity rate of 96%. In CA stenosis, a PSVof 200 cm/second or more predicted stenosis with 87% sensitivity rate and 80% specificity rate (Fig. 13). Although elevations in EDV were observed in stenotic vessels, use of EDV did not improve the sensitivity or specificity of results. In a different study, Moneta [18] found that the ratios of PSV to EDV were not predictive. These studies addressed one important technical factor in acquiring PSV data. In patients with peripheral atherosclerotic disease but no mesenteric occlusive disease, PSVs were elevated over control subjects. This result suggests that tortuousity of the mesenteric vessels in patients with atherosclerosis may limit the sonographers ability to maintain Doppler angles less than 60 [18]. This inability could result in falsely elevated PSVs. Bowersox [20] found that EDV and PSV were elevated in confirmed SMA stenosis . The study accepted 50% or more stenosis as being significant. In normal control subjects, SMA flow was triphasic with a normal PSV of 134 (F 18) cm/second and EDV of 24 (F 4) cm/second. (except in replaced hepatic artery, in which flow was biphasic). PSVs increased with increasing SMA stenosis. PSV of 300 cm/second diagnosed 50% or more stenosis with a sensitivity rate of 63% and specificity rate of 100%. Unlike Moneta, however, Bowersox [20] found that EDV was more sensitive and specific than PSV. An EDV of more than 45 cm/second was found to be 100% sensitive and 92% specific in detecting severe stenosis. Significant CA values could not be established in this study. One proposed reason is that collaterals through the gastroduodenal arcade can restore CA flow in the presence of severe stenosis [20]. Two more recent publications favor the use of EDVs in predicting significant stenosis. Perko et al [44] evaluated 39 patients with suspected intestinal
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Fig. 13. Celiac stenosis. (A) Color Doppler with narrowing at the celiac origin and turbulent flow. (B) Doppler spectrum with elevated PSV (>300 cm/second) and spectral broadening. (C) Angiogram demonstrates narrowing of the CA (arrow) and SMA.
ischemia using Monetas criteria in addition to the following other parameters: EDV, early diastolic velocity (EaDV), and PDV. A control group of hyperthyroid patients was included in this study. They found that the Moneta criteria (PSV >275 cm/second) were 90% accurate for stenoses more than 50%. Accuracy improved dramatically, however, when EDV, EaDV, and PDV were considered. EDV of more than 50cm/second, EaDV of more than 50cm/second, and PDV of more than 70 cm/second predicted significant stenosis with a sensitivity and specificity rate of 100%. PSV in the CA also was examined according to Monetas criteria. An accuracy rate of 94% was demonstrated using a PSV of more than 200 cm/sec-
ond to predict more than 50% stenosis. As with SMA disease, evaluation of EDV, EaDV, and PDV predicted significant CA stenosis with 100% sensitivity and specificity. In this study, two false-positive results were noted using PSV as a criteria, one in a hyperthyroid patient and the other in a hypertensive patient with extensive atherosclerotic calcification. Elevated PSVs occurred in the thyrotoxic group, likely related to increased stroke volume. EDV and EaDV were unaffected. High output states may elevate PSV artificially [48]. Zwolack et al [17] found similar results to the Perko study. In a retrospective study of 243 patients with suspected mesenteric ischemia, an EDV of more
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than 45 cm/second predicted more than 50% stenosis with an accuracy rate of 91% (sensitivity 90%, specificity 91%). Their results for using PSV to predict SMA stenosis were similar to the Bowersox study, with a low sensitivity rate (60%) but high specificity rate (100%) for PSVs of more than 300 cm/second. Similar to the Perko study, a PSVof more than 200 cm/ second and an EDV of more than 55 cm/sec predicted CA stenosis with good accuracy, although EDV demonstrated the greatest accuracy (95% for EDV versus 93% for PSV). This study also demonstrated high-grade CA stenosis or occlusion in 100% of patients with reversed hepatic flow. Because the CA is frequently difficult to visualize, this finding may be particularly helpful in inferring CA stenosis [17]. Several factors may account for disagreement regarding the accuracy in PSV in SMA stenosis. Zwolack et al [17] described several potential explanations for the discrepancies in results. First, in the Moneta study [18], 88% of subjects were men. In the Zwolack study, 70% percent were women. Gender differences in flow characteristics in the mesenteric vasculature may be present, although to date these have not been explored fully. Second, aliasing is more frequent at PSVs more than 200 cm/second and vary according to the type of equipment used. This occurrence may account for the low sensitivity encountered using the Moneta criteria for SMA stenosis of 300 cm/ second, whereas PSVs of 200 cm/second predicted CA stenosis in both studies [17]. Another potential pitfall in the use of PSV, as described by Moneta et al [19], is the difficulty encountered in acquiring velocities at the level of stenosis. Stenoses usually arise at the origin of the vessel. Distal to this, the PSV is expected to fall. The reduced sensitivity in PSV described in some studies may be the result of sampling of the SMA distal to the stenosis. The studies described have used different percent stenoses as significant values. The Moneta criteria use 70% as a critical value, whereas the remaining studies use 50%. Using different percentages to define significant stenoses did not significantly alter the findings between the studies. In the study by Zwolack et al [17], the diagnosis of CII was suspected in all patients. Approximately half were found to have occlusive disease; symptoms in the remaining patients were attributed to other causes. In the CII group, most had stenoses of 70% or more at arteriography. In the group without CII, most had stenosis less than 50%. This finding created a bimodal distribution of vascular lesions. Only 12% of patients fell between these two groups. This result suggests that either value is acceptable and may explain the accuracy the Perko group demonstrated using the Moneta
criteria of PSV 275 cm/second to predict lesions of 50% or more [17]. In conclusion, duplex US scanning of the mesenteric vasculature has been demonstrated to be an effective screening test in patients with suspected CII. An adequate examination of the splanchnic vessels can be achieved in only 60% of the general population. The remaining 40% are limited by body habitus and interposed bowel gas. Patients with CII tend to be thinner than the general population and are easier to scan. Although controversy still exists in the literature as to the sensitivity and specificity of using PSV to predict SMA stenosis, PSV is a reliable parameter for diagnosing CA stenosis. Reversal of hepatic flow also has been shown to predict CA occlusion [17,19]. EDV reliably predicted significant SMA and CA stenosis in several studies. In clinical practice, the US finding of normal vasculature or subcritical stenoses in patients with abdominal pain and weight loss can exclude CII. Most patients with positive duplex US proceed to CT or conventional angiography. Mesenteric US may be a valuable screening tool.
Splanchnic artery aneurysms Historically, splenic artery aneurysms have been the most common visceral artery aneurysms. In recent years, hepatic artery aneurysms have surpassed splenic aneurysms in incidence with increasing use of percutaneous biliary procedures [49]. Posttraumatic pseudoaneurysms in the splanchnic vasculature, most commonly the hepatic artery, have been reported after trauma in children (Fig. 14). Blunt trauma is most frequently implicated, although it has been described in penetrating trauma. Embolization is the treatment of choice, although spontaneous thrombosis has been reported [50,51]. Splenic artery aneurysms are associated with acute pancreatitis. They occur in 10% of elderly patients [52]. In women of childbearing age, more than half of ruptured splenic artery aneurysms are related to pregnancy, and survival is uncommon [53]. Hepatic and splenic artery aneurysms appear as cystic structures in communication with the parent artery, which demonstrates arterial flow within the cystic portion on color Doppler (Fig. 15).
Iliac artery aneurysm Seventy-five percent of iliac artery aneurysms (IAAs) occur in association with AAA either as a
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Fig. 14. Traumatic hepatic artery aneurysm. (A) Cystic central area surrounded by thrombus (arrow). (B) Color Doppler shows turbulent flow within cystic portion of aneurysm.
direct extension of AAA or coincident with AAA [54,55]. The common iliac artery is the most commonly involved (99%), followed by the internal then external iliac [54]. According to standards created by the Subcommittee on Reporting Standards for Arterial Aneurysms, Ad Hoc Committee on Reporting Standards, Society for Vascular Surgery and the North American Chapter of the International Society for Cardiovascular surgery, IAA is defined by a luminal diameter that exceeds 1.5 cm [55]. They may be
fusiform, saccular, or bilobed. Atherosclerotic disease is the most common predisposing factor [54,55]. Pseudoaneurysms are less frequent and may be associated with trauma (accidental or iatrogenic), pregnancy, infection, or collagen vascular disease (Fig. 16) [54]. Several hypotheses have been proposed to explain the association with pregnancy, including trauma and instrumentation associated with delivery, infection, and increased vascular demand associated with pregnancy [56].
Fig. 15. Splenic artery aneurysm. (A) Cystic structure communicates with vessel lumen. Note disordered flow. (B) Color Doppler shows turbulent flow.
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Santilli et al [55] recommended annual screening with B-mode US of IAAs smaller than 3 cm and biannually for those larger than 3 cm. Repair is frequently undertaken in association with AAA repair. Elective IAA repair is indicated in symptomatic IAA and IAA larger than 4 cm. More urgent repair is performed in IAA larger than 5 cm given their higher risk of rupture [55]. IAAs, although uncommon, carry a risk of rupture with high associated mortality. As in AAA, US is a modality well suited to surveillance of IAA. Because 75% of IAAs occur in association with AAA [55], the routing screening for AAA as proposed by Lee [27] could potentially unmask most IAAs.
Other peripheral arterial aneurysms The most common lower extremity aneurysms are popliteal, which comprise 80% of all peripheral arterial aneurysms. They tend to be bilateral (50%). Patients often present with acute limb ischemia secondary to embolization or thrombosis. This carries a poor prognosis, with 15% requiring amputation [59]. Forty percent of patients with popliteal aneurysms have coincident AAA [56]. In a prospective study of patients with AAA, Diwan et al [60] found popliteal or femoral artery aneurysms in 51 of 313 patients. The association of femoral and popliteal aneurysms with AAA suggests a common pathogenesis. Jacob et al [61] found reduced vascular smooth muscle, increased inflammatory infiltrate, and increased expression of signaling molecules involved in cell death in surgical specimens obtained from AAA, iliac, popliteal, femoral, and carotid artery repairs. US is the imaging modality of choice in diagnosing popliteal aneurysm. In a series of 21 patients, MacGowan et al [62] found that sonography was superior to angiography in detecting surgically confirmed popliteal aneurysm. Popliteal aneurysm is diagnosed by focal dilatation of more than 20% of the vessel diameter. As with AAA, popliteal aneurysm can be followed sonographically. Popliteal aneurysm larger than 2 cm generally require surgical intervention regardless of the presence or absence of symptoms although much controversy regarding this still exists [63,64].
Fig. 16. Right internal iliac artery with surrounding hypoechoic fluid collection represents hematoma after stent procedure (arrow).
IAAs are frequently asymptomatic but may cause pelvic, flank, or groin pain [54,55]. Ureteral obstruction may complicate IAA because of the close proximity to the genitourinary tract. Sciatic and femoral root compression may result in symptoms. Arteriovenous fistula with resulting lower extremity ischemia is a less frequent manifestation [54,56,57]. Santilli et al [55] found that rate of expansion depended on aneurysm size. Common IAAs smaller than 3 cm expanded approximately 1 mm per year; IAAs larger than 3 cm expanded 2.6 mm per year. In that study, approximately 50% of the patient population with IAA was symptomatic. All symptomatic patients had aneurysms larger than 4 cm. The risk of rupture increased with increasing aneurysm size. For common IAAs, the risk of rupture for aneurysms smaller than 5 cm in diameter was 0%; for aneurysms larger than 5 cm, it was 33% [55]. Richardson and Greenfield [58] found that internal IAAs tended to be larger at detection and carried a 33% incidence of rupture. Santilli et al [55] found that B-mode US and CT had similar accuracy in measuring iliac aneurysms. US is most effective in diagnosing IAA when it is large enough to cause a palpable mass. Under these circumstances, IAAs are more likely to displace bowel loops, which aids visualization. Gentle graded compression is also helpful in displacing bowel loops [54]. Color Doppler shows a characteristic swirling pattern along with intraluminal thrombus, if present [54].
Summary The role of US in imaging of the abdominal vasculature has broadened over recent years. Long
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K. Hermsen, W.K. Chong / Radiol Clin N Am 42 (2004) 365381 Endoleak as a complication of endoluminal grafting of abdominal aortic aneurysms: classification, incidence, diagnosis, and management. J Endovasc Surg 1997; 4(2):152 68. Pacanowski JP, Dieter RS, Stevens SL, Freeman MB, Goldman MH. Endoleak: the Achilles heel of endovascular abdominal aneurysm exclusion: a case report. Wis Med J 2002;101(7):57 63. Harward T, Smith S, Seeger J. Detection of celiac axis and SMA occlusive disease with use of abdominal duplex scanning. J Vasc Surg 1993;17(4):738 45. Zwolak R, Fillinger M, Walsh D, LaBombard F, Musson A, Darling C. Mesenteric and celiac duplex scanning: a validation study. J Vasc Surg 1998;27(6): 1078 87; discussion 1088. Moneta G, Yeager R, Dalman R, Antonovic R, Hall L, Porter J. Duplex ultrasound criteria for diagnosis of splanchnic artery stenosis or occlusion. J Vasc Surg 1991;14(4):511 8; discussion 518 20. Moneta G, Lee R, Yeager R, Taylor L, Porter J. Mesenteric duplex scanning: a blinded prospective study. J Vasc Surg 1993;17(1):79 84; discussion 85 6. Bowersox J, Zwolak R, Walsh D, Schneider J, Musson A, LaBombard E, et al. Duplex ultrasonography in the diagnosis of celiac and mesenteric artery occlusive disease. J Vasc Surg 1991;14(6):780 6; discussion 786 8. Durham J, Kaufman J. Imaging of acquired thoracic and abdominal aortic disease. In: Strandness DE, Van Breda A, editors. Vascular diseases: surgical and interventional therapy. New York: Churchill-Livingstone; 1994. p. 240 72. Beede S, Ballard D, James E, et al. Positive predictive value in clinical suspicion of abdominal aortic aneurysms. J Gen Intern Med 1990;150:549 51. Mower W, Quinones J, Gambhir S. Effect of intraluminal thrombus on abdominal aortic aneurysm wall stress. J Vasc Surg 1997;26(4):602 8. Brown PM, Zelt DT, Sobolev B. The risk of rupture in untreated aneurysms: the impact of size, gender, and expansion rate. J Vasc Surg 2003;37(2):280 4. Sharp MA, Collin J. A myth exposed: fast growth in diameter does not justify precocious abdominal aortic aneurysm repair. Eur J Vasc Endovasc Surg 2003; 25(5):408 11. Sostek M, Fine SN, Harris TL. Duodenal obstruction by abdominal aortic aneurysm. Am J Med 1993;94(2): 220 1. Lee TY, Korn P, Heller J, Kilaru S, Beaver F, Bush HL. The cost-effectiveness of a quick-screen program for abdominal aortic aneurysms. Surgery 2002;132(2): 399 407. Griffith JF, Yang WT, Lam WWM, Metreweli C. Uncommon features of abdominal aorto-iliac disease. Br J Radiol 1997;70:536 42. Rogoff SM, Lipchik EO. Aneurysms of the abdominal aorta. In: Abrams HL, Cook PH, editors. Angiography. Boston: Little, Brown and Company; 1971. p. 761. Fiorani P, Bondanini S, Faraglia V, Spartera C, Spe-
considered the modality of choice in the detection of AAA, its use has expanded to diagnosing and monitoring IAAs and PAAs, screening for mesenteric ischemia, and posttreatment monitoring of endovascular stents.
[15]
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[1] Bluth E, LoCascio L. Ultrasound evaluation of the abdominal aorta. Echocardiography 1996;13(2): 197 206. [2] Wanhainen A, Bergqvist D, Bjorck M. Measuring the abdominal aorta with ultrasonography and computed tomography: difference and variability. Eur J Vasc Endovasc Surg 2002;24(5):428 34. [3] Downey D. The retroperitoneum and great vessels. In: Rumack CM, Wilson SR, Charboneau JW, editors. Diagnostic ultrasound. St. Louis: Mosby-Year Book; 1998. p. 453 86. [4] Naganuma H, Ishida H, Konno K, Sato M, Ishida J, Watanabe S. Mycotic abdominal aneurysm: report of a case with emphasis on the presence of gas echoes. Abdom Imaging 2001;26(4):420 2. [5] Hollinshead WH. The abdomen. In: Hollinshead WH, editor. Textbook of anatomy. New York: Harper and Row; 1967. p. 662 3. [6] Pedersen OM, Aslaksen A, Vik-Mo H. Ultrasound measurement of the luminal diameter of the abdominal aorta and iliac arteries in patients without vascular disease. J Vasc Surg 1993;17(3):596 601. [7] Ross MH, Romrell LJ, Kaye GI. Cardiovascular system. In: Histology: a text and atlas. Baltimore: Williams and Wilkins; 1995. p. 304 9. [8] Moneta G. Diagnosis of chronic intestinal ischemia. Semin Vasc Surg 1990;3(3):176 85. [9] Nebesar RA, Kornblith PL, Pollard JJ, Michels N. Anatomic considerations in celiac and superior mesenteric arteries: a correlation of angiograms and dissections. Boston: Little, Brown and Company; 1969. p. 26. [10] Moneta GL, Taylor DC, Helton WS, Mulholland MW, Strandness DE. Duplex ultrasound measurement of post prandial intestinal blood flow: effect of meal composition. Gastroentereology 1988;95(5):1294 301. [11] Guyton AC, Hall JE. General principles of gastrointestinal function: motility, nervous control, and blood circulation. In: Textbook of medical physiology. Philadelphia: WB Saunders; 1996. p. 800 1. [12] Lanne T, Sandgren T, Mangell P, Sonesson B, Hansen F. Improved reliability of ultrasonic surveillance of abdominal aortic aneurysms. Eur J Vasc Endovasc Surg 1997;13(2):149 53. [13] Pages S, Favre JP, Cerisier A, Pyneeandee S, Boissier C, Veyret C. Comparison of color Duplex ultrasound and computed tomography scan for surveillance after aortic endografting. Ann Vasc Surg 2001;15(2): 155 62. [14] White GH, Yu W, May J, Chaufour X, Stephen MS.
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Radiol Clin N Am 42 (2004) 383 396
Arterial injuries: a sonographic approach

Brian D. Davison, MDa,*, Joseph F. Polak, MD, MPHb
a
Department of Radiology, Harvard Medical School, Brigham and Womens Hospital, 75 Francis Street, Boston, MA 02115, USA b Department of Radiology, Tufts Medical School, New England Medical Center, Box 299, 750 Washington Street, Boston, MA 02111, USA
Acute arterial emergencies can arise from direct traumatic injury to the artery or be spontaneous. In the case of spontaneous injuries, the likelihood of a specific arterial event increases in the presence of certain risk factors or medical conditions. For example, the incidence of acute arterial occlusions is increased in the presence of popliteal artery aneurysms or atrial fibrillation. This article emphasizes the various presentations of arterial emergencies. These include acute arterial occlusions; excessive bleeding; and hematoma formation caused by penetrating arterial wall injuries, pseudoaneurysms, and arteriovenous fistulas. The broad category of arterial occlusions includes traumatic lacerations, embolizations, and arterial dissections. The caliber of the artery can also, on occasion, be significantly narrowed because of spasm. This often exacerbates the clinical impact of the injury. Modern ultrasound equipment is a rapid and convenient imaging approach in many of these clinical scenarios. In combination with MR angiography and CT angiography, these noninvasive tests can diagnose the presence of most arterial injuries, and be used to measure their impact. Conventional angiography is reserved for problem solving or directed therapy.
Validation studies: pathologic validation In the emergency setting color Doppler imaging and duplex ultrasound have shown use in the evaluation of potential vascular injuries, especially in the
setting of proximity injuries or where a mechanism of injury is not in accordance with other physical findings. Since the late 1980s studies have been conducted to screen patients with vascular injuries that need possible surgical management. Ultrasound can be up to 95% to 100% sensitive for diagnosing vascular injuries in the hands of highly qualified personnel with a high index of suspicion [1]. This high diagnostic accuracy has actually been validated with animal studies. Panetta et al [2] created different types of arterial injuries in the femoral and carotid arteries of dogs. These injuries including intimal flaps, crush injuries, and lacerations, and were compared with control limbs. The studies were performed by a sonographer blinded to the type and location of the injury. Results were correlated against operative observation and pathologic study of the injured artery 1 month after the injury. The sensitivity and specificity of ultrasound were 96.5% and 86.4%, respectively, with an accuracy of 95%. The ultrasound findings correlated well with the histopathologic examination. All arteries subjected to crush injury in these studies showed abnormal duplex findings with measurable changes in the arterial wall thickness. The site of the crush injury showed intramural hemorrhage or mural thrombus at the site of injury. Most intimal flaps had healed at the time of pathologic examination, 1 month after the injury. Overall, the findings of Doppler ultrasound suggested that it has clinical use in the evaluation of acute arterial trauma.
Nonimaging Doppler techniques

* Corresponding author. E-mail address: bddavison@partners.org (B.D. Davison).
The ankle-brachial index is a quick comparison of blood pressure readings. Doppler is used instead of a stethoscope. Systolic pressures are obtained in both
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brachial arteries. Pressures are obtained in the posterior tibial artery, or the dorsalis pedis in both legs. By dividing the highest left and right ankle values by the highest brachial value an ankle-brachial index is calculated. Someone with no disease should have a ratio of greater than 0.96. For evaluation of peripheral vascular disease a value of 0.81 to 0.95 suggests mild disease, 0.51 to 0.80 suggests moderate disease, 0.31 to 0.50 suggests moderate to severe disease, and 0.30 or below suggests severe disease. Simple measurement of the ankle-brachial index can be used to screen for lower-extremity arterial injuries. This adds value to the clinical finding of depressed pulses or pulses that change strength, waxing and waning over a few minutes. More direct comparisons of pressure in one limb with the other can also be done. Johansen et al [3] used the Doppler arterial-pressure index to compare the systolic arterial pressure in the injured extremity to the arterial pressure in the uninvolved side. A ratio of 0.9 or less was indicative of major arterial injury with a sensitivity and specificity of 95% and 90%, respectively. The negative predictive value was high. Most physicians, however, consider a negative arterial-pressure index as a poor indicator of potentially unstable injuries, such as arterial dissections, disruptions, and pseudoaneurysms. These findings were confirmed in a study by Lynch and Johansen [4] where the arterial-pressure index calculated in 100 consecutive injured limbs in 93 trauma victims. All of these patients subsequently had angiography. An arterial-pressure index of less than 0.9 had a sensitivity of 80% and specificity of 97% for the presence of arterial disruption. Overall, the sensitivity of the pressure index for detecting injuries requiring intervention ranges from 44% to 95%, depending on clinical circumstances and extent of the injury. Angiography remains the gold standard for the evaluation of traumatic arterial injuries. There are several disadvantages include cost, time delay, and a 0.6% major complication rate. Vascular injuries requiring intervention are present on only 1% to 1.5% of angiograms in patients missing true signs of vascular injury. Impaired renal function and the amount of iodinated contrast already given should be weighed before an angiographic procedure.
Pseudoaneurysm Pseudoaneurysm or false aneurysm is defined by the loss of integrity of the three layers of the arterial wall. This results in a contained rupture of the blood vessel. The most common origin of pseudoaneurysms is traumatic, secondary to a penetrating injury. Of
these, iatrogenic compromise of the arterial wall following medical interventions is most common. Diagnostic and interventional arterial catheterizations are the most common sources of iatrogenic pseudoaneurysms. Other common sources are postsurgical, typically at the site of an arterial anastomosis or following an arterial repair. Pseudoaneurysms following femoral artery catheterization have a reported incidence of 7% to 8% [5]. The likelihood of an iatrogenic pseudoaneurysm following arterial catheterization increases with the size of the catheter, the length of the procedure, and the concurrent use of anticoagulants. Additional factors include poor puncture [6] and compression techniques [5]. Antegrade punctures and use of compression devices increase the likelihood of pseudoaneurysm formation. Other factors include poor coagulation factors caused by liver failure and thrombocytopenia, and other patient factors, such as obesity, hypertension, and stresses to the catheter entry site [5,7]. The patient who presents acutely to the emergency room typically has suspicious physical signs, such as swelling in the injured region, a pulsatile mass, or the presence of a thrill. This occurs in the case of postcatheterization pseudoaneurysm 1 to 10 days after the actual catheterization. Ecchymotic skin changes are often present starting 1 to 2 days postinjury. If the mass of the pseudoaneurysm presses sufficiently on the native arteries, then blood flow can be decreased despite intact or even increased pulses. A bruit may be heard on auscultation. Gray-scale ultrasound analysis reveals anechoic or hypoechoic areas resembling fluid collections (Fig. 1A). These are located adjacent to or can abut the arterial wall. Color Doppler ultrasound, however, is most useful in identifying the nature of the lesion. Classically, the description of the blood flow pattern as seen on color Doppler ultrasound has been described as the yin and yang sign (Fig. 1B). These signals are caused by swirling motion of blood within the pseudoaneurysm cavity. The inflow jet of blood is directed along one wall causing a positive frequency shift (red color), and the outflow is along the opposite wall causing a negative frequency shift (blue color). The presence of a communicating channel or neck between the artery and the collection is needed, however, to confirm the diagnosis. Blood flow in this communicating channel has a very typical pattern. Inflow of blood causes the pseudoaneurysm collection to expand during systole. Sampling of the Doppler waveform in the neck of the pseudoaneurysm shows a positive inflow into the channel. During diastole, blood flows out of the collection into the artery. This is caused by the release of elastic energy stored by the
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Fig. 1. (A) Color Doppler image in a patient with a knife wound shows a superficial hematoma (arrow) and a collection containing flow signals. (B) The presence of a pseudoaneurysm is confirmed by the alternating to-and-fro signals at the neck of the pseudoaneurysm.
soft tissues surrounding the pseudoaneurysm cavity. Blood flow is directed out of the collection into the artery. This biphasic to-and-fro blood flow pattern with pandiastolic reversal of flow is characteristic of a pseudoaneurysm. Once diagnosed, gray-scale ultrasound can be used to estimate the size of the neck of the pseudoaneurysm. Smaller diameter and long necks are more suitable for percutaneous interventions than pseudoaneurysms with short (less than 1 cm) and wide necks (larger than 2 3 cm), and location must be considered. The natural history is varied. Most pseudoaneurysms spontaneously thrombose [8]. Over time pseudoaneurysms can mature and a fibrous capsule may form. The dreaded complication of a pseudoaneurysm is continued expansion and bleeding into the thigh or retrograde bleeding into the pelvis. With rapid enough expansion, the dissecting blood can cause a compartment syndrome, compromise blood flow to the distal limb, and lead to ischemia and irreversible tissue loss. Many pseudoaneurysms at presentation contain varying degrees of clotted blood. Pseudoaneurysms can have multiple separate compartments or collections connected by thin tracts or canals. Expanding pseudoaneurysms can cause limb ischemia through compression. The thrombus forming within them theoretically can escape and cause distal emboli [9].
Pseudoaneurysms involving surgical sites, most often the anastomosis of bypass grafts, typically have very wide necks. They tend to be large and have wellformed capsules. They often contain mural thrombus. Pseudoaneurysms caused by gunshot wounds or penetrating knife wounds should be considered as potentially being infected. This type of pseudoaneurysm seldom resolves spontaneously, and often requires direct surgical intervention. Historically, treatment of pseudoaneurysms has been by open surgical repair, but evolution in endovascular devices has allowed multiple options for treating these lesions. Ultrasonography should be used to assess the neck of the pseudoaneurysm. If it is wide or in a position not directly accessible for compression, other therapies should be considered. Ultrasound-guided manual compression of the pseudoaneurysm has been used for over 15 to 20 years as a treatment for pseudoaneurysms. The procedure allows natural thrombosis of the pseudoaneurysm cavity. Using gray-scale imaging as a guide, force can be applied directly to the skin overlying the neck. With enough pressure, blood flow stops and the contents of the pseudoaneurysm thrombose. Success rates are reported in the range of 51% to 73% [10 13]. The procedure is noninvasive, but can be time consuming and painful for both the patient and operator. Unfortunately, this technique may require several
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attempts before complete obliteration of the pseudoaneurysm. Patients treated with anticoagulants can be refractory to this form of therapy. The recurrence rate of pseudoaneurysms after ultrasound-guided compression may be as high as 20% [5]. Direct thrombin injection using a sterile technique and real-time Doppler ultrasound guidance into a pseudoaneurysm causes thrombosis of the pseudoaneurysm within seconds. The procedure usually takes less than 15 minutes. This procedure is safe and can be performed on outpatients. A 20-gauge can be used and the tip should be directed away from the neck. Percutaneous thrombin injection for the treatment of pseudoaneurysm has been described in the subclavian, brachial, radial, and tibial arteries and carotid and temporal arteries [14 16]. The proximity to these key arteries requires that the operator have great technical skills to prevent excess injection of thrombin and thrombosis of the native artery. Success rates for thrombin injection vary between 93% and 100% in the literature [12,14 19]. Patients on antiplatelet therapy or heparin can have thrombin injection without decreasing success rates [14,19]. Pseudoaneurysms that have very short and wide necks or that are located posterior to the artery are at higher risk for failure or complications than those with long necks and located near the skin. Complications include inadvertent direct injection of thrombin into the artery, or subsequent emboli emission through a large neck. Sensitivity or allergy to thrombin has been reported [20]. The long-term effects of bovine thrombin injection are not known. Percutaneous transcatheter embolization and other endovascular techniques, such as exclusion of the pseudoaneurysm with covered stent placement, are
successful but invasive. Covered wall grafts have been percutaneously placed to treat internal carotid artery aneurysms [21]. In a small series, 16-month follow-up did not show evidence of occlusion or stenosis or reperfusion to the pseudoaneurysm. Indications included penetrating trauma and complications of percutaneous interventions [5,7,22]. Temporary balloon occlusion has been tried and can be successful in properly selected patients. Repair of large neck aneurysm with balloon occlusion and thrombin injection has not been shown to be an acceptably safe procedure. In the event that the previously described procedures fail or rupture is threatened by the rapid expansion of the pseudoaneurysm, surgery should be performed. Other surgical indications include infection, distal ischemia, an embolic event, or extensive tissue damage. There is significant morbidity associated with emergently performed surgery [12].
Hematoma A hematoma is the natural outcome of a vascular disruption. This can occur spontaneously in smaller arteries especially in the setting of anticoagulation [2,23,24]. The hematoma can be the result of blunt or penetrating trauma or represent a thrombosed pseudoaneurysm (Figs. 2 4). The hematoma may remain restricted to the surrounding soft tissue especially if it occurs in a muscle, or it can tract through fascial planes when caused by a larger arterial disruption. Hematomas commonly occur in the retroperitoneum [23,25], the rectus sheath [26], and in the extremities around joints associated with muscle tears [24].
Fig. 2. (A) Transverse scan of the right groin in a patient with acute pain following a fall shows an avascular mass (arrow) medial to the vein. (B) The CT of the pelvis shows a right pubic ramus fracture (arrow) and the hematoma lying superior to it.
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Fig. 3. (A) Arteriogram of the upper limb shows an intact duplicated brachial artery (arrows) and a distal humeral fracture. (B) The corresponding color Doppler image shows a hematoma (within calipers) and no evidence of a pseudoaneurysm. A, duplicated brachial artery.
Physical finding include swelling in the injured region, which is most often nonpulsatile, and silent on auscultation. Ecchymotic skin changes are almost always present. If causing compression and narrowing, hematomas can present with diminished blood flow and pulses to the affected limb. If bleeding is severe and within a fascial compartment, then a compartment syndrome can ensue, causing severe pain, markedly diminished pulses, pallor, and paresthesias. Hematomas should be delineated with a marking pen on the skin and measured carefully on ultrasound to rule out a rapidly evolving hematoma. Although not a common site of arterial puncture, a high brachial puncture used for catheterization is difficult to compress following catheter removal. This can result in an extensive hematoma. Extension into the axilla is of great concern because the resulting hematoma can compress and injure the brachial plexus [27,28]. The common femoral artery remains the preferred site for arterial access for catheterization procedures. Hematomas
here usually result in local groin swelling adjacent to the puncture site. Rarely, they can expand to pelvis, leg, or retroperitoneum. Vigorously compressed to break apart, the hematoma ultimately decreases patient discomfort. Careful fluoroscopic checking of the anatomic landmark of the femoral head ensures proper needle placement, and is paramount in minimizing the risk of postprocedure hematoma. Gray-scale ultrasound analysis shows variable findings dependent on the time interval since the original hemorrhage and possibly intermittent nature of bleeding episodes. In the acute period (hours) hematoma may present as solid or mixed echogenic structures because of mixing of liquid with clotting blood [11,26]. It can be well or ill defined, and should be imaged carefully to document its extent, location, and dimensions. The size seen on ultrasound should be compared with the physical effect on the extremity. Hematomas can often dissect in a diffuse fashion and not form a well-circumscribed mass. A baseline
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Fig. 4. (A) Color flow Doppler image shows a large hematoma in a patient following penetrating trauma. (B) Doppler signals confirm the presence of an additional arteriovenous fistula.
measurement of size should be done because this can help document possible rebleeding and expansion of the hematoma. Over the course of days the clotted blood breaks down to fluid in areas, giving a complex cystic and solid appearance. At this point, without proper history, the collection can be misdiagnosed an abscess cavity or perhaps a pseudoaneurysm. Cystic, necrotic, or hemorrhagic neoplasms may also have similar imaging findings, and should be excluded with follow-up. As discussed previously, however, color flow Doppler is most useful in identifying and differentiating these lesions from pseudoaneurysms (see Fig. 1). Over weeks liquefactive necrosis of the entire hematoma usually occurs [11,26]. Ultrasound at this point shows all fluid signals, but a hematocrit level may be seen within. A 2- to 3-month follow-up scan is recommended to assess for decreasing size or resolution to differentiate the hematoma from a mass. Secondary infections are relatively rare. Their likelihood increases if there is a persistent foreign body in the case of penetrating trauma. Other examples where foreign material remains in the soft tissues include after the use of closure devices used to seal the needle access site following catheterization, or post synthetic graft placement.
Arteriovenous fistulas Arteriovenous fistulas represent a direct connection between a vein and an artery. Like hematomas and pseudoaneurysms, arteriovenous fistulas can be spontaneous, but are often the result of penetrating
trauma. Arteriovenous fistulas are often asymptomatic, but when significant can cause rapid shunting with return of oxygenated blood to the right heart. Rarely, they can contribute to high-output cardiac failure [29]. They can also shunt away blood from the extremity and cause symptoms of distal ischemia. Arteriovenous fistulas are often caused by low-arterial punctures, large-diameter catheters, anticoagulant use, and they are associated with pseudoaneurysms [2,30 32]. The femoral artery and vein are parallel and side-by-side in the region of the groin. Variant anatomy or punctures in the lower thigh (where the femoral vein travels behind superficial femoral and profunda arteries) are risk factors for the formation of iatrogenic arteriovenous fistulas. Iatrogenic arteriovenous fistulas are not uncommon elsewhere in the body, and not infrequently seen as a consequence of a biopsy, such as in the kidney. Physical examination can reveal little to no swelling or ecchymosis, but a palpable thrill is often present. Patients may present with pain but are most often asymptomatic, but have a bruit on local auscultation. Gray-scale ultrasound imaging is not helpful in the evaluation of arteriovenous fistulas unless the arteriovenous fistula is chronic and the high flow state has caused dilatation of the vein and artery. Color Doppler imaging and pulsed wave Doppler are usually diagnostic. Tissue vibrations caused by turbulent flow are the most notable color Doppler finding (see Fig. 4). Also, the track between artery and vein can sometimes be directly visualized. The Doppler waveform in the feeding artery shows a low resistance pattern with increased diastolic flow. The
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jet of arterial flow entering the vein can cause a marked flow disturbance and chaotic waveform or in more severe case an arterial waveform is present. Compression repair is usually not successful for closing arteriovenous fistulas. Small arteriovenous fistulas can spontaneously remit [8]. Percutaneous placement of a covered stent or surgical repair is often indicated.
Craniocervical dissections There are two types of dissections likely to affect the carotid and vertebral arteries. The first is a primary dissection of the artery, sometimes associated with a vague history of trauma or rapid movement of the head. This is seen more often in young patents less than 50 years of age. Secondary dissections occur as an extension of a type A dissection of the aortic arch into the origins of the brachycephalic, carotid, and subclavian arteries. This is typically seen in older patients or patients with a weakness of the media in the aortic wall, typically with cystic medial necrosis. Primary dissections Although any of the arteries in the neck may be affected, primary dissections of the internal carotid
artery are the most common. Internal carotid artery dissections typically occur in the proximal internal carotid artery, just beyond the carotid bulb. Primary dissections of the intracranial portion of the internal carotid artery can occur but they are much less common than the classic primary dissection of the internal carotid artery (Fig. 5). Dissections of the vertebral arteries are also seen but a careful investigation is rarely done because symptoms, if present, tend to be minimal. Patients with an internal carotid artery dissection have nonspecific presenting symptoms, such as a sensory or motor deficit. The classic presentation is that of a headache. The dissection often happens in a previously healthy individual and develops either spontaneously or following various degrees of trauma. As medical imaging equipment has evolved, better visualization of this area is possible. This fact coupled with more awareness has made this diagnosis less difficult. A dissection is the disruption of the media or second layer of the artery. Once the dissection starts, the intima along with a portion of the media is lifted from the artery wall. Collagen is exposed to blood and this usually starts a clotting cascade. The pathology of the primary dissection of the internal carotid artery is one of an intramural blood clot. If the size and volume of the blood clot is large enough, the artery occludes. If the size of the clot is intermediate,
Fig. 5. (A) Spectral Doppler waveform demonstrates a high resistance and low amplitude in the internal carotid artery of a 25-year-old patient. (B) The corresponding arteriogram shows abrupt termination of the internal carotid artery (arrow) at the site of an internal carotid artery dissection.
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with proved dissections. Internal carotid artery dissections may or may not cause symptoms depending on the integrity of the circle of Willis. Atherosclerotic disease may be present in the adjacent arterial segment. Spectrum analysis may demonstrate two separate frequency curves when the dissected lumen is still open. Doppler ultrasound has been used to monitor and follow patients with internal carotid artery dissection. Secondary dissections These dissections extend into the neck arteries from a primary dissection arising from the ascending aorta (Fig. 7). The patients present with the symptoms of acute chest pain, radiating to the back. Because these type A dissections are, a priori, triaged to surgical intervention, it is very likely that the aorta will be repaired. The extension of the dissection into the neck arteries is rarely symptomatic, probably because the dissecting lumen re-enters the lumen at variable locations in the common or, less often, the internal carotid arteries. Neurologic symptoms are rare. Gray-scale imaging shows the typical luminal flap. Doppler waveforms are altered. If there is a site of re-entry, forward blood flow is mainly seen. If one of the lumens (the false lumen) does not re-enter the
Fig. 6. This patient was found to have an acute traumatic intimal tear of the internal carotid artery on the carotid arteriogram (not shown). The internal carotid artery color Doppler image demonstrates evidence of a periarterial soft tissue mass consistent with a hematoma (arrow). The intimal tear seen in arteriogram could not be seen on color flow Doppler.
then the lesion causes a stenosis or even occlusion of the proximal internal carotid artery (see Fig. 5). If relatively small, the patient can present with acute symptoms and no neurologic deficit because the lesion does not compromise blood flow in the internal carotid artery. This can occur in spontaneous and posttraumatic dissections (Fig. 6). The latter scenario is typical of up to 40% of patients with primary internal carotid artery dissections. Physical examination can reveal motor weakness or a sensory deficit. Rarely, the patient can present clinically with cranial nerve palsy, such as Horners syndrome [33 35]. A double lumen with a separating intimal flap can be seen on gray-scale imaging in cases of primary internal carotid artery dissections, but is less common than an intramural hematoma. Typically, the dissection consists of an intramural hematoma or thrombus that is hypoechoic and hard to perceive. The Doppler findings are variable. In the absence of a significant obstruction, the signals can be normal. A more significant dissection with large intramural hematoma shows direct evidence of a stenosis with a zone of elevated blood flow velocities. Very severe dissections can occlude or subtotally occlude the internal carotid artery. Doppler ultrasound is quite specific for the detection of significant vessel obstruction when the Doppler waveform is altered and shows a highresistance pattern (see Fig. 5). This pattern, however, is the least common of the patterns seen in patients
Fig. 7. Gray-scale ultrasound image shows the leading edge of an aortic dissection extending from the arch into the common carotid artery. The leading edge of the dissection has re-entered the lumen of the artery.
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carotid lumen, then an alternating systolic-diastolic waveform is seen in that lumen.
Stroke and carotid artery stenosis The patient who presents with a stroke (or significant transient ischemic attack) likely has an arterial embolus in the intracranial circulation or primary disease of the intracranial branches. Other and more common sources of stroke include emboli from the heart and from the aorta. In the aggregate, most
patients with strokes have nonsignificant lesions in the carotid arteries. If a significant lesion is detected, then the focus shifts to this lesion. It is then considered to be a culprit lesion. Significance is defined in one of three ways. A 50% or greater narrowing of the internal carotid artery is considered a hemodynamic significant stenosis. In asymptomatic patients, a 60% or greater narrowing of the lumen diameter of the internal carotid artery is considered significant. In symptomatic patients, the definition varies. The North American Symptomatic Carotid Endarterectomy Trial (NASCET) study showed that
Fig. 8. (A) Color Doppler image shows an abrupt termination of color Doppler signals before an echogenic filling defect in the proximal internal carotid artery. This corresponds to an embolus in a 35-year-old patient. (B) Transverse gray-scale ultrasound image shows the filling defect. (C) The spectral Doppler waveform shows a high resistance pattern consistent with the presence of the obstructing embolus.
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a 70% diameter stenosis was a threshold above which there was a high-risk for a permanent stroke in the next few months or years [36]. A second NASCET report indicated that a 50% or greater stenosis should be considered to be significant [37]. Rarely, an acute embolus can occlude the carotid artery proper; the source of the embolus is then the heart or even the aortic arch (Fig. 8). Physical examination shows diminished pulses only for the most severe stenoses. Presence of a carotid bruit can be heard on auscultation. A carotid bruit is, however, an unreliable sign of significant stenosis. Gray-scale imaging can show the fibrofatty changes (hypoechoic) of carotid artery plaque. The most common finding, however, is the presence of a heterogeneous plaque with mixed dense and hypoechoic elements. Calcium deposits cause acoustic shadowing. Pulsed wave Doppler is the most important ultrasound approach to evaluating the degree of carotid stenosis. The degree of carotid stenosis is graded by the blood flow velocity elevation caused at the site of stenotic narrowing. The peak systolic and end-diastolic velocity is correlated to the degree of internal carotid artery stenosis. The ratio of the internal carotid artery to common carotid artery peak systolic velocities is considered a sturdy diagnostic criterion that accounts for changes in blood flow velocities caused by altered (either lowered or increased) cardiac output. When a stenosis in the internal carotid arteries lumen is reduced by 50%, a noticeable change in blood flow velocity can be measured. This corresponds to a 50% diameter stenosis. When flow values approach and exceed 230 cm/second, then the presence of a 70% or greater stenosis is very likely. Rarely, a critical stenosis is so severe as to decrease blood flow volume and blood flow velocity to the point that the Doppler signal is no longer detectable. This remains a limitation of Doppler ultrasound: mistaking a subtotal occlusion to be a total occlusion is still a diagnostic limitation of ultrasound imaging. Patients with a subtotal occlusion could still benefit from an intervention, whereas there is no lasting benefit to opening a previously occluded internal carotid artery. In the setting of recurrent transient ischemic attacks in a patient with an ipsilateral high-grade carotid lesion, carotid endarterectomy should be considered. Currently, appropriate therapy in an acute setting is not necessarily surgical endarterectomy. Percutaneous stenting of the carotid is a viable option in the emergent setting, especially if the patient is evolving toward a major stroke. There is increasing controversy as to how and when to treat the culprit lesion in the neck, especially if an acute revascularization of the intracranial arteries is being attempted. In this context,
a fully percutaneous approach with stenting of the carotid and lysis of the embolus offers a reasonable therapeutic option.
Acute limb ischemia: arterial embolization The normal appearance of an extremity artery is triphasic (Fig. 9). Pulse Doppler waveform shows an initial narrow antegrade systolic peak, followed by an early diastolic retrograde peak or notch. Finally, a variable antegrade diastolic peak is seen. Under the arterial envelope a clear area is seen. Extremity arterial waveforms convert to a lower resistance pattern during exercise, with a broadened spectral peak, and pandiastolic antegrade flow. Acute limb ischemia is usually caused by a sudden arterial obstruction. There are two main causes: acute thrombosis of an existing arterial lesion; and embolism from the heart or from a more central arterial lesion, such as an aneurysm or an ulcerated plaque. Emboli usually lodge at major branch points in the arteries. Symptom onset is rapid. Depending on the physiologic impact of the occlusion, the patient may have severe claudication, rest pain, or sensory loss. Emergent intervention by surgical embolectomy, surgical bypass, or percutaneous thrombolysis is required to save the limb from necrosis of the muscles. In severe cases, amputation may be needed because further myonecrosis causes release of myoglobin and can trigger further metabolic pathways that lead to organ failure and finally death. The impact of the arterial occlusion depends on the extent of arterial disease and the presence of arterial collaterals. For example, acute occlusion of an artery in a young, relatively healthy patient can be devastating, because there are almost no collateral branches to feed the more distal leg arteries. A patent with claudication and slowly progressing arterial disease likely has
Fig. 9. Triphasic spectral Doppler waveform. The systolic peak is marked (arrowhead) followed by an area of flow reversal (short arrow). This is followed by a small area of antegrade flow (long arrow).
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Fig. 10. (A) This patient with acute onset of calf pain had evidence of a Baker cyst (within calipers) on ultrasound examination. (B) Imaging lower in the calf shows a hypoechoic mass extending along the fascia. This is consistent with an acute dissecting Baker cyst.
well-developed collateral branches. An acute occlusion in this patient may only cause an abrupt increase in the severity of claudication. Gray-scale imaging from the groin to the calf arteries is relatively easy, as is the upper arm. Difficulty can be experienced, especially in diabetic patients, when calcium deposits in the arterial walls impair ultrasound beam penetration. Sometimes an alternative diagnosis for acute pain can be made with gray-scale imaging (Fig. 10). Long-standing occlusion can result in contraction of the artery to a small scarred cord that runs parallel to the deep vein. New thrombus in the vessel lumen can appear hyper-
echoic, especially if it originates from the heart. Thrombus is most often anechoic with echogenicity similar to that of blood. Dilation of the artery proximal to an occlusion is rarely seen. Acute occlusions are most likely diagnosed by combining color flow Doppler with pulsed wave Doppler waveform analysis. Absence of flow or low amplitude signal in the affected vessel is diagnostic of occlusion (Fig. 11), whereas high-grade stenosis is associated with increased blood flow velocities. Care should be taken to reduce the pulse repetition frequency and to scan in orthogonal planes to assess for the presence of very slow blood flow.
Fig. 11. (A) Transverse color flow Doppler image shows low-amplitude signals in the brachial artery. (B) The corresponding spectral Doppler waveform shows low-amplitude signals in the artery just proximal to an acute embolus to the brachial artery.
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Fig. 12. (A) Spectral Doppler waveform from the superficial femoral artery shows a reversing component to blood flow during diastole. This is caused by high peripheral resistance from a distal (calf) compartment syndrome following trauma. (B) The contralateral normal superficial femoral artery spectral Doppler waveform is shown for comparison.
This helps distinguish an occlusion from a stenosis. In transverse plane, tortuous small collaterals may be seen in both cases. One should look for reconstitution of the occluded vessel, distal to the occlusion. Extensive thrombosis extending over long segments is more difficult to treat using endovascular approaches than shorter occlusions. Thrombolysis can be used alone or in combination with a surgical bypass operation. Surgical thrombectomy alone or in combination with surgical bypass operations is a very common therapeutic option. Uncommonly, a compartment syndrome can occur where tissue pressures in the compartment exceed systolic pressure (Fig. 12).
Diabetic foot Vascular disease in the diabetic patient is usually insidious in its presentation and slowly progressive. Close control of the diabetic status and medical examination of known diabetics is the best way to avoid an emergency. Careful routine clinical examination and self-inspection of the diabetic foot on a regular basis is the most effective preventive measure. Peripheral neuropathy is a risk factor associated with poor outcome. Loss of sensory feedback adds to the effects of arterial obstruction because symptoms are ignored and the extent of tissue loss can increase without the patient noticing. The prevalence of lowerextremity occlusive arterial disease in diabetics is four times more prevalent than in nondiabetics of a similar age [38]. Calcification of the arterial wall is generally
widespread, and the larger vessels of the pelvis are less affected than the small vessels of the calf and foot. Falsely elevated pressures that are measured with external pressure cuffs, typically greater than 30 mm Hg above the brachial pressure, suggest the presence of noncompliant arteries. Of the run-off vessels, the dorsalis pedis artery is often spared [39]. The calcification of the peripheral vasculature generally affects the more distal vessels to a lesser degree. Distal pedal pulses can be intact and the vessels remain compressible. This allows pressures measured at the toe to be used as an alternative noninvasive approach to assess lower-extremity arterial disease. A toe-to-brachial index of greater than 0.6 is considered normal. A vascular work-up including transcutaneous oxygen measurement [40], the ankle-brachial index, and the absolute toe systolic pressure [41] is appropriate. In the acute setting, where lower-extremity ischemia is strongly suspected, arteriography or MR imaging should be performed to confirm or rule out ischemia.
Ischemia of the upper limbs Acute ischemia in the upper extremity can be caused by other etiologies than arterial embolization from central arteries, heart, and aorta. An accurate diagnosis can sometimes be difficult in the presence of an underlying vascular disease. The most noticeable signs and symptoms are changes in color and sensation in the hand caused by Raynauds phenomenon. This can be seen in as much as a fifth of the
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population, and is four times more likely to occur in women. The disorder affects the smallest blood vessels in the hand with exposure to stress, vibration, or cold triggering arterial-arteriole contraction and vasospasm. This contraction results in blanching or bluing of the skin of the digits from diminished blood supply. There is marked rubor and paresthesias as hyperemia results on rewarming. Raynauds phenomenon is a manifestation of many diseases, most often collagen vascular processes, whereas primary or idiopathic Raynauds phenomenon is called Raynauds disease. The etiology of these changes is thought to be multifactorial and variable. Noninvasive vascular testing is occasionally used to evaluate patients with Raynauds disease and includes digital pulse volume recordings and measurement of digital systolic blood pressure and digital blood flow. Stress testing for cold sensitivity should be considered. Past medical history is most important diagnosing the etiology of Raynauds. Laboratory testing for antinuclear antibody, cryoglobulins, rheumatoid factor, sedimentation rate, and others may suggest a specific secondary cause of Raynauds phenomenon. Atherosclerosis, thromboembolism, acrocyanosis, reflex sympathetic dystrophy, thromboangiitis obliterans, and hypothenar hammer syndrome are in the differential diagnosis. These entities may all result in macrothrombus or microthrombus in the circulatory system and can all present acutely. Noninvasive diagnosis is limited in the acute, limb-threatening situation. Arteriography and possibly MR angiography are more useful for confirming the diagnosis on morphologic basis. Doppler ultrasound is useful when it confirms patency of the large conduit arteries to the hand. It can also be used to confirm the presence of arterial aneurysms as are seen in cases of hypothenar hammer syndrome.
[5]
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[1] Bynoe RP, Miles WS, Bell RM, Greenwold DR, Sessions G, Haynes JL, et al. Noninvasive diagnosis of vascular trauma by duplex ultrasonography. J Vasc Surg 1991;14:346 52. [2] Panetta TF, Sales CM, Marin ML, Schwartz ML, Jones AM, Berdejo GL, et al. Natural history, duplex characteristics, and histopathologic correlation of arterial injuries in a canine model. J Vasc Surg 1992;16:867 74; discussion 874 6. [3] Johansen K, Lynch K, Paun M, Copass M. Non-invasive vascular tests reliably exclude occult arterial trauma in injured extremities. J Trauma 1991;31:515 9; discussion 519 22. [4] Lynch K, Johansen K. Can Doppler pressure measure[16]
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ment replace exclusion arteriography in the diagnosis of occult extremity arterial trauma? Ann Surg 1991; 214:737 41. Katzenschlager R, Ugurluoglu A, Ahmadi A, Hulsmann M, Koppensteiner R, Larch E, et al. Incidence of pseudoaneurysm after diagnostic and therapeutic angiography. Radiology 1995;195:463 6. Rapoport S, Sniderman KW, Morse SS, Proto MH, Ross GR. Pseudoaneurysm: a complication of faulty technique in femoral arterial puncture. Radiology 1985; 154:529 30. Forster T, Kardos A, Kiss E, Varga A, Gaal T, Csanady M. Diagnosis of femoral pseudoaneurysm and factors contributing to its incidence after heart catheterization. Orv Hetil 1991;132:2897 9. Toursarkissian B, Allen BT, Petrinec D, Thompson RW, Rubin BG, Reilly JM, et al. Spontaneous closure of selected iatrogenic pseudoaneurysms and arteriovenous fistulae. J Vasc Surg 1997;25:803 8; discussion 808 9. Perry MO. Complications of missed arterial injuries. J Vasc Surg 1993;17:399 407. Morgan R, Belli A. Current treatment methods for postcatheterization pseudoaneurysms. J Vasc Interv Radiol 2003;14:697 710. Paulson EK, Sheafor DH, Kliewer MA, Nelson RC, Eisenberg LB, Sebastian MW, et al. Treatment of iatrogenic femoral arterial pseudoaneurysms: comparison of US-guided thrombin injection with compression repair. Radiology 2000;215:403 8. Taylor BS, Rhee RY, Muluk S, Trachtenberg J, Walters D, Steed DL, et al. Thrombin injection versus compression of femoral artery pseudoaneurysms. J Vasc Surg 1999;30:1052 9. Trertola SO, Savader SJ, Prescott CA, Osterman Jr FA. US-guided pseudoaneurysm repair with a compression device. Radiology 1993;189:285 6. Kang SS, Labropolous N, Mansour MA, Michelini M, Filliung D, Baubly MP, et al. Expanded indications for ultrasound-guided thrombin injection of pseudoaneurysms. J Vasc Surg 2000;31:289 98. Partap VA, Cassoff J, Glikstein R. US-guided percutaneous thrombin injection: a new method of repair of superficial temporal artery pseudoaneurysm. J Vasc Interv Radiol 2000;11:461 3. Sheiman RG, Brophy DP, Perry LJ, Akbari C. Thrombin injection for the repair of brachial artery pseudoaneurysms. AJR Am J Roentgenol 1999;173:1029 30. Kang SS, Labropolous N, Mansour MA, Baker WH. Percutaneous ultrasound guided thrombin injection: a new method for treating postcatheterization femoral pseudoaneurysms [comment]. J Vasc Surg 1998; 27:1032 8. Liau CS, Ho FM, Chen MF, Lee YT. Treatment of iatrogenic femoral artery pseudoaneurysm with percutaneous thrombin injection [comment]. J Vasc Surg 1997;26:18 23. Brophy DP, Sheiman RG, Amatulle P, Akbari CM. Iatrogenic femoral pseudoaneurysms: thrombin injec-
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B.D. Davison, J.F. Polak / Radiol Clin N Am 42 (2004) 383396 tion after failed US-guided compression. Radiology 2000;214:278 82. Sheldon PJ, Oglevie SB, Kaplan LA. Prolonged generalized urticarial reaction after percutaneous thrombin injection for treatment of a femoral artery pseudoaneurysm. J Vasc Interv Radiol 2000;11:759 61. Kubaska S, Greenberg R, Clair D, Barber G, Srivastava S, Green R, et al. Internal carotid artery pseudoaneurysms: treatment with the wall graft enoprosthesis. J Endovasc Ther 2003;10:182 9. Hood DB, Mattos MA, Douglas MG, Barkmeier LD, Hodgson KJ, Ramsey DE, et al. Determinants of success of color-flow duplex-guided compression repair of femoral pseudoaneurysms. Surgery 1996;120:585 8; discussion 588 90. Sharp KW, Spees EK, Selby LR, Zachary JB, Ernst CB. Diagnosis and management of retroperitoneal hematomas after femoral vein cannulation for hemodialysis. Surgery 1984;95(1):90 5. Bianchi S, Martinoli C, Abdelwahab IF, Derchi LE, Damiani S. Sonographic evaluation of tears of the gastrocnemius medial head (tennis leg). J Ultrasound Med 1998;17:157 62. Tomlinson MA, Beese R, Banwell M, Loosemore T, Buckenham TM, Dormandy JA. Sequential retroperitoneal venous hemorrhage and embolism of an angio-seal puncture closure device complicating iliac artery angioplasty. J Endovasc Surg 1999;6:264 9. Fukuda T, Sakamoto I, Kohzaki S, Uetani M, Mori M, Fujimoto T, et al. Spontaneous rectus sheath hematomas: clinical and radiological features. Abdom Imaging 1996;21:58 61. Elesber AA, Kent PD, Jennings CA. Compressive neuropathy of the brachial plexus and long thoracic nerve: a rare complication of heparin anticoagulation. Chest 2001;120:309 11. Klein SR, Bongard FS, White RA. Neurovascular injuries of the thoracic outlet and axilla. Am J Surg 1988; 156:115 8. Abreo G, Lenihan DJ, Nguyen P, Runge MS. Highoutput heart failure resulting from a remote traumatic aorto-caval fistula: diagnosis by echocardiography. Clin Cardiol 2000;23:304 6. [30] Cwikiel W, Midia M, Williams D. Non-traumatic vascular emergencies: imaging and intervention in acute arterial conditions. Eur Radiol 2002;12:2619 26. [31] Knudson MM, Lewis FR, Atkinson K, Neuhaus A. The role of duplex ultrasound arterial imaging in patients with penetrating extremity trauma. Arch Surg 1993;128:1033 7; discussion 1037 8. [32] Pellerito JS. Current approach to peripheral arterial sonography. Radiol Clin North Am 2001;39:553 67. [33] Patel S, Ilsen PF. Acquired Horners syndrome: clinical review. Optometry 2003;74:245 56. [34] Aanonsen NO, Kerty E, Nyberg-Hansen R, Nakstad P. Spontaneous dissection of the internal carotid artery. Tidsskr Nor Laegeforen 1991;111:330 2. [35] Anzola GP, Gualandi GF, Orlandini A, Scipione V. Lower cranial nerve palsy produced by internal carotid artery dilatation: report of two cases. Ital J Neurol Sci 1987;8:375 9. [36] North American Symptomatic Carotid Endarterectomy Trial Collaborators. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. N Engl J Med 1991;325:445 53. [37] Barnett HJ, Taylor DW, Eliasziw M, Fox AJ, Ferguson GG, Haynes RB, et al. Benefit of carotid endarterectomy in patients with symptomatic moderate or severe stenosis. North American Symptomatic Carotid Endarterectomy Trial Collaborators. N Engl J Med 1998; 339:1415 25. [38] Kannel WB, McGee DL. Diabetes and glucose tolerance as risk factors for cardiovascular disease: the Framingham study. Diabetes Care 1979;2:120 6. [39] LoGerfo FW, Coffman JD. Current concepts: vascular and microvascular disease of the foot in diabetes. Implications for foot care. N Engl J Med 1984;311: 1615 9. [40] Bacharach JM, Rooke TW, Osmundson PJ, Gloviczki P. Predictive value of transcutaneous oxygen pressure and amputation success by use of supine and elevation measurements. J Vasc Surg 1992;15:558 63. [41] Apelqvist J, Castenfors J, Larsson J, Stenstrom A, Agardh CD. Prognostic value of systolic ankle and toe blood pressure levels in outcome of diabetic foot ulcer. Diabetes Care 1989;12:373 8.
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Emergency Doppler evaluation of the liver and kidneys

Michelle M. McNamara, MD*, Mark E. Lockhart, MD, MPH, Michelle L. Robbin, MD
Abdominal Imaging Section, Department of Radiology, University of Alabama at Birmingham, 619 19th Street South, JTN 353, Birmingham, AL 35249-6830, USA
Vascular complications of hepatic and renal transplants are potentially catastrophic. They may result in loss of the allograft with significant morbidity for the recipient. Doppler evaluation of renal and hepatic transplants may provide data that are essential for preserving allograft function. Timely recognition of these problems improves the likelihood that intervention to correct vascular abnormalities will be successful. Emergent applications of Doppler in the native liver and kidneys are more limited. Sonographic evaluation of patients with cirrhosis, with or without a transjugular intrahepatic portosystemic shunt (TIPS), may elucidate a cause for acute clinical decompensation. Ultrasound is a readily available means of assessing patients with acute renal dysfunction. Importantly, ultrasound can be used to determine if active hemorrhage is present at liver or renal biopsy sites in the postbiopsy patient with a decreasing hematocrit level.
Hepatic ultrasound Anatomy and appearance The liver is divided into lobes and segments by three fissures. The main lobar fissure divides the right and left lobes. The boundaries of this fissure are the middle hepatic vein superiorly, the gallbladder neck in the midportion, and the inferior vena cava inferi-
* Corresponding author. E-mail address: mmcnamara@uabmc.edu (M.M. McNamara).
orly. The left intersegmental fissure separates the left lobe into the lateral and medial segments. The anatomic boundaries of this fissure are the left hepatic vein superiorly and the falciform ligament inferiorly. The ascending portion of the left portal vein is at the midportion of this fissure. The right intersegmental fissure separates the right lobe into anterior and posterior segments. The right hepatic vein defines this fissure superiorly. The main portal vein divides into right and left branches in the liver hilum. The left portal vein courses horizontally (horizontal segment) and then changes to a more vertical orientation in the left intersegmental fissure, termed the ascending portion, or umbilical segment of the left portal vein. The right portal vein divides into anterior and posterior divisions. The anterior and posterior divisions of the right portal vein course centrally in the anterior and posterior right hepatic lobe segments, respectively, and are equidistant from the middle and right hepatic veins. The hepatic veins, surrounded by liver parenchyma, drain into the inferior vena cava. They are in open communication with the right heart. Cardiac physiology and hepatic parenchymal compliance influence the hepatic vein waveform. The normal hepatic vein waveform is phasic, similar to the inferior vena cava (Fig. 1A). Two large antegrade waves reflect atrial diastole and ventricular systole. A small reversal in flow is seen between the larger antegrade waves at atrial systole. The main portal vein provides 70% to 80% of hepatic blood flow. Normal portal venous waveforms reflect minimal undulations from respiratory and cardiac activity, because they are normally isolated from the central venous system (Fig. 1B). The hepatic
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Fig. 1. Spectral Doppler of normal hepatic waveforms. (A) Right hepatic vein shows triphasic flow. (B) Portal vein waveform demonstrates monophasic flow. (C) Hepatic artery with sharp systolic upstroke.
artery, which provides 20% to 30% of hepatic blood flow, originates from the celiac trunk. The common hepatic artery (Fig. 1C) becomes the proper hepatic artery after it gives rise to the gastroduodenal artery. The proper hepatic artery bifurcates into the right and left hepatic arteries. Variations in hepatic anatomy are common, however, and may not be sonographically apparent [1].
Transplant liver Clinical Hepatic artery thrombosis is the most common vascular complication of orthotopic liver transplant, and it occurs in 3% to 10% of all recipients [2,3]. The incidence is at the higher end of the spectrum in pediatric recipients, and it occurs in up to 12% of transplant recipients [3,4]. If this complication occurs, it is most often seen in the first 2 weeks after
transplant [4]. Clinical manifestations include biliary dysfunction and sepsis [4]. Hepatic artery anastomotic stenosis usually precedes thrombosis [5]. Hepatic artery stenosis and thrombosis can be detected with Doppler ultrasound. Early arterial occlusion is associated with liver failure and may require retransplantation. Alternatively, if significant hepatic artery stenosis can be detected before life-threatening ischemia occurs, angioplasty or surgical revascularization may salvage the liver transplant [4 6]. Doppler spectral analysis is an effective tool for evaluating a patient for hepatic artery thrombosis or stenosis, and it has sensitivity and specificity rates of 97% and 64%, respectively [6]. Other vascular complications include portal vein, hepatic vein, and inferior vena cava (IVC) stenosis and thrombosis, and pseudoaneurysm formation at the arterial anastomosis [7]. The narrowing that results from nonocclusive thrombus cannot always be differentiated sonographically from stenosis secondary to other causes [6]. These less frequent complications
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Sonographic criteria Hepatic artery stenosis Hepatic artery stenosis is suspected if RIs are less than 0.5 [5] or if there is a focal peak systolic velocity (PSV) more than 200 to 300 cm/second [2]. Other indicators of significant hepatic arterial narrowing include a systolic acceleration time (end diastole to first systolic peak) more than 0.08 seconds [5]. In the first 48 hours after transplant, RIs may be low or high (Fig. 2) [10]. Essentially, the presence of an arterial signal in the immediate postoperative period is satisfactory, as long as a focal gradient is not found [6]. In the authors experience, a PSV ratio at the anastomosis of more than approximately 3:1 correlates with a hemodynamically significant stenosis. A low resistance arterial waveform may be seen downstream from the stenosis (Fig. 3). Portal vein thrombus The portal vein is evaluated for presence or absence of flow, nonocclusive filling defects, and flow direction. In the authors experience, a PSV gradient equal to or more than approximately 3:1 at the anastomosis is consistent with a hemodynamically significant stenosis, a finding rarely encountered.
Fig. 1 (continued).
Hepatic veins and inferior vena cava Flow direction and pulsatility are evaluated in the hepatic veins with spectral Doppler. Monophasic flow in the hepatic veins after transplant is a rela-
may develop independently or concomitantly. Prompt diagnosis and treatment of vascular complications are crucial to graft and patient survival [8]. Sonographic technique For most adult patients, a 3.5-MHz or lower frequency transducer is preferred, especially in the immediate posttransplant period, when available sonographic imaging windows may be limited. Lower frequency transducers facilitate adequate tissue penetration without compromising resolution for Doppler evaluation. Optimum Doppler angle is less than 60. Low wall filter settings increase sensitivity for detection of low flow [9]. Direct gray scale inspection of the vessels is performed, as is color and spectral Doppler analysis of the main, right, and left hepatic arteries, the main, right, and left hepatic veins, the main, right, and left portal veins, IVC, and splenic vein. Patency, flow direction, velocities, resistive indices (RIs), and waveforms are assessed. Anastomotic sites are interrogated for narrowing [7].
Fig. 2. Immediate post liver transplant hepatic artery Doppler. Color and spectral Doppler documents antegrade flow with RI of 1. In the perioperative period, a high resistance waveform does not necessarily indicate a pathologic condition.
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Pathologic mechanisms include cell death, fibrosis, and regeneration, which result in the formation of nodules. In the micronodular type of cirrhosis, nodules measure less than 1 cm, whereas in the macronodular type, nodules of varying size may measure up to 5 cm. Alcoholism and viral hepatitis are common causes. Other causes include biliary cirrhosis, sclerosing cholangitis, Wilsons disease, and hemochromatosis. Cirrhosis is a common cause of intrahepatic portal hypertension, with resultant ascites, portosystemic collateral formation, and gastrointestinal bleeding. Doppler ultrasound is a useful noninvasive means of assessing the status of a TIPS and portal vein flow in patients with cirrhosis who present with acute decompensation [11]. Depending on criteria selected to define abnormal, Doppler ultrasound sensitivity rate for detection of TIPS malfunction ranges from 92% to 94% [12], with a specificity rate of 72% to 100% [12].
Fig. 3. Hepatic artery stenosis in a transplant liver. Color and spectral Doppler of the right hepatic artery (Doppler gate) shows abnormal waveform with RI of 0.37. RIs in the left and main hepatic arteries (not shown) were 0.32 and 0.44, respectively. Angiography documented 80% stenosis at the hepatic artery surgical anastomosis.
Sonographic technique Comprehensive evaluation of the hepatic vessels includes acquiring angle-corrected color and spectral Doppler to determine flow direction, pulsatility, PSV, and patency. As with transplant liver Doppler evaluation, a lower frequency transducer may facilitate penetration [13]. Low pulse repetition frequency settings increase color Doppler sensitivity but may result in aliasing, which can mimic flow reversal [11,14]. Direction of flow should be confirmed by modifying pulse repetition settings or with spectral Doppler [14]. High wall filter settings should be avoided because they may decrease the ability to detect low velocity flow [2]. The main, right, and left portal veins, middle left and right hepatic veins, hepatic artery, splenic vein, and IVC are evaluated with gray scale followed by assessment with color and spectral Doppler. Varices are sought in the coronary, periumbilical, peripancreatic, and splenic regions, typically the most fruitful locations for sonographic variceal detection. Vessels are sampled proximal to (upstream) and at any abnormality. Parenchymal abnormalities are imaged in transverse and longitudinal planes. Doppler interrogation of any thrombus seen is performed to aid in determining if it is bland or tumor thrombus, particularly in the presence of a liver mass. Tumor thrombus may demonstrate flow on color or spectral Doppler. Sonographic evaluation of TIPS is complex. Velocities in as much of the shunt as is acoustically visible should be evaluated. A complete assessment
tively common finding. Although it is not always clinically significant, monophasic flow in the hepatic veins can be a result of outflow stenosis or obstruction at the cranial IVC anastomosis. In the authors experience, a distended IVC with a peak systolic ratio of more than approximately 3:1 can be seen in cases with IVC anastomotic stenosis (Fig. 4A C). An IVC venogram with measurement of pressures across the stenosis can be a useful confirmation of clinically significant abnormality. Hepatic vein thrombosis is uncommonly seen on Doppler (Fig. 5). Pseudoaneurysm Pseudoaneurysms appear as a simple or complex hypoechoic lesion on grayscale ultrasound. Unless a pseudoaneurysm is completely thrombosed, typical to-and-fro color and spectral Doppler findings should be elicited (Fig. 6) [9].
Cirrhotic native liver Clinical Cirrhosis is a diffuse process characterized by fibrosis and alteration of normal liver architecture.
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Fig. 4. IVC stenosis after liver transplant. (A) Narrowing is visually apparent on gray scale images (arrows). (B) Spectral Doppler demonstrates PSV of 24 cm/second 2 cm caudal to the infrahepatic anastomosis. (C) PSV at the anastomosis is 115 cm/second, which results in a PSV ratio of 115/24, or 4.8. IVC venogram (not shown) showed stenosis without significant pressure gradient at this level.
may require changes in patient position during the examinationincluding the left lateral decubitus and prone positionsto get the best angle and shunt visualization. Main portal vein velocity and flow direction should be assessed. Values for the hepatic venous end within the stent, mid-shunt and portal venous end within the stent, and highest and lowest intrashunt velocities (if at a different location) are recorded [2,13,15]. Flow direction and PSV in the intrahepatic right and left portal veins and in the right, middle, and left hepatic veins are also evaluated [2]. Stent diameter is measured.
Sonographic criteria Portal vein thrombosis The presence of occlusive low-level echoes, or a nonocclusive filling defect, may be observed at gray scale imaging. Color Doppler may be useful in finding hypoechoic thrombus not apparent on gray scale imaging (Fig. 7). Normal portal vein caliber ranges from 9 to 13 mm [16]. A small vessel in the region of the portal vein is suspicious for prior portal vein thrombus, with subsequent vein sclerosis or collateral formation. Cavernous transformation,
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Fig. 5. Hepatic vein thrombosis after liver transplant. Color Doppler shows a hypoechoic linear structure (arrows) in the region of the right hepatic vein without Doppler flow.
Fig. 7. Cirrhotic liver with nonocclusive portal vein thrombus. Color Doppler demonstrates linear hypoechoic thrombus (asterisks) within the portal vein (arrows). Spectral Doppler (not shown) also documented vessel patency.
which represents multiple small periportal venous collaterals, suggests chronic portal vein thrombosis. Portal hypertension Portal venous hypertension may manifest sonographically as slow antegrade, stagnant, or hepatofugal flow in the main portal vein, intrahepatic branches only, or extrahepatic collaterals only [11]. The portal vein may be enlarged and measure more than 1.3 cm, a sensitive but not specific sign of portal venous
hypertension [17]. Bi-directional flow may precede reversal of flow [11]. Although cirrhosis is the most common cause of hepatofugal flow, there are exceptions. Large portosystemic collaterals may persist after transplantation and result in reversed flow in the absence of recurrent portal hypertension. Liver function and portal vein patency may be compromised as a result. Hepatofugal flow in one or more intrahepatic portal veins may occur with a focal arterioportal shunt from a biopsy or tumor and is not specific for portal hypertension [11]. Transjugular intrahepatic portosystemic shunt malfunction TIPS is an effective and widely used means of treating symptomatic portal hypertension. Timely identification of TIPS malfunction increases the probability of successful shunt revision with a consequent decrease in recurrence of complications of portal hypertension. Sensitivity and specificity rates for detection of TIPS dysfunction range from 92% to 94% and 72% to 100%, respectively, depending on the number of abnormal criteria present [12,18]. Clinical manifestations of TIPS dysfunction may include ascites recurrence, variceal bleeding, and splenomegaly. A wide range of velocities is seen in patent shunts [13,15], which necessitates determination of baseline velocities in individual patients for long-term followup [13]. Integration of data from several parameters is needed to suggest TIPS malfunction. If multiple abnormalities are identified, the likelihood of TIPS dysfunction increases [12,18,19]. Stenosis most commonly involves the draining hepatic vein.
Fig. 6. A 6.2-cm hepatic artery pseudoaneurysm at the arterial anastomosis. Liver transplant was performed at an outside institution. Color and spectral Doppler show typical biphasic to and fro pattern.
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Direct signs of TIPS malfunction include lack of flow with color and spectral Doppler, consistent with shunt occlusion. Stenosis is suggested by a velocity within the shunt that is less than 90 cm/second or exceeds 189 cm/second. Velocity gradient across the shunt also correlates with stenosis. Similar sensitivity and specificity for detection of stenosis has been shown when either 50 cm/second or 100 cm/second is selected as the upper limit of normal for velocity
gradient [12,20]. Normal main portal vein velocity when a TIPS is present is approximately 43 cm/ second. Velocities in the main portal vein less than 30 to 33 cm/second correlate with TIPS malfunction (Fig. 8A C) [12,18,20]. Comparison with prior studies is helpful for evaluating for TIPS malfunction. Decrease in main portal vein velocity of 20% from baseline or peak shunt velocity decrease of more than 40 cm/second
Fig. 8. Stenotic TIPS. (A) Main portal vein velocity is abnormally low, 28 cm/second. (B) Spectral Doppler shows a velocity gradient within the TIPS. Velocity at the hepatic vein side is 135 cm/second. Velocities mid-shunt and at the portal vein side (not shown) were 60 and 50 cm/second, respectively. (C) The stenosis is located in the draining hepatic vein, where the velocity is 206 cm/second.
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Table 1 Indicators of transjugular intrahepatic portosystemic shunt stenosis [12] Criteria Main portal vein velocity Velocity within the TIPS Diagnostic threshold Less than 30 cm/sec Decrease of 20% from baseline <90 or >189 cm/sec Decrease of >40 cm/sec or increase of >60 cm/sec from baseline More than 100 cm/sec Sensitivity/specificity Sensitivity Sensitivity Sensitivity Sensitivity 82%, 78%, 84%, 71%, specificity specificity specificity specificity 77% 75% 70% 88%
Gradient across the TIPS
Sensitivity 56%, specificity 78%
or increase more than 60 cm/second correlates with stenosis [12]. A change from retrograde to antegrade flow in a portal vein not drained by the TIPS and reappearance of varices or patent periumbilical collateral strongly suggests shunt malfunction [13] but may be a relatively late sign (Table 1). Main portal vein velocity after TIPS placement may be influenced by the size of the stent. Higher flow velocities may be observed with 12-mm versus 10-mm shunts. A higher main portal vein velocity threshold for shunt malfunction may be necessary; however, significant differences in maximum and minimum intrashunt velocities are not likely [19]. Portal vein aneurysmal ectasia Aneurysmal ectasia of the portal vein is uncommonly seen and may be congenital or secondary to portal venous hypertension or vessel wall weakening related to inflammatory processes, such as acute pancreatitis. There is considerable variation in the size of the portal vein. The measurement at which dilatation is called aneurysmal is somewhat arbitrary. Aneurysmal ectasia is present if there is significant focal portal vein diameter enlargement compared with the rest of the vessel, especially if a saccular or fusiform appearance is identified [21,22]. It generally appears as a cystic structure. Turbulent or to and fro flow is identified with Doppler interrogation [23], unless the vein is thrombosed.
aneurysm are rare, usually sequelae to inflammatory processes such as pancreatitis or septicemia. Portal vein thrombus also may be seen with hypercoagulable states and malignancy. Sonographic technique Comprehensive sonographic evaluation is similar to evaluation of the cirrhotic native liver. All anechoic structures are evaluated for flow. If the evaluation is for a postbiopsy complication, evidence of active hemorrhage also is sought. Sonographic criteria Postbiopsy complications Active hemorrhage may be observed as a jet on color Doppler (Fig. 9) and demonstrate an arterial spectral waveform. Additional findings consistent with hemorrhage include the presence of hematoma or fluid adjacent to the liver or in the pelvis. A non-
Noncirrhotic native liver Clinical Applications of urgent Doppler ultrasound in patients without cirrhosis include evaluation for post liver biopsy complications, sequela of inflammatory processes, and determination of the cause of acutely elevated liver function tests. An acute drop in hematocrit or unusual pain after biopsy may warrant sonographic evaluation for active hemorrhage or pseudoaneurysm. Portal vein thrombus and pseudo-
Fig. 9. Postbiopsy hemorrhage. Color Doppler of native liver after biopsy shows active hemorrhage demonstrated by a jet from the biopsy tract to the liver surface (arrow).
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thrombosed pseudoaneurysm demonstrates the typical to and fro color and spectral pattern. Portal vein thrombosis Evaluation is the same as for a cirrhotic liver. Portal vein thrombosis is rare in the native noncirrhotic liver and may not be detected on a routine abdominal ultrasound. The authors have found that a brief look at the main portal vein with gray scale and color Doppler on routine abdominal ultrasound examination occasionally has been useful in detecting clinically unsuspected portal vein thrombus.
diastolic velocity. Flow should be laminar without aliasing. In the normal kidney, diastolic flow should be present in the artery, and the upper limit of RI has been described as 0.7 in adults [26,27]. Flow in the main renal vein should have normal mild respiratory phasicity.
Transplant kidney Clinical Ultrasound is the best initial imaging modality in the renal transplant patient with elevated creatinine level. Using ultrasound as the initial screening test avoids the use of radiation, increased cost, and the potential nephrotoxic effects of iodinated contrast associated with CT. Common allograft abnormalities include hydronephrosis with ureteral obstruction, renovascular disease, acute tubular necrosis, and rejection. Peritransplant seromas or lymphoceles may cause hydronephrosis or compress the renal vessels. Rarely, a mass from posttransplant lymphoproliferative disorder may cause renal artery stenosis or hydronephrosis [28]. Many of these etiologies overlap in their clinical symptomatology, and the underlying problem must be diagnosed accurately to guide therapy. Doppler ultrasound can document patency of a transplant renal artery and vein and may aid in the detection of renal artery stenosis or an arteriovenous fistula. Decreased or absent perfusion in the postoperative allograft is rare but requires immediate intervention [29]. Gray scale ultrasound is sensitive and specific for hydronephrosis, which is caused by obstruction in up to 8% of transplanted kidneys [30]. Ultrasound may evaluate delayed function of the kidney or a sudden functional decline after good initial results. Sonographic technique Sonographic characteristics of the renal transplant are similar to native kidneys with a few significant differences. Renal transplants are most commonly placed within the right or left pelvis. The superficial location may allow easier visualization of the transplant vessels and anastomoses compared with the vessels of the native kidneys. A higher frequency transducer3.5 mHz or higher (usually a curved transducer, which allows good visualization of the near and far portions of the kidney)is used. The entire course of the renal artery and vein should be
Renal ultrasound Anatomy and appearance The kidney has several distinct anatomic features that may be differentiated by ultrasound. The renal cortex and medullary pyramids are similar in echotexture in the normal kidney. Each pyramid and surrounding cortex converges into a renal papilla and collecting system infundibulum. In echogenic kidneys, the pyramids of the renal medullary region are hypoechoic to the renal cortex. Each of these structures may be distinguished easily from the echogenic fat of the central sinus. The anechoic renal calyces course into the renal pelvis and proximal ureter, structures that may be visualized if distended with urine. Normal cortical thickness averages 10 mm, but differentiation of medulla and cortex may be difficult. Instead, the combined thickness of the capsule to the renal sinus may be better depicted and normally measures approximately 15 to 16 mm [24]. The length of kidneys varies with patient height, but their median length is 11 cm; most kidneys measure 9.8 to 12.3 cm long and are symmetric in length [24]. A single renal artery arises from each side of the abdominal aorta caudal to the superior mesenteric artery to supply each kidney. In up to 30% of kidneys, however, accessory renal arteries may be present [25]. Accessory arteries may arise near the main renal artery, distal aorta, or common iliac arteries. The main renal artery bifurcates or trifurcates into branches that supply the dorsal and ventral portions of the kidney. Segmental renal arteries course within the renal parenchyma near the pyramids. Multiple renal vein branches join to form the main renal veins, which drain directly into the inferior vena cava. The normal spectral waveform in the native renal artery is a rapid systolic upstroke with a small early systolic peak followed by smooth tapering to the end
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visualized, with special attention paid to the anastomoses, usually at the external iliac artery and vein. Rarely, a transplant may be placed in the midabdomen with anastomoses to visceral vessels. The kidney is often best visualized from an anterolateral approach with displacement of any overlying bowel loops with gentle graded compression by the ultrasound transducer. Adynamic ileus in the perioperative period may hinder the sonographic examination, however. Once the allograft is localized, the renal vessels can be traced to the areas of anastomosis. Anglecorrected flow evaluation should maintain an angle less than 60 from the sonographic beam. An initial scan with power or color Doppler to demonstrate areas of decreased flow is useful. Regional decreased flow may be the only suggestion of a segmental stenosis or infarction. Subsequently, a representative segmental renal artery waveform in the upper pole, midportion, and lower pole is evaluated with spectral Doppler, and an RI is calculated. The detection of an abnormal acceleration time or absence of the early systolic peak may suggest transplant renal artery stenosis [31]. Color Doppler is used to identify turbulent vessel flow by the depiction of aliasing. Spectral Doppler is obtained in the areas of aliasing to evaluate for potential stenosis. PSV measurements are obtained at and approximately 2 cm proximal to the area of aliasing or visual narrowing, which allows the calculation of a PSV ratio. The main renal artery anastomosis is specifically evaluated with color and spectral
Doppler at each examination, because it is a relatively common site of abnormality. If a stenosis at the renal artery anastomosis is suspected, a PSV is obtained in the proximal iliac artery approximately 2 cm from the anastomosis, which allows for the calculation of a renal artery anastomosis to proximal iliac artery PSV ratio. The main renal vein is also evaluated with color and spectral Doppler, which usually demonstrates a normal antegrade venous waveform.
Sonographic criteria Postbiopsy complications Interrogating the transplant kidney after instrumentation or biopsy is important to assess for complications that could result in loss of life or loss of the allograft. Color Doppler can detect active extravasation (Fig. 10A, B) of blood from the margin of the kidney at the point of biopsy. The biopsy tract is often visible, and active hemorrhage presents as a jet of color that projects from this region into the perinephric fat. Pseudoaneurysm is a documented complication of renal biopsy [32]. In a kidney with history of instrumentation, any anechoic structure should be evaluated with Doppler to exclude a vascular structure [33]. Flow that fills a cavity that does not conform to the renal vessels confirms a pseudoaneurysm. Spectral Doppler may detect the to and fro waveform that diagnoses pseudoaneurysm in other sites.
Fig. 10. Postrenal biopsy hemorrhage. (A) Color Doppler of kidney after biopsy shows jet of active extravasation through the capsule (arrow) into a perinephric hematoma. Renal parenchymal denoted by asterisk. (B) Spectral Doppler of the jet demonstrates arterial waveform.
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artery resistance downstream in the segmental arteries, from an inflow, or intrinsic transplant abnormality with high-resistance arterial waveforms. Transplant vascular compromise Severe vascular complications can result in rapid loss of the transplant allograft. In this setting, emergent Doppler may identify the cause of the dysfunction and allow intervention in a timely manner. In one series, emergent ultrasound and intervention in patients decreased loss of the organ from 4.7% to 1.05%. In that series, the most common cause of severe perfusional failure of the transplant was renal artery stenosis [29], which may occur in as many as 8% to 16% of renal transplant allografts [39,40]. In the authors experience, there is an increased incidence of transplant renal artery stenosis in living related donor allografts compared with cadaveric kidneys. This is likely because of different surgical techniques in the cadaveric renal transplant versus living related donor. In the cadaveric transplant, a patch of the aorta is taken around the main renal artery aorta takeoff. The anastomosis in the cadaveric transplant is actually a larger anastomosis than just that of the main renal artery, from the aortic patch to the iliac artery, with resultant decrease in technical complications. Taking an aortic patch would not be desirable in the living related transplant. The main renal artery anastomosis with the iliac artery is generally a much smaller diameter anastomosis, with increased potential for technical problems that cause stenosis. Critical vascular compromise of a transplant kidney may be demonstrated with abnormal color Doppler perfusion. In the setting of rapid allograft failure, reduced or absent flow in the kidney and main renal artery suggests renal artery thrombosis [29]. This is a rare occurrence but may have severe impact on the allograft. Occasionally, only segmental arteries are thrombosed. In these cases, segmental infarctions may be detected on color Doppler [41]. Power Doppler may increase confidence for detection of perfusional defects associated with areas of allograft infarction, however [42]. Renal artery stenosis also may cause allograft dysfunction. In transplant renal artery stenosis, high PSVs of more than 200 cm/second have been described at the site of a significant renal artery stenosis (Fig. 12A) [43]. The accuracy is improved if a PSV of more than 350 cm/second criterion is used in combination with acceleration time and evaluation for dampened intrarenal waveforms [31]. Measurement of a tardus-parvus waveform (slow systolic acceleration with low peak flow velocity) of poststenotic flow in the allograft also may suggest main renal artery stenosis
Fig. 11. Postbiopsy 0.6-cm arteriovenous fistula (cursors) in a transplant kidney. Spectral Doppler (not shown) demonstrated bidirectional flow in the renal parenchyma denoted by asterisks. Also, a needle track pseudoaneurysm is seen (arrows).
Arteriovenous fistula is a common complication of renal biopsy (Fig. 11), and it is detected on followup imaging in 10% to 15% of biopsies [34,35]. It is important to find a fistula if present, because it can cause a significant steal from normal parenchyma, which causes transplant dysfunction. A fistula may be suspected based on low resistance main renal artery flow in the absence of a vascularized collection. There may be aliasing of signal on color Doppler [35]. On color Doppler, tissue reverberation may cause color artifact in the renal parenchyma [35,36]. High volume of flow may be present on spectral Doppler in the renal artery and vein [37]. Close to the arteriovenous fistula (AVF), the draining vein typically has an arterialized waveform [35,38]. Intraoperative renal ultrasound Although intraoperatively the surgeon may note by visual inspection that kidney perfusion is failing, the cause of the abnormal perfusion may not be clear. The sonologist can be helpful to the surgeon during a difficult surgical procedure by documenting renal flow characteristics. Doppler ultrasound can document patency of the main renal artery and main renal vein. It can detect an arterial dissection and may be able to differentiate it from renal artery thrombosis. Intraoperative Doppler may assist the surgeon in differentiating an inflow problem with low renal
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Fig. 12. Renal artery stenosis in a transplant kidney. Spectral Doppler shows an elevated velocity of 469 cm/second at the arterial anastomosis (A) and parvus-tardus waveform (B) in an intrarenal segmental artery.
(Fig. 12B) [31,44]. Iliac artery stenosis proximal to the transplant artery may affect a renal transplant adversely in much the same way as renal artery stenosis [45,46]. Renal vein thrombosis is rare, but it may cause allograft loss if the diagnosis remains unrecognized. Diastolic reversal of flow (Fig. 13) or absent flow in the main renal artery has been documented in renal transplant allografts with renal vein thrombosis [43,47,48]. Both findings are nonspecific and may occur with severe rejection [49], acute tubular necrosis, or acute interstitial nephritis [47]. Recognition of the arterial waveform abnormality is useful to prompt directed main renal vein evaluation for thrombus, however. The normal main renal vein flow should be antegrade with minimal variability, unlike the rapid pulsatile waveforms of the renal artery.
Posttransplant allograft dysfunction In a functioning, normal renal transplant, an RI of 0.5 to 0.7 has been generally reported [29]. Elevation of the RI in a transplant has been described as an indicator of allograft dysfunction (Fig. 14A) [50 52], but it is not specific in determining the cause of the allograft failure [52,53]. Elevated RIs may be associated with hydronephrosis (Fig. 14B). More worrisome is a change in RIs over time without a morphologic cause, such as hydronephrosis [54]. Interval increases in RI are also nonspecific, however, and may be caused by acute rejection, chronic rejection, acute
Fig. 13. Spectral Doppler shows reversal of diastolic flow in the main renal artery. The renal vein was not definitely identified (not shown). At surgery, a large peritransplant hematoma was evacuated, which restored flow in the renal vein.
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Fig. 14. Elevated RIs in two separate renal allografts. Spectral Doppler demonstrates increased RIs in segmental arterial branches. (A) The RI of 0.91 was secondary to acute rejection 3 days after transplant, documented by Tc 99m MAG 3 study and clinical findings. (B) The cause of the RI of 1 was severe hydronephrosis.
tubular necrosis, or cyclosporine toxicity. The RI in a transplant kidney may be elevated in the perioperative period because of acute tubular necrosis [55].
Native kidney Clinical Sonography is commonly used in the evaluation of abnormal renal function or evidence of urinary pathology. In the emergency setting, ultrasound is often the first imaging test to evaluate acute renal failure, flank pain, hematuria, or a postbiopsy drop in hematocrit because it is rapid and inexpensive and does not use ionizing radiation or potentially nephrotoxic contrast agents. Ultrasound may help differentiate between various causes of renal dysfunction that may be clinically similar in physical examination and laboratory tests. For most chronic renal pathologic conditions, gray scale ultrasound is adequate to differentiate medical renal disease from hydronephrosis or renovascular
abnormality. Renal vascular abnormality and hydronephrosis must be discerned from medical renal disease, because the therapies differ. Renal artery stenosis may be suggested by hypertension and renal atrophy on gray scale images. Renal artery occlusion may occur secondary to embolus or thrombus and may affect the main renal artery or branches. Renal vein thrombosis is another cause of renal failure. Renal vein thrombosis may occur acutely and is usually secondary to an underlying abnormality of the kidney, abnormal hydration, or coagulation status. The cause may be suggested in the presence of the nonspecific finding of an enlarged kidney [56]. There are several situations in which the use of Doppler ultrasound is more controversial. Doppler ultrasound is not considered adequate for exclusion of acute renal trauma [57]. Although gray scale ultrasound may grade the severity of hydronephrosis caused by acute obstruction by a renal stone, Doppler assessment of RIs in this clinical setting is no longer generally performed. If hydronephrosis is detected and there is clinical concern for ureteral calculus, a noncontrast CT for urinary calculi is obtained.
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Sonographic technique Sonographic settings and imaging technique for evaluation of the kidneys must be optimized individually because the patient and scanning situation are often suboptimal in the emergent setting. Flow detection by color Doppler should be maximized without introducing too much color artifact in the adjacent tissues. The gain should be increased until artifact occurs and then slightly reduced below the level where artifacts are noted. Spectral Doppler should use a gate that overlies most of the vessel diameter and is angled with the direction of flow. If evaluating for renal artery stenosis, complete color and spectral Doppler of renal artery always should be attempted. Any areas of turbulent flow or aliasing on color Doppler should be evaluated closely with gray scale and spectral Doppler for stenosis. The arterial waveform of the aorta at the level of the renal arteries should be obtained if renal artery stenosis is suspected. If there is a focal site of injury, such as in a renal biopsy, the biopsy site should be investigated carefully with gray scale for adjacent hematoma and Doppler for active hemorrhage. In this setting, any intrarenal anechoic structure should be checked with Doppler for the possibility of pseudoaneurysm. Sonographic findings Postbiopsy complications Immediately after renal biopsy, color Doppler is useful for evaluating active bleeding from the site of biopsy. The authors generally wait approximately 2 minutes after the biopsy before looking for significant bleeding, however, because brief bleeding is common with the large 14- to 16-gauge biopsy needles used. Hemorrhage and urinoma are the most common complications after renal biopsy [32]. Active hemorrhage is detected as a fountain of color that originates from the edge of the renal parenchyma on color Doppler. The scale and filters must be adjusted to optimize for detection of flow. Typically there is no sonographic evidence of arteriovenous fistula in the immediate postprocedural setting. Arteriovenous fistulas and pseudoaneurysms from renal biopsies occasionally can be seen on subsequent ultrasound evaluations, however. Severe acute urinary obstruction Severe acute urinary obstruction may be associated with Doppler abnormalities. The RI may be elevated in a severely hydronephrotic kidney [58 60]. Comparison of RIs with the contralateral normal kidney also may be helpful [26]. The usefulness of
RI criteria is limited because of the lack of sensitivity of Doppler for partial obstruction or moderate hydronephrosis [61]. In pregnant patients with clinical concern for ureteral obstruction and additional concern about exposure to ionizing radiation, an RI more than 0.7 or more than the contralateral kidney may be accurate and useful for detecting obstruction [62]. Current clinical practice includes evaluating most patients with suspected renal colic with noncontrast CT rather than ultrasound.
Pyelonephritis Pyelonephritis is a common clinical diagnosis in the emergent setting that is often referred to a radiologist for imaging. The differentiation between pyelonephritis and cystitis may be difficult in a patient with leukocytes in the urine. Ultrasound may be requested to evaluate for renal abscess or perinephric abscess. Color and power Doppler have been documented to show focal peripheral areas of decreased perfusion in an infected kidney [63]. Although not approved in the United States for clinical use within the urinary system, microbubble contrast agents may demonstrate focal areas of infarction associated with pyelonephritis with good detail and may obviate the need for CT (Fig. 15) [64].
Fig. 15. Pyelonephritis in a native kidney. Interval delay transverse image using ultrasound contrast with agent detection imaging shows focal area of decreased perfusion (arrow) in the mid-kidney. Ps, psoas; SP, spleen.
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Renal vein thrombosis Renal vein thrombosis is associated with dehydration, hypercoagulability, renal disease, tumor, surgery, extension of existing venous thrombus, and trauma [65]. Color or power Doppler may detect absent renal vein flow or thrombus as a filling defect within the detected flow [66,67] or demonstrate absent or slow flow. It is important to realize that venous collaterals develop quickly after native renal vein thrombosis, in contradistinction to the renal transplant. It is important to evaluate the entire renal veinand not just the renal vein at the hilumif this diagnosis is a clinical consideration. Monophasic venous flow is also abnormal and may indicate collateral flow or incomplete thrombosis [65]. Absent diastolic flow may be noted in the native renal artery. Absent or reversed diastolic flow is neither sensitive nor specific for renal vein thrombosis in the native kidney, however [68]. Renal trauma Gray scale ultrasound may detect a renal laceration or contusion in the emergency setting; however, there is little use of color or spectral Doppler evaluation of the kidneys in the setting of acute abdominal trauma. The ability of ultrasound to visualize a renal
injury is low [57]. Although demonstration of active hemorrhage may direct a surgeon to the appropriate area of the body, absence of visualization does not exclude a significant renal injury. Patients with active extravasation of urine or blood are often treated with conservative management [69] or angiographically directed embolization. Renal artery stenosis Many sonographic criteria are reported for the evaluation of renal artery stenosis in the native kidneys with variable degrees of success [70]. The most widely accepted criteria are based on direct visualization of the main renal artery with elevated PSV of more than 180 to 200 cm/second [70 72]. Stenosis may be detected as a focal area of turbulence or an area aliasing on color Doppler, confirmed by spectral Doppler [67,73]. Other direct criteria include a ratio of the PSV within the renal artery divided by the PSV of the aorta of at least 3.5:1 (Fig. 16A, B) [74 76]. Several indirect criteria also have been suggested and are sometimes reported in conjunction with direct criteria to increase detection of renal artery stenosis. The loss of the normal early systolic peak was the most sensitive of the indirect criteria in one series
Fig. 16. Renal artery stenosis in a native kidney. (A) Spectral Doppler demonstrates normal aorta (Doppler gate) waveform with a PSV of 57 cm/second. (B) Elevated PSV of 610 cm/second is detected in the proximal main renal artery (Doppler gate), which resulted in a renal artery to aorta PSV ratio of 10.7.
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[77]. Other criteria include the tardus-parvus waveform in the segmental renal arteries [67,78]. Delayed acceleration time of the systolic upstroke has been useful in some studies [79]. A difference in the RI between the kidneys may suggest renal artery stenosis [80]. A low RI can be seen downstream from an area of focal narrowing in renal artery stenosis [81,82]. Poor detection of stenosis of accessory renal arteries has been a limitation of ultrasound. In one sonographic study of renal artery stenosis, nearly half of the false-negative results were caused by stenosis of an accessory renal artery [82]. A recent article suggested that significant stenosis isolated to an accessory renal artery occurs in only 1.5% of patients with clinically significant renal artery stenosis [83]. Another important consideration in the assessment of renal artery stenosis deals with the potential to correct hypertension by angioplasty or surgery. In patients with renal artery stenosis and RI more than 0.8, there may be little improvement in a patients hypertension, kidney survival, or renal function after repair of the focal stenosis [84]. Renal artery occlusion is less common than renal vein thrombosis, but it is also devastating to the kidney. No flow is documented in the renal artery if complete occlusion is present. Partial arterial thrombosis may be more difficult to detect, however, and careful insonation of the entirety of the renal artery is necessary. Segmental arterial occlusion is sonographically indistinguishable from decreased perfusion secondary to pyelonephritis, which presents as a focal area of decreased or absent flow on color or power Doppler.
References
[1] Martinez-Noguera A, Montserrat E, Torrubia S, Villalba J. Doppler in hepatic cirrhosis and chronic hepatitis. Semin Ultrasound CT MR 2002;23(1):19 36. [2] Withers CE, Wilson SR. The liver. In: Rumack CM, Wilson SR, Charboneau JW, editors. Diagnostic ultrasound. 2nd edition. St. Louis: Mosby Year Book; 1998. p. 87 154. [3] Cook GJR, Crofton ME. Hepatic artery thrombosis and infarction: evolution of the ultrasound appearances in liver transplant recipients. Br J Radiol 1997;70: 248 51. [4] Nishida S, Kato T, Levi D, et al. Effect of protocol Doppler ultrasonography and urgent revascularization on early hepatic artery thrombosis after pediatric liver transplantation. Arch Surg 2002;137:1279 83. [5] Rode A, Ducerf C, Adham M, et al. Influence of systematic echo Doppler arterial survey on hepatic artery thrombosis after liver transplantation in adults. Transpl Int 1998;11(Suppl 1):S292 5. [6] Dodd III GD, Memel DS, Zajko AB, Baron RL, Santaguida LA. Hepatic artery stenosis and thrombosis in transplant recipients: Doppler diagnosis with resistive index and systolic acceleration time. Radiology 1994; 192(3):657 61. [7] Hamper UM. Doppler sonography in the evaluation of liver transplants: advances in sonography. Presented at the SRU 12th Annual Meeting. San Francisco, October 26, 2002. [8] Kok T, Slooff MJH, Thijn CJP, et al. Routine Doppler ultrasound for the detection of clinically unsuspected vascular complications in the early postoperative phase after orthotopic liver transplantation. Transpl Int 1998; 11:272 6. [9] Grant EG, Schiller VL, Millener P, et al. Color Doppler imaging of the hepatic vasculature. AJR Am J Roentgenol 1992;159:943 50. [10] Garcia-Criado A, Gilabert R, Salmeron JM, et al. Significance of and contributing factors for a high resistive index on Doppler sonography of the hepatic artery immediately after surgery: prognostic implications for liver transplant recipients. AJR Am J Roentgenol 2003; 181:831 8. [11] Wachsberg RH, Bahramipour P, Sofocleous CT, Barone A. Hepatofugal flow in the portal venous system: pathophysiology, imaging findings, and diagnostic pitfalls. RadioGraphics 2002;22(1):123 60. [12] Kanterman RY, Darcy MD, Middleton WD, et al. Doppler sonography findings associated with transjugular intrahepatic portosystemic shunt malfunction. AJR Am J Roentgenol 1997;164:467 72. [13] Foshager MC, Ferral H, Finlay DE, Castaneda-Zuniga WR, Letourneau JG. Color Doppler sonography of transjugular intrahepatic portosystemic shunts (TIPS). AJR Am J Roentgenol 1994;163:105 11. [14] Ralls PW. Color Doppler sonography of the hepatic artery and portal venous system. AJR Am J Roentgenol 1990;155:517 25.
Summary Doppler ultrasound is useful in the emergent evaluation of the liver and kidney transplant patient. Arterial stenosis, pseudoaneurysm, and venous thrombosis are treatable causes of allograft failure that can be detected easily with color and spectral Doppler. Doppler has a limited but important role in the emergent evaluation of the native liver and kidneys, usually involving prior biopsy or instrumentation.
Acknowledgments The authors would like to thank Trish Thurman for her assistance in manuscript preparation and Anthony Zagar for photographic assistance.
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M.M. McNamara et al / Radiol Clin N Am 42 (2004) 397415 [63] Dacher JN, Pfister C, Monroc M, Eurin D, Dosseur PL. Power Doppler sonographic pattern of acute pyelonephritis in children: comparison with CT. AJR Am J Roentgenol 1996;166:1451 5. [64] Robbin ML, Lockhart ME, Barr RG. Renal imaging with US contrast: current status. Radiol Clin N Am 2003;41(5):963 78. [65] Mulligan SA, Koslin DB, Berland LL. Duplex evaluation of native renal vessels and renal allografts. Semin Ultrasound CT MR 1992;13(1):40 52. [66] Platt JF, Ellis JH, Rubin JM. Intrarenal arterial Doppler sonography in the detection of renal vein thrombosis of the native kidney. AJR Am J Roentgenol 1994;162: 1367 70. [67] Helenon O, el Rody F, Correas JM, et al. Color Doppler US of renovascular disease in native kidneys. RadioGraphics 1995;15(4):833 54. [68] Platt JF. Doppler ultrasound of the kidney. Semin Ultrasound CT MR 1997;18(1):22 32. [69] Husmann DA, Gilling PJ, Perry MO, Morris JS, Boone TB. Major renal lacerations with a devitalized fragment following blunt abdominal trauma: a comparison between nonoperative (expectant) versus surgical management. J Urol 1993;150:1774 7. [70] Stavros AT, Harshfield D. Renal Doppler, renal artery stenosis, and renovascular hypertension: direct and indirect duplex sonographic abnormalities in patients with renal artery stenosis. Ultrasound Q 1994;4: 217 63. [71] House MK, Dowling RJ, King P, Gibson RN. Using Doppler sonography to reveal renal artery stenosis: an evaluation of optimal imaging parameters. AJR Am J Roentgenol 1999;173:761 5. [72] Pellerito J.S. Renal artery stenosis: advances in sonography. Society of Radiologists in Ultrasound, 12th Annual Meeting and Postgraduate Educational Course, San Francisco, October 25 27, 2002. [73] Dubbins PA. Renal artery stenosis: duplex Doppler evaluation. Br J Radiol 1986;59:225 9. [74] Kohler TR, Zierler RE, Martin RL, et al. Noninvasive diagnosis of renal artery stenosis by ultrasonic duplex scanning. J Vasc Surg 1986;4(5):450 6. [75] Taylor DC, Kettler MD, Moneta GL, et al. Duplex ultrasound scanning in the diagnosis of renal artery stenosis: a prospective evaluation. J Vasc Surg 1988;7(2): 363 9. [76] Strandness Jr DE. Duplex scanning in diagnosis of renovascular hypertension. Surg Clin N Am 1990;70(1): 109 17. [77] Stavros T, Harshfield D. Renal Doppler, renal artery stenosis, and renovascular hypertension: direct and indirect duplex sonographic abnormalities in patients with renal artery stenosis. Ultrasound Q 1994;12(4): 217 63. [78] Downey DB. The retroperitoneum and great vessels. In: Rumack CM, Wilson SR, Charboneau JW, editors. Diagnostic ultrasound. 2nd edition. St. Louis: Mosby Year Book; 1998. p. 453 86. [79] Handa N, Fukunaga R, Uehara A, et al. Efficacy of
[46] Nghiem DD, Ercolani L, Corry RJ. Stenosis of the iliac artery: an unusual cause of hypertension in the renal transplant recipient. Transplant Proc 1983;15(4): 2161 3. [47] Kaveggia LP, Perella RR, Grant EG, Tessler FN, Rosenthal JT, Danovitch GM. Duplex Doppler sonography in renal allografts: the significance of reversed flow in diastole. AJR Am J Roentgenol 1990;155: 295 8. [48] Baxter GM, Morley P, Dall B. Acute renal vein thrombosis in renal allografts: new Doppler ultrasonic findings. Clin Radiol 1991;43:125 7. [49] Reuther G, Wanjura D, Bauer H. Acute renal vein thrombosis in renal allografts: detection with duplex Doppler US. Radiology 1989;170:557 8. [50] Rifkin MD, Needleman L, Pasto ME, et al. Evaluation of renal transplant rejection by duplex Doppler examination: value of the resistive index. AJR Am J Roentgenol 1987;148:759 62. [51] Rigsby CM, Taylor KJW, Weltin G, et al. Renal allografts in acute rejection: evaluation using duplex sonography. Radiology 1986;158:375 8. [52] Genkins SM, Sanfilippo FP, Carroll BA. Duplex Doppler sonography of renal transplants: lack of sensitivity and specificity in establishing pathologic diagnosis. AJR Am J Roentgenol 1989;152:535 9. [53] Perrella RR, Duerinckx AJ, Tessler FN, et al. Evaluation of renal transplant dysfunction by duplex Doppler sonography: a prospective study and review of the literature. Am J Kidney Dis 1990;15(6):544 50. [54] Hollenbeck M, Hilbert N, Meusel F, Grabensee B. Increasing sensitivity and specificity of Doppler sonographic detection of renal transplant rejection with serial investigation technique. Clin Invest 1994;72: 609 15. [55] Harris DCH, Antico V, Allen R, et al. Doppler assessment in renal transplantation. Transplant Proc 1989; 21(1):1895 6. [56] Braun B. Ultrasonic demonstration of renal vein thrombosis. Radiology 1981;138:157 8. [57] McGahan JP, Richards JR, Jones CD, Gerscovich EO. Use of ultrasonography in the patient with acute renal trauma. J Ultrasound Med 1999;18:207 13. [58] Platt JF, Rubin JM, Ellis JH. Acute renal obstruction: evaluation with intrarenal duplex Doppler and conventional US. Radiology 1993;186(3):685 8. [59] Rodgers PM, Bates JA, Irving HC. Intrarenal Doppler ultrasound studies in normal and acutely obstructed kidneys. Br J Radiol 1992;65(771):207 12. [60] Gottlieb RH, Luhmann IV K, Oates RP. Duplex ultrasound evaluation of normal native kidneys and native kidneys with urinary tract obstruction. J Ultrasound Med 1989;8:609 11. [61] Chen JH, Pu YS, Liu SP, Chiu TY. Renal hemodynamics in patients with obstructive uropathy evaluated by duplex Doppler sonography. J Urol 1993;150:18 21. [62] Shokeir AA, Mahran MR, Abdulmaaboud M. Renal colic in pregnant women: role of renal resistive index. Urology 2000;55(3):344 7.
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Radiol Clin N Am 42 (2004) 417 425
Emergency ultrasound in trauma patients

John P. McGahan, MDa,*, John Richards, MDb, Maria Luisa C. Fogata, MDa
a
Division of Diagnostic Radiology, University of California, Davis, School of Medicine, 4860 Y Street, Suite 3100, Sacramento, CA 95817, USA b Division of Emergency Medicine, University of California, Davis, School of Medicine, 2315 Stockton Boulevard, PSSB 2100, Sacramento, CA 95817, USA
Although ultrasound (US) was first described in the detection of blunt traumatic splenic injuries more than 30 years ago [1], it was never widely advocated until approximately 10 years ago [2 4]. There are probably two reasons for the initial limited use of sonography in blunt traumatized patients. The first is that the use of CT evolved at approximately the same time and was shown to be highly sensitive for evaluation of blunt abdominal trauma [5]. CT not only detected free fluid but also directly demonstrated the organ injury. Sonography also was used initially to detect specific organ injury rather than the free fluid associated with the injury. There were limitations in the ability and sensitivity of sonography in directly demonstrating the injured organ. It was not until the 1990s that the focused abdominal sonography for trauma (FAST) was developed for the main objective of detecting free fluid in patients with blunt abdominal trauma [2 4].
Sonographic examination The initial focus of sonographic examination was a single view of the hepatorenal fossa (Morisons pouch) [2]. It was soon realized that a more comprehensive examination of the abdomen improved detection of free fluid, however [4]. This included examinations of both upper quadrants, the paracolic gutters, and pelvis. In 1997, McGahan et al [4]
documented that sonographic sensitivity for the detection of free fluid could be improved by having a full bladder. Often in traumatized patients a Foley catheter is placed and the bladder is decompressed, which eliminates the acoustic window in the pelvis needed to detect small or moderate amounts of free fluid. More recently, in an article by Hahn et al [6], patients with proven intra-abdominal injuries after blunt abdominal trauma were evaluated and it was demonstrated that the finding of free fluid with sonography was important. Seventy-eight percent of patients with free fluid on sonography required laparotomy, whereas only 27% without free fluid needed laparotomy. They also showed that examination of Morisons pouch had the highest detection rate of free fluid in these patients (66%), whereas free fluid was detected 56% of the time in the upper quadrants, 48% of the time in the paracolic gutters, and 36% of the time in the pelvis. Examination of all areas was important, however, because 3 of the 604 patients with intra-abdominal injuries had free fluid only in paracolic gutters [6]. At our institution we always include an examination of the heart for pericardial fluid as a part of the FAST scan. US is also useful in examinations of the chest for pneumothorax or pleural effusion, which are discussed later in this article.
Sonographic findings Free fluid
* Corresponding author. E-mail address: john.mcgahan@ucdmc.ucdavis.edu (J.P. McGahan).
Free fluid typically appears as a hypoechoic region within the peritoneal cavity or pelvis and is usually linear or triangular in shape (Fig. 1). The
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Fig. 1. Patterns of free fluid. (A) Real-time US examination of the right upper quadrant demonstrates small triangular-shaped hypoechoic region (arrow) that corresponds to free fluid. (B) Real-time US of the right upper quadrant demonstrates larger hypoechoic region, with acute angles (arrow), noted just inferior to the liver and the right kidney that corresponds to free fluid. (C) In the same patient as B, linear hypoechoic region in the hepatorenal fossa (Morisons pouch) corresponds to free fluid (arrow).
shape of the fluid depends on its compression by the surrounding structures. For instance, in Morisons pouch, the fluid between the kidney and liver usually has a linear shape (see Fig. 1). Fluid that surrounds bowel often appears triangular. Fluid often accumulates at the site of injury but then flows throughout the abdomen and into the pelvis. At the site of injury, the blood may appear echogenic as it forms a clot adjacent to the injured organ (Figs. 2, 3). There maybe several pitfalls in recognition of free fluid within the abdomen (Box 1). Pitfalls Patients with pre-existing ascites or iatrogenic free fluid (eg, dialysis patients) may have falsepositive sonogram results. It is impossible in these patients to know if the free fluid is caused by preexisting ascites, traumatic injury, or a combination of the two. In women of childbearing age, a small amount of physiologic free fluid may be noted in the pelvis. It is important to recognize that although this free fluid is most likely pre-existing and probably
physiologic, it may be secondary to an injury. In this situation, searching for free fluid in other sites is important. Loops of fluid-filled bowel should not be confused with free intraperitoneal fluid. Bowel loops can be distinguished from free fluid because they are round and have peristalsis. This should cause little confusion. In almost all recent studies of the use of sonography for detection of free fluid in patients with blunt abdominal trauma, the specificity of sonography is high [4]. In some cases sonography may detect small amounts of free fluid that are not visualized with CT [4]. Sonographic sensitivity in detecting injuries in patients with blunt abdominal trauma may be decreased for several reasons. The sensitivity of sonography for detection of free fluid in the pelvis may be decreased if a full bladder is not used. With the bladder decompressed after placement of a Foley catheter, free fluid in the dependant portion of the pelvis can be missed. Another potential pitfall of US detection of free fluid is that hematomas may appear echogenic. With severe injury, clotted blood at the
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Fig. 2. Echogenic clot/liver laceration. (A) Real-time US examination of the right upper quadrant of the abdomen shows right kidney (RTK) and echogenic clot anterior to the liver (RT LOBE). (B) Real-time examination of the liver demonstrates fairly well marginated echogenic region in the liver (arrows) that corresponds to liver laceration.
site of the injury may be echogenic and should not be overlooked (see Figs. 2, 3). Finally, there is often no free fluid associated with contained injuries of solid organs, such as the liver, spleen, or kidney. In the article by Hahn et al [6], in several patients no free fluid was detected, yet 27% of these patients required laparotomy. This may be the greatest pitfall of the FAST scan and is discussed later in this article. Finally, sonography is limited and unable to show some types of injuries, including spinal and pelvic fractures, bowel and mesentery injuries, pancreatic injuries, vascular injuries, diaphragmatic ruptures, and adrenal injuries [4].
Free fluid scoring systems Scoring systems have been developed to help stratify patients into groups who may or may not require laparotomy. Others have stratified patients based on either the amount of free fluid in one location or the number of locations in which free fluid was detected. For instance, Sirlin et al [7,8] described a scoring system based on the location of the fluid. For each anatomic region in which fluid was detected, one point was given. The percentage of patients with a score of 0 who had intra-abdominal injury or required surgical intervention (based on this scoring system) was 1.4% and 0.4%, respectively. For the score of 1, the rate of intra-abdominal injury was 59%, and the rate of surgical intervention was 13%. The rate of intra-abdominal injury increased to 85% and rate of surgical intervention was 36%, for a score of 2. For a score of 3, the percentage of pa-
Box 1. Pitfalls in examination of the abdomen for free fluid

Pre-existing fluid (ascites) Iatrogenic free fluid as in dialysis or Fig. 3. Subcapsular hematoma of the spleen. Longitudinal real-time US of the spleen demonstrates well-demarcated, slightly hyperechoic region along the anterior aspect of the spleen (arrow) that corresponds to subcapsular hematoma. (From McGahan JP, Wang L, Richards JR. From the RSNA refresher courses: focused abdominal US for trauma. Radiographics 2001;21(Spec No):S191 9; with permission.)
direct peritoneal lavage Pelvic fluid (female) Loops of fluid filled bowel Incomplete or empty bladder Echogenic clot Contained injury
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tients with intra-abdominal injury remained static at 83%, but rate of surgical intervention was 63%. The higher the score, the higher the injury rate and the greater the need for laparotomy. Others have advocated scoring systems based on the number of free fluid sites or the vertical height of free fluid [9,10]. A common theme would be the more the amount of free fluid, the greater the likelihood of injury or the need for surgical intervention. Sensitivity of sonography The sensitivity of sonography depends on what is used as the gold standard to which US is compared. When sonographic results are compared with clinical outcome, the sensitivity rates of sonography are high, usually more than 95% [11 13]. McGahan et al [4] calculated a sensitivity rate of only 63% when sonography was compared with CT or laparotomy and not using clinical observation as a gold standard. The probable reason for this discrepancy in sensitivities is that McGahan et al [4] showed that several minor lacerations of the liver or spleen were detected on CT but not detected by FAST. These patients did not require surgical intervention, and all improved clinically. If clinical improvement had been used as the gold standard, these patients would have been deemed as having true negative results. When using CT as the gold standard, however, they were deemed as having false-negative results. This is the main reason for discrepancies in the sensitivities of FAST scan. Numerous other studies have been published on the topic of the sensitivity of FAST. For instance, in 744 pediatric patients with blunt abdominal trauma, Richards et al [14] demonstrated a sonographic sensitivity rate of 68% for detecting free fluid or solid organ injuries. In a large review of 3264 patients, this same study group showed that sonography had a sensitivity rate of 67% in detection of intra-abdominal injury [15]. Other results from recent literature vary. Miller et al [16] reported a sensitivity rate of 42% for the FAST scan when compared with CT. Polletti et al [17] demonstrated a sensitivity rate of 93% for sonography, however. Other studies have shown that sonography may miss injuries that may require surgery. Dolich et al [18] reported on 43 patients with false-negative sonography results, 10 of whom (33%) required surgery. Shanmuganathan et al [19] studied the use of sonography in more than 11,000 patients with blunt abdominal trauma: 467 patients had intraabdominal injury, 310 (66%) of whom had free fluid detected by sonography. This detection rate is similar to past studies. In this larger study by Shanmuga-
nathan et al, 157 patients (34%) with intra-abdominal injury had no free fluid, and 26 of these patients required surgery or further intervention. Sonography can be used to triage patients, but one must remember that it may miss significant injuries that require further intervention. CT should be used for patients with a negative sonography result in whom there is a suggestion of intra-abdominal injury [20,21].
Solid organ injury After the initial studies on the use of sonography in detecting organ injuries in the 1970s [1], more recent studies focused on the detection of free fluid [11 13]. A few recent studies have demonstrated the ability of sonography to detect parenchymal organ abnormalities directly. Rothhin et al [12] reported a sensitivity rate of 41.4% for the direct detection of solid organ injuries by sonography. McGahan et al [4] also reported a sensitivity rate of 41% detection in solid organ injuries. More recently, Polletti et al [17] showed a sensitivity rate of 41% for direct demonstration of organ injury. Stengel et al [22] showed that a 7.5-MHz linear ray probe detected solid organ injuries much more readily than a 3.5-MHz convex probe.
Sonographic appearance of solid organ injuries Much of the work on sonographic classification and appearance of solid organ injuries has been performed by McGahan et al [23,24] and Richards et al [25,26]. When identified, acute solid organ injuries are often echogenic on sonography. A diffuse heterogeneous echogenic pattern is the predominant
Fig. 4. Splenic laceration. US examination of the left upper quadrant demonstrates poorly marginated spleen with mixed echo pattern (arrows), which corresponds to severe splenic laceration.
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pattern identified with splenic injuries (Fig. 4). A discrete hyperechoic or diffuse hyperechoic pattern is seen with hepatic injuries (see Fig. 2). Renal injuries are echogenic, with a disorganized appearance that occurs with severe renal lacerations (Fig. 5). More recently, contrast-enhanced abdominal US has been used in the evaluation of solid organ injuries in trauma patients (Fig. 6). For instance, Martegani et al [27] presented the preliminary evaluation of micro-bubble enhanced US of abdominal organs in blunt and penetrating trauma. They evaluated 14 patients with abdominal trauma who were scanned with unenhanced US and contrast-enhanced sonography. These authors use SonoVue (Bracco/ ALTANA Pharm, Konstanz, Germany), a phospholipid coated micro-bubble, at the dose of 1.2 to 2.4 mL scanned with a low mechanical index. The liver, spleen, and kidneys were studied over a 3- to 5-minute interval. They demonstrated that on the unenhanced scan, no lesions were confidently visualized. Excellent enhancement of the parenchymal organs was obtained in all cases using contrast-enhanced sonography, however. They detected injuries in the liver in 5 patients, the spleen in 5 patients, and the kidney in 4 patients. In 7 patients there was confirmation with CT, and there was good correlation between contrastenhanced sonography and contrast-enhanced CT in terms of the position and size of the abnormality. The authors believed that the contrast-enhanced sonography might expedite management of trauma patients [27]. The chest Sonography has been shown to detect pleural effusions [28]. In traumatized patients, sonography
can be used to diagnose pneumothorax or free fluid within the thorax. More recently, sonography also has been shown to be helpful in diagnosing pericardial effusions [29,30] in traumatized patients. The main reason for diagnosing pericardial effusions is to prevent patients from having a traumatically induced pericardial tamponade. We incorporate the subcostal view of the heart as a portion of the FAST scan in all patients with blunt abdominal trauma. This is helpful in diagnosing pericardial effusions (Fig. 7). It must be emphasized that inexperienced examiners often have problems diagnosing pericardial effusions. For instance, Blavias et al [30] set up a study with emergency medicine residents and fellows trained in sonography. They had trouble discerning the epicardial fat, which appeared hypoechoic on US, from a true pericardial effusion. Sonography had a sensitivity rate of 73% and a specificity rate of only 44% in this study [30]. With more experienced examiners, sonography may be useful in detecting moderate pericardial effusions. More recently, sonography also has been proved to be useful in diagnosing pneumothorax [31,32]. The parietal pleura adheres to the inner muscle of the thorax, whereas the visceral pleura adheres to the lung. During inspiration and expiration the visceral pleura slides back and forth adjacent to the parietal pleura. The bright echogenic line of the visceral pleura, which adheres to the lung as it moves and slides during normal inspiration and expiration, may be observed on real-time sonography and is a normal finding (Fig. 8). Absence of the sliding lung is a direct sign of pneumothorax (Fig. 9). Remembering that the free air within the thorax rises to the most nondependent portion of the thoracic cavity, the US probe is placed in this area to check for pneumotho-
Fig. 5. Renal laceration. (A) Longitudinal scan of the right upper quadrant of the abdomen demonstrates ill-defined region without reniform shape, which corresponds to severe renal laceration (shattered kidney) (arrows). Right nephrectomy was performed immediately after the US examination. (B) Real-time US examination of the right paracolic gutter demonstrates an echogenic region inferior to the kidney in the right paracolic gutter that corresponds to hematoma (arrow).
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Fig. 6. Contrast-enhanced US of splenic laceration. (A) Noncontrast US of the spleen appears normal. (B) Contrast-enhanced US with SonoVue demonstrates a large, wedge-shaped defect in the central portion of the spleen. (C) Correlative CT demonstrates splenic laceration. (Courtesy of Thomas Albrecht, MD, FRCR, Berlin, Germany.)
rax. Either a curved array probe or, better yet, a linear array probe may be used to detect pneumothorax. The US probe is placed in the intercostal space. The normal to and fro motion of the visceral pleura against the parietal pleura is observed in a normal
Fig. 7. Pericardial effusion. Subcostal real-time US of the heart demonstrates anechoic region (long arrow) anterior to the heart, which corresponds to pericardial effusion.
patient. The normal motion of the visceral pleura against the parietal pleura is absent with pneumothorax, however. In a normal patient, a reverberation artifact usually is noted posterior to the parietal visceral pleura interface in a normal patient (see Fig. 8). This is observed as lines that are equally spaced from one another and gradually decrease in echogenicity. This is the reverberation of the US beam as it strikes the interface between the parietal and visceral pleura and the air in the lung and is reflected back to the transducer. This reverberation produces multiple equally spaced echoes. The reverberation artifact is not identified when there is a pneumothorax. A pneumothorax may produce acoustic shadowing. Absence or decrease of the reverberation artifact also may occur in a normal patient if the gain settings are set too low. An article by Rowan et al [33] compared the accuracy of sonography with that of the supine chest radiograph in detecting traumatic pneumothorax, with CT serving as the reference or gold standard. They studied 27 patients who sustained
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Fig. 8. Normal lung. (A) Real-time US examination using linear array probe demonstrates the appearance of the normal lung on US. Note that the first echogenic line (open arrow) corresponds to the interface between the parietal and the visceral pleura. Parallel equally spaced lines of decreasing echogenicity are observed posterior to this, which corresponds to reverberation artifacts (arrows). (B) Drawing of reverberation artifact. The US probe is placed on the skin surface (S). R refers to the interface between the parietal and visceral pleura. Lines labeled as numbers 1 and 2, which are of decreasing echogenicity posterior to this, correspond to reverberation artifacts caused by the US beam reverberating or bouncing between the pleura and transducer. (C) Similar pattern is seen with sector scan of the lung in another patient.
blunt thoracic trauma and had US. The radiographic and US findings were compared with CT findings. Eleven of 27 patients had pneumothoraces as seen with CT. All of the pneumothoraces were detected by sonography, for a sensitivity rate of 100%. The
specificity rate of sonography was 94%, and 1 of 16 patients had a false-positive diagnosis of pneumothorax. Supine chest radiography had a sensitivity rate of only 36% (4 of 11 patients), with a specificity rate of 100%. In their study, US was more sensitive
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shown to be sensitive in detecting pneumothoraces in traumatized patients.
References
[1] Kristensen JK, Buemann B, Kuehl E. Ultrasonic scanning in the diagnosis of splenic haematomas. Acta Chir Scand 1971;137:653 7. [2] Jehle D, Guarino J, Karamanoukian H. Emergency department ultrasound in the evaluation of blunt abdominal trauma. Am J Emerg Med 1993;11:342 6. [3] Kimura A, Otsuka T. Emergency center ultrasonography in the evaluation of hemoperitoneum: a prospective study. J Trauma 1991;31:20 3. [4] McGahan JP, Rose J, Coates TL, Wisner DH, Newberry P. Use of ultrasonography in the patient with acute abdominal trauma. J Ultrasound Med 1997;16: 653 62. [5] Federle MP, Griffiths B, Minagl H, Jeffrey Jr RB. Splenic trauma: evaluation with CT. Radiology 1987; 162:69 71. [6] Hahn DD, Offerman SR, Homes JF. Clinical importance of intraperitoneal fluid in patients with blunt intra-abdominal injury. Am J Emerg Med 2002;20: 595 600. [7] Sirlin CB, Casola G, Brown MA, Patel N, Bendavid EJ, Hoyt DB. Patterns of fluid accumulation on screening ultrasonography for blunt abdominal trauma: comparison with site of injury. J Ultrasound Med 2001;20:351 7. [8] Sirlin CB, Casola G, Brown MA, Patel N, Bendavid EJ, Hoyt DB. Quantification of fluid on screening ultrasonography for blunt abdominal trauma: a simple scoring system to predict severity of injury. J Ultrasound Med 2001;20:359 64. [9] Huang MS, Liu M, Wu JK, Shih HC, Ko TJ, Lee CH. Ultrasonography for the evaluation of hemoperitoneum during resuscitation: a simple scoring system. J Trauma 1994;36:173 7. [10] McKenney KL, McKenney MG, Nunez DB, et al. Interpreting the trauma ultrasound: observations in 62 positive cases. Emerg Radiol 1996;3:113 7. [11] McKenney MG, Martin L, Lentz K, Lopez C, Sleeman D, Aristide G, et al. 1,000 consecutive ultrasounds for blunt abdominal trauma. J Trauma 1996;40:607 10. [12] Rothlin MA, Naf R, Amgwerd M, Candinas D, Frick T, Trentz O. Ultrasound in blunt abdominal and thoracic trauma. J Trauma 1993;34:488 95. [13] Rozycki GS, Ochsner MG, Jaffin JH, Champion HR. Prospective evaluation of surgeons use of ultrasound in the evaluation of trauma patients. J Trauma 1993; 34:516 26. [14] Richards JR, Knopf NA, Wang L, McGahan JP. Blunt abdominal trauma in children: evaluation with emergency US. Radiology 2002;222:749 54. [15] Richards JR, Schleper NH, Woo BD, Bohnen PA, McGahan JP. Sonographic assessment of blunt ab-
Fig. 9. Small pneumothorax. Real-time US examination of thorax in this patient with a small pneumothorax demonstrates the echogenic line that corresponds to the parietal and visceral pleura, which is noted to the left side of image. Note more distal reverberation artifacts. To the right side of the image there is loss of this pattern because of a small pneumothorax.
than chest radiography in the detection of traumatic pneumothoraces.
Summary US will be used more frequently in the future for the evaluation of traumatized patients. Previously, the main focus of the sonographic examination was for the detection of free fluid. Unstable patients with free fluid often can be triaged to the operation room without further imaging tests. In patients who are more stable or in whom US results are negative, CT is required. Based on recent studies, sonography has a sensitivity rate of approximately 40% in direct detection of solid organ injuries. In the future, however, with the use of contrast-enhanced agents, sonography may more reliably detect solid organ injuries. Within the chest, US has been shown to be helpful in detecting pleural effusions and may be useful in detecting pericardial effusions. US has been
J.P. McGahan et al / Radiol Clin N Am 42 (2004) 417425 dominal trauma: a 4-year prospective study. J Clin Ultrasound 2002;30:59 67. Miller MT, Pasquale MD, Bromberg WJ, Wasser TE, Cox J. Not so fast. J Trauma 2003;54:52 9. Polletti PA, Kinkel K, Vermeulen B, Irmay F, Unger PF, Terrier F. Blunt abdominal trauma: should US be used to detect both free fluid and organ injuries? Radiology 2003;227:95 103. Dolich MO, McKenney MG, Varela JE, Compton RP, McKenney KL, Cohn SM. 2,576 ultrasounds for blunt abdominal trauma. J Trauma 2001;50:108 12. Shanmuganathan K, Mirvis SE, Sherbourne CD, Chiu WC, Rodriguez A. Hemoperitoneum as the sole indicator of abdominal visceral injuries: a potential limitation of screening abdominal US for trauma. Radiology 1999;212:423 30. McGahan JP, Richards J, Gillen M. The focused abdominal sonography for trauma scan: pearls and pitfalls. J Ultrasound Med 2002;21:789 800. McGahan JP, Richards JR. Blunt abdominal trauma: the role of emergent sonography and a review of the literature. AJR Am J Roentgenol 1999;172:897 903. Stengel D, Bauwens K, Sehouli J, Nantke J, Ekkernkamp A. Discriminatory power of 3.5 MHz convex and 7.5 MHz linear ultrasound probes for the imaging of traumatic splenic lesions: a feasibility study. J Trauma 2001;51:37 43. McGahan JP, Richards JR, Jones CD, Gerscovich EO. Use of ultrasonography in the patient with acute renal trauma. J Ultrasound Med 1999;18:207 13. McGahan JP, Wang L, Richards JR. From the RSNA refresher courses: focused abdominal US for trauma. Radiographics 2001;21(Spec No):S191 9.
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[16] [17]
[18]
[19]
[20]
[21]
[22]
[23]
[24]
[25] Richards JR, McGahan JP, Jones CD, Zhan S, Gerscovich E. Ultrasound detection of blunt splenic injury. Injury 2001;32:95 103. [26] Richards JR, McGahan JP, Pali MJ, Bohnen PA. Sonographic detection of blunt hepatic trauma: hemoperitoneum and parenchymal patterns of injury. J Trauma 1999;47:1092 7. [27] Martegani A, Cosgrove DO, Del Favero C, Aiani L, Harvey CJ. Contrast enhanced abdominal ultrasound in trauma using SonoVue. Radiology 2002;225(P):358. [28] Ma OJ, Mateer JR. Trauma ultrasound examination versus chest radiography in the detection of hemothorax. Ann Emerg Med 1997;29:312 6. [29] Aaland MO, Bryan III FC, Sherman R. Two-dimensional echocardiogram in hemodynamically stable victims of penetrating precordial trauma. Am Surg 1994;60:412 5. [30] Blaivas M, DeBehnke D, Phelan MB. Potential errors in the diagnosis of pericardial effusion on trauma ultrasound for penetrating injuries. Acad Emerg Med 2000;7:1261 6. [31] Dulchavsky SA, Schwarz KL, Kirkpatrick AW, et al. Prospective evaluation of thoracic ultrasound in the detection of pneumothorax. J Trauma 2001;50:201 5. [32] Sargsyan AE, Hamilton DR, Nicolaou S, et al. Ultrasound evaluation of the magnitude of pneumothorax: a new concept. Am Surg 2001;67:232 6. [33] Rowan KR, Kirkpatrick AW, Liu D, Forkheim KE, Mayo JR, Nicolaou S. Traumatic pneumothorax detection with thoracic US: correlation with chest radiography and CT. Initial experience. Radiology 2002;225: 210 4.
Radiol Clin N Am 42 (2004) 427 443
Priapism
Hossein Sadeghi-Nejad, MDa,b,*, Vikram Dogra, MDc, Allen D. Seftel, MDd, Mamdouh A. Mohamed, MDd,e
Division of Urology, University of Medicine and Dentistry of New Jersey, Medical School, 185 South Orange Avenue, MSB G536, Newark, NJ 07103-2714, USA b Center for Human Sexuality and Male Reproductive Medicine, Hackensack University Medical Center, 20 Prospect Avenue, #711, Hackensack, NJ 07601, USA c Division of Ultrasound, Department of Radiology, Case Western Reserve University, University Hospitals, 11100 Euclid Avenue, Cleveland, OH 44106, USA d Department of Urology, Case Western Reserve University, University Hospitals of Cleveland, Cleveland Veterans Affairs Medical Center, 11100 Euclid Avenue, Cleveland, OH 44106 5046, USA e Department of Urology, El-Mina University Hospital, El-Mina, Egypt
a
Priapism is a relatively uncommon medical condition that is defined as a pathologic prolonged engorgement or erection of the penis or clitoris that is unrelated to sexual arousal. Recent advances in the study of erectile physiology and the pathophysiology of erectile dysfunction have resulted in better understanding of the processes leading to various subtypes of priapism and the factors implicated in its resolution or recurrence. Despite these advances, there is a paucity of randomized studies and basic science investigations pertaining to priapism. The recently published American Urological Association (AUA) Guideline on the management of priapism sheds further light on the management of this potentially emergent condition, but the guideline does not establish a fixed set of rules or define the legal standard of care for the treatment of priapism [1].
Definition The term priapism is derived from Priapus, a minor god of fertility, luck, and the deity of gardens and fields in Greek mythology [2]. A famous painting in the entrance to the House of Vettii in Pompeii depicts Priapus with a disproportionately large phallus, leaning against a pillar and weighing his massive penis. Conditions related to the prolonged engorgement of the penis were associated with Priapus in the Greek language and were later assimilated into Latin and modern languages [2]. In the early twentieth century, Hinman [3] classified priapism as either mechanical or nervous in etiology and suggested corporal vein thrombosis as the cause of mechanical priapism. The condition is more common in men and typically involves the paired corpora cavernosa, although rare exceptions with involvement of the corpus spongiosum and sparing of the cavernosal spaces have been reported [4]. Priapism is broadly classified as low-flow (ischemic) or high-flow (arterial and nonischemic). Lowflow priapism and the associated severe decrease in venous drainage from the corpora cavernosa is a potential medical emergency and may lead to irreversible ischemic tissue changes. High-flow priapism is less commonly encountered and involves unregu-
* Corresponding author. Division of Urology, University of Medicine and Dentistry of New Jersey, Medical School, 185 South Orange Avenue, MSB G536, Newark, NJ 07103-2714. E-mail addresses: hossein@ix.netcom.com, www.hsadeghi.com (H. Sadeghi-Nejad).
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H. Sadeghi-Nejad et al / Radiol Clin N Am 42 (2004) 427443
lated inflow that is typically secondary to some form of arterial trauma. One of the earliest reports of arterial priapism was published in 1960 following a case of traumatic coitus that was surgically managed by ligation of the internal pudendal artery [5]. Unlike the ischemic subtype, arterial priapism is not considered an emergency: the patient does not have pain and spontaneous resolution is the likely outcome in more than half the cases. Hauri et al [6] elaborated on the different management approaches to arterial versus veno-occlusive priapism and was one of the first to suggest that the prognosis of the latter is far less favorable than arterial priapism. Nonetheless, the long-term outcome of nonischemic priapism has not been thoroughly investigated and it is clear that completely normal erectile function after these episodes cannot be guaranteed in all cases. Stuttering priapism refers to a condition of recurrent, intermittent, painful erections. These episodes are more common in patients with various hemoglobinopathies. Stuttering priapism is especially troublesome for both the affected patient, facing repeated painful episodes and potential emergency room visits, and the physician challenged to arrive at a practical and efficacious management plan for the patient. Malignant priapism is a rare clinical entity that is caused by metastasis of solid tumors to the penis.
The penile blood vessels arise from the internal pudendal artery. The common penile artery continues in the Alcocks canal above the perineal membrane and terminates in three branches to supply the erectile bodies. The bulbourethral artery supplies the urethra, spongiosum, and the glans. The cavernosal artery enters the corpora cavernosa on the superomedial surface of the penis. The cavernosal artery travels in the center of each corporal body and gives off straight and helicine arteries. Helicine arteries form a bridge between the cavernosal artery and the lacunar spaces in the corpora cavernosa [7]. It is the cavernosal artery and its branches that dilate and bring extra blood to the erectile tissue during penile erection. The dorsal artery of the penis passes between the crus penis and the pubis to reach the dorsal surface of the corporal bodies. The dorsal artery mainly supplies blood to the glans and runs between the dorsal vein and the dorsal penile nerve. The venous blood is returned by the venous plexus beneath the tunica albuginea. The emissary veins perforate the tunica albuginea, and the blood is drained by the venae circumflexae into the deep dorsal veins.
Sonographic technique A penile sonographic examination is performed with the patient supine with the penis lying on the anterior abdominal wall or supported with towels between the thighs. High frequency (7.5 12 MHz) linear array ultrasound transducers provide high-resolution images of the penis [7]. Copious amounts of acoustic gel should be used on the surface of the penis to optimize visualization and avoid excessive compression by the transducer. Transverse images of the penis are recorded starting at the level of the glans and moving down to the base of the penis. The two corpora cavernosa are identified as two adjacent circular hypoechoic structures. The tunica albuginea is identified as a hyperechoic linear structure covering the corpora. The cavernosal artery is visualized on the medial portion of each corpora cavernosa. The corpus spongiosum is often compressed and is difficult to visualize from the ventral aspect (see Fig. 1). Longitudinal evaluation of the corporal bodies should also be obtained and recorded. During the transverse and longitudinal scanning, close attention should be given to any plaques, calcific foci, or arteriovenous fistulas. In the case of veno-occlusive priapism, the sonographer should be extremely gentle while performing the sonographic examination because this is an exceedingly painful condition.
Sonographic anatomy of the penis The penis is composed of two dorsal corpora cavernosa and one ventral corpus spongiosum. The two corpora cavernosa are enclosed in a fibrous sheath, the tunica albuginea, which partially covers the corpus spongiosum. The tunica albuginea is composed of elastic fibers that form an irregular, latticed network on which collagen fibers rest. The septum between the two corpora cavernosa is complete proximally and is incomplete in its distal two thirds. The corpora cavernosa join beneath the pubis (penile hilum) to form the major portion of the body of the penis. The corpora cavernosa are composed of sinusoidal spaces lined by smooth muscles (erectile tissue) and endothelium. The glans penis is formed by the expansion of the corpus spongiosum. The corpus spongiosum is traversed throughout its length by the anterior urethra, which begins at the perineal membrane. The corpus spongiosum provides support to the urethra and helps with the expulsion of semen from the urethra. Bucks fascia surrounds both cavernosal bodies dorsally and splits to surround the spongiosum ventrally (Fig. 1).
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A
Dorsal Artery Cavernosal Artery Dorsal Veins Tunica Albuginea
Corpus Cavernosum Corpus Spongiosum
Buck's Fascia Urethra
C
Internal Pudendal Artery Dorsal Artery Helicine Arteries Cavernosal Artery
Bulbar Artery
Spongiosal Artery
Fig. 1. (A) Diagrammatic representation of penile anatomy in cross-section. (B) Corresponding gray-scale ultrasound image. (C) Diagrammatic representation of penile anatomy in longitudinal view. (From Fitzgerald SW, Erickson SJ, Foley WD, et al. Color Doppler sonography in the evaluation of erectile dysfunction. Radiographics 1992;12(1):3 17; with permission.)
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The presence of the cavernosal artery in each corpora cavernosa along with a spectral Doppler waveform of each should be obtained and recorded. Color Doppler images in both transverse and longitudinal views should also be obtained.
Epidemiology and etiology Eland et al [8] have evaluated the incidence of priapism in the general population. These investigators conducted a population-based retrospective cohort study using a longitudinal observational database from the patient records of a group of general practitioners in The Netherlands. They found an overall incidence rate of 1.5 per 100,000 person-years. The incidence rate in men 40 years old and older was 2.9 per 100,000 person-years. The authors acknowledged that not all patients with priapism seek medical care and the reported data may be an underestimation of the actual rate in the general population. The incidence of priapism in special at-risk subpopulations is much higher. At-risk populations include men with cocaine drug use, advanced pelvic or hematologic malignancy, and those on antipsychotic medications [9 12]. Pohl et al [13] evaluated various etiologies for priapism in a study of 230 single case reports in the literature: idiopathic causes comprised one-third of the cases, whereas 21% were attributed to alcohol abuse or medications, 12% to perineal trauma, and 11% to sickle cell anemia (SCA) [13]. For individuals on intracorporal injection therapy for erectile dysfunction, the incidence range of priapism episodes is from 1% for those on prostaglandin E1 and as high as 17% for patients who receive intracorporeal injections of papaverine [14]. The most likely cause of prolonged erection as a result of intracavernous injection therapy is overdosage. Proper injection technique and gradual upward titration of the dose by the patient helps decrease this adverse event. Priapism associated with sickle cell disease is classically described as ischemic, although rare exceptions of high-flow priapism in association with sickle cell disease have been reported. The pathophysiology of high-flow priapism in patients with sickle cell disease is not known [15]. Fowler et al [16] evaluated the incidence and prevalence of priapism in sickle cell conditions. The authors reported frequent self-limited priapistic episodes, mostly occurring during sleep, which last less than 3 hours. Priapism associated with SCA was unusual before puberty and in keeping with the previously reported 6% prevalence of priapism in children with SCA
[16,17]. No correlations are observed between the average number of priapism episodes per year and the duration of a typical episode. A similar study from Jamaica documented a 42% prevalence of priapism in SCA patients [18]. Priapism was significantly associated with low hemoglobin F levels and high platelet counts and over one fourth of those who had suffered priapism had some degree of impotence. A more recent survey of patients with homozygous SCA (hemoglobin SS) and sickle cell b(0) thalassemia (hemoglobin S-b[0]) between 5 and 20 years of age found an 89% actuarial probability of experiencing priapism by 20 years of age. The mean duration of an episode in this study was 125 minutes. Episodes typically occurred around 4:00 AM, and 75% of the patients surveyed had at least one episode starting during sleep or on awakening from sleep [19]. Drug-induced priapism has been reported with a variety of medications, most commonly related to the antihypertensive drugs guanethidine, prazosin, and hydralazine and psychotropic medications [20]. Antipsychotics are associated with a small, but definite risk of priapism and the most commonly cited agents are trazodone (Desyrel), thioridazine, and chlorpromazine [21]. Abber et al [22] investigated the mechanism of drug-induced priapism in dogs by intravenous and intracorporeal injection of the antipsychotic agent chlorpromazine and the antidepressant trazodone. The authors demonstrated that both drugs induced erection in a manner similar to that of intracorporeal injection of papaverine and showed venous restriction and slight increases in internal pudendal arterial flow at the beginning of tumescence. The authors stated that the a-adrenergic antagonist properties of chlorpromazine and trazodone probably cause priapism by local action. Psychotropic-induced priapism is almost always associated with low-flow pathology and is currently believed to be caused by the a1-adrenergic antagonism of these medications. Chlorpromazine and thioridazine are conventional antipsychotics with the greatest a1-adrenergic affinity and have been most frequently reported to be associated with priapism [9]. The exact pathophysiology has not been elucidated, but is likely multifactorial and may be related to the ratio of a-adrenergic blockade to anticholinergic activity. Risperidone, olanzapine, and clozapine are the atypical antipsychotics that have been reported to cause priapism on rare occasions [9]. It has been reported that trazodone and cocaine may have synergistic effects in promoting priapism and their combination may pose an additional risk of priapism. Clinicians should be aware of the possible additive risk of priapism in this patient population,
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because trazodone is commonly used as a hypnotic and is often chosen for polysubstance abusers because of its low abuse potential [23]. Cocaine-induced priapism has been reported in association with topical application to enhance sexual performance, and intranasal and intracavernous injections [24 26]. Priapism has also been reported in association with the recreational drug ecstasy [27]. Androgens have been implicated as an important etiologic factor with reports of priapism in hypogonadal men receiving gonadotropin-releasing hormone or high-dose testosterone, testosterone-induced priapism in adolescents with SCA, and priapism after androstenedione intake for athletic performance enhancement [28 31]. Examples of neurologic etiologic factors include priapism in patients with degenerative stenosis of the lumbar canal, where symptoms may be fully relieved by surgical decompression, and priapism secondary to cauda equina syndrome (following degenerative stenosis of the lumbar canal and lumbar arachnoiditis), herniated disk, or blockage of the central inhibitory influences as seen during general or regional anesthesia. Noteworthy reports of systemic illnesses implicated as etiologic factors include reports of priapism occurring in widespread amyloidosis [32]. Other uncommon etiologies include glucose phosphate isomerase deficiency (third most commonly occurring erythroenzymopathy), which can cause priapism through increased rigidity of red blood cell membrane and resultant increased blood viscosity, cell sludging in the corpora, and increased acidity; Fabrys disease (glycosphingolipid lipidosis) presenting with a combination of renal insufficiency and priapism; high concentration (ie, 20% rather than 10%) fat emulsion in total parenteral nutrition; and paradoxical thromboembolic events in heparin- or warfarin-induced priapism [33 37]. Possible etiologies for increased thromboembolic events in total parenteral nutrition induced priapism include increased blood coagulability and fat emboli and direct cellular effects by high fat content. Increased platelet function assessed by the levels of antiheparin platelet factor 4 and b-thromboglobulin has been documented in priapism following 20% fat emulsion total parenteral nutrition [35]. The mechanism of malignant priapism has not been definitively elucidated, but may be caused by extensive organ replacement by carcinoma, venous obstruction by the tumor, or continual stimulus to the erectile afferent or efferent neural pathways [38]. Tumor infiltration is most frequently from the bladder and prostate (32% and 28%, respectively) followed by kidney (17%), gastrointestinal tract (8%), and rarely
from testis, lung, liver, bone, and sarcomas as the primary source [39]. It has been reported that 20% to 53% of cases of penile metastasis from other primary tumors initially present with priapism [40]. When Witt et al [41] published their paper on traumatic laceration of intracavernosal arteries and the pathophysiology of nonischemic high-flow priapism in 1990, only five additional cases of priapism with similar features to the reported case were cited. Although more attention has been focused on this subtype of priapism and numerous related papers have been published since the early 1990s, there is general agreement that arterial priapism is far less common than the ischemic variant. It is estimated that the condition is rare enough that few urologists treat more than two cases in their lifetime [42]. Nonetheless, because the presentation of arterial priapism is painless and far less distressful to the patient, it is entirely possible that many more cases of arterial priapism are unreported. Nonischemic priapism has been described in a variety of conditions causing perineal trauma including bicycling and other straddle injuries [43 47]. The resultant injury to the arterial system and formation of an arteriolacunar fistula is most often implicated as the causative factor in nonischemic high-flow priapism. The venous outflow system is typically unaffected in these conditions and the blood in the corpora remains well oxygenated. The condition may also be iatrogenic following deep dorsal vein arterialization for vasculogenic impotence [48]. This etiology is exceedingly unlikely to be reported in the future, however, because deep dorsal vein arterialization is rarely performed anymore. The most common etiology for high-flow priapism in children is traumatic arterial laceration, but cases associated
Box 1. Etiology (AFUD classification)

Drug induced Hematologic Sickle cell disease and other hemo-
globinopathies
Thrombophilia states (protein C and
other thrombophilias, lupus)

Hyperviscosity states (hyperleukocy-
tosis, polycythemia)
Idiopathic Central nervous system mediated Other
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Box 2. Etiologic factors in priapism Low-flow states (veno-occlusive or ischemic type)

Hemoglobinopathies and sickle cell
logic Disease (AFUD) Thought Leader Panel on Priapism [43,52]. A more detailed list of etiologic factors based on low-flow versus high-flow subtypes of priapism is shown in Box 2.
disease
Thrombophilia states (lupus,
Pathophysiology In broad terms, priapism may be regarded as an imbalance between arterial inflow and outflow. Burnett [53] has recently reviewed the pathophysiology of priapism and suggested derangements in the diverse systems of regulatory control in erectile function. These dysregulatory functions include possible overactivity of the veno-occlusive mechanism, arterial inflow, or neurogenic processes that can affect inflow or outflow. Conversely, the problem may be secondary to malfunction of the normal contractile activities of cavernosal smooth muscle cells. Low flow Ischemic or veno-occlusive priapism is a medical emergency and the most common form of priapism. It is characterized by a painful, rigid erection; absent cavernosal blood flow; and severely acidotic corpora (Fig. 2). The spectrum of clinical symptoms and signs is analogous to those found in other compartment syndromes and mandates immediate decompression to minimize the chances of long-term sequelae. The combination of venous outflow obstruction, highpressure chambers, and poor-to-absent inflow can lead to trabecular interstitial edema and ultrastructural changes in trabecular smooth muscle cells and functional transformation to fibroblast-like cells. In priapism lasting more than 24 hours, severe cellular damage and widespread necrosis may occur [54]. Destruction of the endothelial lining, formation of blood clots within the corpora, and widespread transformation of the smooth muscle cells to fibroblast-like cells or necrosis occurs in cases lasting beyond 48 hours and eventually results in irreversible erectile dysfunction [54]. Lack of these changes in priapism lasting less than 12 hours emphasizes the importance of patient education and early intervention. In an animal model, anoxia has been shown to eliminate spontaneous and drug-induced contractile activity, suggesting a likely explanation for the failure of penile injection of a-adrenergic agonists to reverse prolonged ischemic priapism when the penis is in its maximal rigid state [55]. The failure of detumescence seen in low-flow priapism may be secondary to failed a-adrenergic neurotransmission, endothelin deficit, or

protein C) Warfarin or heparin induced Fabrys disease Dialysis Total parenteral nutrition (high fat content) Vasculitis Hematologic malignancies Pelvic or lower genitourinary tract (bladder and prostate) cancer and metastatic (ie, renal) malignancies Psychotropics and antidepressants (chlorpromazine, trazodone, risperidol) Antihypertensives (guanethidine, hydralazine, prazosin) Erectogenic agents (intracavernosal vasoactives; sildenafil; intraurethral prostaglandin E1) Spinal cord stenosis Amyloidosis Glucose phosphate isomerase deficiency Alcohol Androgens or testosterone
High-flow states (arterial or nonischemic type)

Penile or perineal trauma Straddle injury Cavernosal artery injury Arteriosinusoidal fistula Cocaine Metastatic malignancy Fabrys disease Iatrogenic (following deep dorsal vein arterialization)
with inherited metabolic disorders (ie, Fabrys disease) or hematologic diseases, such as SCA, also have been described [49 51]. Box 1 is a classification of priapism by etiology as agreed on by the American Foundation for Uro-
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Fig. 2. Low-flow priapism in a patient with sickle cell disease. Longitudinal sonogram of the corpora cavernosa demonstrates high-resistance flow in the cavernosal artery suggestive of priapism. Cavernosal arterial flow is usually absent in patients with low-flow priapism; however, highresistance flow may be observed.
inactivation of intracellular cofactors of smooth muscle contraction caused by hypoxia or hypercarbia [55]. Recurrent episodes of veno-occlusive priapism, occurring anywhere from a few times monthly to recurrent daily episodes, are quite disabling and often have an idiopathic etiology. Levine et al [56] evaluated six patients with recurrent veno-occlusive priapism and ruled out mechanical occlusion of corporeal venous drainage by demonstrating elevated flows to maintain intracavernosal pressures following smooth muscle contraction and markedly decreased flow rates following smooth muscle relaxation. The authors proposed that a functional alteration of the adrenergic or endothelial-mediated mechanisms that control penile tumescence and maintain penile flaccidity may develop secondary to the initial ischemic episode and reported that the use of oral phenylpropanolamine reduced the frequency and duration of the recurrences, and markedly reduced the need for adrenergic selfinjection. Treatment of the recurrent episodes with intracavernous self-injection of phenylephrine resulted in successful detumescence in that series and the authors experience with similar cases. The pa-
tients must be instructed on the proper and early use of phenylephrine self-injections. Most recently, Lin et al [57] have postulated that the mechanism of stuttering priapism in patients with sickle cell hemoglobinopathies may involve abnormally low expression of phosphodiesterase type 5 secondary to hypoxia. In the human corpus cavernosum, phosphodiesterase type 5 is responsible for degradation of cGMP and phosphodiesterase type 5 inhibitors, such as sildenafil and vardenafil, have become the mainstay of oral pharmacotherapy in the treatment of erectile dysfunction. Seftel et al [58] have reported on two cases of veno-occlusive priapism refractory to conventional therapy that later converted to high-flow priapism. The authors suggested that the high-flow state observed after treatment of veno-occlusive priapism may represent a variant of nonischemic priapism or, alternatively, may be the pathophysiology of recurrent idiopathic priapism. Neurologic control of the efferent erectile pathway is by the pelvic nerves that are joined by the preganglionic parasympathetic nerves. The pelvic nerves join the pelvic plexus that gives rise to the cavernous nerve of the penis. Normally, penile stimulation causes reflexogenic erections that are primarily controlled by the sacral parasympathetic nerves originating from the S2-4 segment located at the T11-L1 vertebral levels. The afferent limb of the erection response is mediated by the dorsal penile nerve (a branch of the pudendal nerve), which transmits sensory impulses to the spinal cord. The role of the sympathetic nervous system in penile erection is not entirely clear, but its activation is generally associated with contraction of corpus cavernosal smooth muscle and penile detumescence. The neuropathophysiology of priapism in patients with lumbar stenosis has not been fully elucidated, but it is postulated that it may be caused by parasympathetic efferent hyperactivity in the S2-4 cauda equina nerve roots within the narrowed thecal sac. The parasympathetic hyperactivity may be secondary to increased intrathecal pressure at the stenotic level and altered circulation within the cauda equina during walking [59]. Sickle cell hemoglobinopathy results from the inheritance of one or two genes coding for an abnormal S hemoglobin and manifests in 0.15% of black Americans in the form of sickle cell disease (homozygous for hemoglobin S) and in 8% as sickle cell trait (heterozygous for hemoglobin S). Inheritance of a combination of a hemoglobin S gene and a second gene coding for abnormal hemoglobin (ie, B + thalassemia or C hemoglobin) is possible and, as in the homozygous type, may result in ischemic complica-
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tions [16]. The pathophysiology of SCA-induced priapism is thought to result from decreased oxygen tension and pH developing in stagnant blood within the corporal sinusoids, which in turn leads to a cycle of erythrocyte sickling and sludging followed by even more hypoxemia and acidosis [60]. Although most cases are of the low-flow ischemic type, high-flow priapism may be observed in patients with sickle cell hemoglobinopathy in rare instances [15]. High flow Nonischemic or arterial priapism is a less common form of priapism that presents clinically as a painless erection that typically follows some type of penile or perineal trauma leading to unregulated arterial inflow into the sinusoidal space. Unlike the veno-occlusive variant, high-flow priapism is not an emergency: the outflow mechanism is intact and the cavernosal milieu is not anoxic. The penis is often not maximally rigid in these cases, but intercourse may be possible. Other clinical observations include delayed onset of priapism after perineal trauma and a state of constant suboptimal rigidity that may become more rigid with arousal [61]. Diagnosis is typically based on the aforementioned clinical history and physical examination, and demonstration of arterial blood on aspirated cavernosal blood gas studies. A number of recent studies have pointed to cycling trauma as the cause of both transient neurogenic impotence and vasculogenic pathologies in the form of arterial priapism or permanent erectile dysfunction [43,46,62]. Spycher and Hauri [54] have shown that at the level of trabecular smooth muscle cells, the ultrastructural changes and fibroblast-like cellular transformation seen in low-flow states do not occur with arteriogenic priapism, even when the latter has been present for prolonged (as late as 5 months) periods. A mechanism for the pathophysiology of high-flow priapism is described by Goldsteins group in Boston: unlike a traditional arteriovenous fistula, the condition is described as an arterial-lacunar fistula where the helicine arteries are bypassed and the blood passes directly into the lacunar spaces. In turn, the high flow in the lacunar space creates shear stress in adjacent areas, leading to increased nitric oxide release, activation of the cGMP pathway, and smooth muscle relaxation and trabecular dilatation [61]. The authors also postulate that the delay in onset of high-flow priapism may be secondary to a delay in the complete necrosis of the arterial wall after the initial penile or perineal trauma. Alternatively, the delay may be secondary to clot formation at the site of injury followed by the normal lytic pathways, which follow in a few days.
Diagnosis Physicians caring for patients with priapism should remember at all times the significant anxiety and fear experienced by most patients with this condition and make a genuine effort to alleviate their apprehension. A thorough history and physical examination are prerequisites to diagnostic accuracy. The sexual and medical history should especially focus on medications, trauma, and predisposing comorbidities. Presence or absence of pain is a fairly reliable predictor of low-flow versus high-flow priapism, respectively. The latter diagnosis is further suggested by a history of penile or perineal trauma. Absence of pain in arterial priapism frequently results in less patient anxiety and discomfort as compared with veno-occlusive priapism. Consequently, those with arterial priapism may present days or even weeks after the original injury. The fundamental aim of the initial phase of assessment is to distinguish arterial from ischemic priapism. The AFUD panel recommendations for the management of priapism are illustrated in Fig. 3 and follow a step-care model that has been modified and refined over the years [43,52,63]. Physical examination of the penis is critical and typically reveals firm corpora cavernosa and a soft glans, indicating sparing of the corpus spongiosum in low-flow priapism. Findings in high-flow states usually reveal a partial to full erection and sparing of the corpus spongiosum in most cases (as in low-flow states). General diagnostic tests include urine toxicology screening for psychoactive drugs and metabolites of cocaine [10,43]. These tests are particularly helpful if the diagnosis is unclear. The AFUD panel has additionally suggested reticulocyte count (if indicated); urinalysis (if indicated); complete blood count; platelets, and differential white blood cell count; and urologic consultation. The reticulocyte count is often elevated in men with SCA. The most important warning with regard to hematologic testing is to remember that hemoglobinopathies are not restricted to African American men and other groups, especially those of Mediterranean descent, may be affected (ie, thalassemia or sickle-thalassemia). The sickledex test and examination of the peripheral smear are less time consuming than hemoglobin electrophoresis and may be more appropriate for the emergency room setting. These recommendations are similarly emphasized in the more recent AUA guideline on priapism [1]. Urologic management of priapism includes history and physical (including penile) examination, and assessment of corporal blood flow status (corporal aspirate and visual inspection by color and consist-
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Fig. 3. Step-care treatment model for the management of priapism recommended by the AFUD thought leader panel. CA, cavernosal artery; CBC, complete blood count; DDU, duplex Doppler ultrasonography; HB, hemoglobin; NB, nerve block; PE, physical examination; PSA, prostate-specific antigen; UA, urinalysis; VS, vital signs. (Data from references [43] and [52].)
ency or corporal blood gas including pH, PO2, and PCO2, or penile duplex Doppler ultrasound) [43]. Low-flow priapism is suggested by finding low oxygen, high carbon dioxide, and low pH in the blood gas analysis of the aspirate. When a high-flow state is suspected based on the bright red appearance or blood gas analysis of the corporal aspirate, duplex Doppler sonography may identify a dilated caver-
nosal artery or pseudocapsule formation at the site of arterial sinusoidal fistula. These findings are helpful if superselective arterial embolization is performed [64]. The AUA Guideline states that the use of penile arteriography for the identification of the site of a cavernous artery fistula may be warranted in some cases, but that arteriography has been largely replaced by color duplex sonography and the former is only
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used as part of an embolization procedure [1]. Furthermore, penile aspiration has mainly a diagnostic role in the management of arterial priapism (not therapeutic). Although the data reviewed by the AUA guideline panel did not reveal any instances of arterial priapism resolution after aspiration or irrigation, two separate case reports in the literature have documented the rare resolution of arterial priapism after aspiration or irrigation in cases of adult and pediatric posttraumatic priapism [65,66]. Patients presenting with refractory low-flow priapism who later convert to a high-flow state represent a less common cohort of priapism patients. Because the management of the low-flow and highflow states is radically different, sonography should be considered if conventional corporal irrigation and intracavernosal sympathomimetics (ie, phenylephrine) fail to resolve the initial veno-occlusive priapism [58]. When a hemoglobinopathy is suspected, hemoglobin electrophoresis may be performed. The AFUD panel has also recommended testing for prostate-specific antigen when indicated.
Role of radiology in the diagnosis and treatment of priapism Most of the reports on the use of sonographic imaging in the diagnostic and therapeutic algorithms of priapism are focused on the high-flow variant, although sonography may be used instead of blood gas sampling to differentiate ischemic (low-flow priapism) from high-flow priapism. Color duplex Doppler sonography has replaced arteriography as the imaging modality of choice for the diagnosis of priapism. Penile color duplex Doppler sonography is noninvasive, does not expose the patient to ionizing radiation, and can reveal important information regarding the location of arterial injury in high-flow priapism. Most published studies on the subject indicate that in experienced hands, differentiation of the increased color flow on the affected side from the normal flow on the contralateral side is not problematic. Two important papers from Goldsteins group at Boston University have shown color Doppler ultrasound to be as sensitive as angiography for the diagnosis of high-flow priapism [61,67]. More specifically, penile duplex Doppler sonography had a sensitivity of 100% and a specificity of 73% with a predictive value of 81% for a positive test and 100% for a negative test [67]. Mabjeesh et al [68] have reported therapeutic use of color duplex Doppler ultrasound in one patient in whom sonography was
used to localize the fistula and subsequently apply external compression to achieve permanent fistula occlusion and resolution of priapism. In a posttraumatic case of priapism with an arterial tear, gray-scale ultrasound reveals an irregular hypoechoic region secondary to tissue injury or distended lacunar spaces in the corpus cavernosum. This irregular area appears with well-circumscribed margins analogous to a capsule formation if the injury has been long-standing [69]. The arteries exhibit normal or increased flows within the cavernosal arteries and an irregular flow from the artery to the cavernosal body at the site of injury. Arterial signs may be seen in the pseudoaneurysm and, unlike veno-occlusive priapism, increased venous flow may be observed in high-flow priapism [42]. The arterial lacunar fistula seen in high-flow priapism essentially bypasses the helicine arteries and appears as a characteristic color blush extending into the cavernosal tissue on color duplex sonography. It is reported that 90% of fistulas in adults appear as unilateral, whereas at least 50% of arterial priapism in children is associated with bilateral or multiple arterial lacerations [42,51]. Bertolotto et al [69] recommend increasing the color Doppler velocity scale for better detection of the cavernosal artery tear region as a focal area with very high flow. Because aspiration is only used for diagnostic purposes in cases of arterial priapism, if the history is suggestive of high-flow pathology and color duplex sonography is conclusive, the patient may be spared the discomfort of needle aspiration. Kang et al [70] warn about the potential difficulty of accurate lesion localization caused by pubic bone sonic attenuation when the injury is in the region of the proximal cavernosal artery or the distal common penile artery. They further reiterate the importance of accurate sonographic localization in cases where embolization may be anticipated because internal iliac artery or internal pudendal artery cannulization is easier from the contralateral femoral artery. The use of selective arterial embolization for the management of arterial priapism is somewhat controversial. The embolization of an arteriolacunar fistula in nonischemic priapism with an autologous clot was first reported by Wear et al [71] in 1977. Numerous reports in the literature have since documented use of this approach in high-flow priapism with variable success [72 82]. The recently published AUA guideline recommends that the initial management of nonischemic priapism should be observation [1]. This approach is based on the finding that expectant management results in spontaneous resolution in 62% of the reported cases (with erectile dysfunction in one third of cases) reviewed by the AUA Guideline
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panel. Many investigators have shown complete resolution of posttraumatic high-flow priapism without any invasive measures and the historical trend on the management of high-flow priapism gradually seems to be moving from surgery to embolization to expectant management [1,67,83]. Selective arterial embolization with autologous clot and absorbable gels are recommended for patients who request treatment [1]. The AUA guideline further states that any discussion of invasive treatment modalities including
surgery or embolization must be preceded by a thorough discussion of the various aspects of expectant management and the chances of spontaneous resolution. It should be noted that autologous clot is reported to be unstable by some investigators and is not widely used [80]. Superselective transcatheter embolization (Fig. 4) has been performed to occlude the source of arterial inflow with potential preservation of potency in up to 80% of patients in one recent report [84]. In rare
Fig. 4. A 40-year-old man with cocaine-induced priapism. He was confirmed to have low-flow priapism on ultrasound examination. After failure of urologic treatment, he was referred to radiology for embolization of the penile artery. The angiography (A, B) demonstrates the internal pudendal artery (straight arrow), the artery to the scrotal wall (curved arrow), and the dorsal artery of the penis (arrowhead). (C) Complete occlusion of the penile artery (arrowhead) after embolization with absorbable gelatin sponge using coaxial microcatheter. Arrow indicates the artery to the scrotal wall. B, bladder; P, priapism. (Courtesy of A. Blum, MD, and P. Kang, MD, Cleveland, OH.)
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instances, this treatment has been associated with perineal abscess formation [85]. When embolization is used, serial penile duplex studies should be performed in follow-up to assure complete resolution of the arterial lacunar fistula and ultimate restoration of normal cavernosal blood flow [67]. Based on the AUA Guideline recommendations and earlier work by the Boston University group, a course of watchful waiting with regular follow-up examinations should be discussed with the patient as a reasonable (if not preferred) alternative to maximize the chances of preserving potency and avoiding nonessential intervention in high-flow priapism [67]. When available, arterial embolization of arteriocavernous fistulas has been advocated by Volkmer et al [51] as the first line of therapy in prepubertal boys with traumatic high-flow priapism when hematologic or metabolic causes have been eliminated [51]. The authors report 26-month mean follow-up in three cases of high-flow priapism diagnosed by color Doppler ultrasound that presented 4 to 7 days after the injury. After diagnosis of the fistula location by angiography (branches of the internal pudendal artery in two and the bulbourethral artery in one patient), gelatin sponge (bulbourethral artery) or microcoil (internal pudendal artery) were used to occlude the fistula and achieve detumescence with preservation of erectile function in all three cases [51]. Traditionally, when embolization is performed, a unilateral approach has been recommended to avoid the dreaded complications of penile gangrene, gluteal ischemia, or erectile dysfunction [61,86]. Langenhuijsen et al [80], however, have described highly selective embolization of bilateral cavernous arteries in a case where unilateral embolization was unsuccessful. The authors advocate the use of the highly selective technique (cannulization of the cavernosal arteries) to minimize the risk of distal embolization of embolic material and use of resorbable materials (gelatin sponge) to allow for later recanalization and potential preservation of potency. The disadvantage of the absorbable materials is that they are not radiopaque and accurate placement can only be accomplished by frequent control arteriography during the procedure [80,87,88]. Callewaert et al [89] were the first to report superselective embolization in children using microcoils. Again, the advantage of the microcoils is that they allow precise placement into the branch supplying the fistula and may be performed bilaterally and yet maintain adequate penile blood flow to potentially preserve erectile function. Volkmer et al [42] advocate a combined interventional approach with intraoperative penile color Doppler ultrasound while performing arterial embolization to minimize iodinated contrast use and radiation exposure. This
approach allows precise angiographic catheter placement and is especially useful for reducing radiation exposure in children because of the higher likelihood of multiple arterial lacerations. For patients requesting treatment in areas with no access to tertiary care centers and angiographic expertise, a trial of cavernosal aspiration and corporal irrigation with a-adrenergic agents may be tried early in the course of priapism and has been associated with a positive outcome (resolution of priapism and ability to achieve normal erections with follow-up) in at least one case report [66].
Treatment The duration of the veno-occlusive period in priapism has a significant impact on the potential for recovery of spontaneous erections. Conservative measures and a trial of medical therapy should always be attempted before surgical therapy. Immediate reduction of intracorporeal pressure in low-flow states is of paramount importance. Treatment options are further separated based on the etiology. For patients with non sickle cell priapism, initial comfort measures include local penile or systemic anesthesia in the form of dorsal nerve block, circumferential penile block, subcutaneous local penile shaft block, and oral conscious sedation for the pediatric patient [43]. The initial diagnostic penile aspiration is also used as a therapeutic measure and, except where contraindicated, should be combined with intracavernosal instillation of a sympathomimetic agent (ie, phenylephrine injection after aspiration) to induce detumescence. This combination addresses the two important goals of therapy in low-flow states: decreased inflow (phenylephrine), and increased outflow and reduced pressures (aspiration). Transient increases in systemic blood pressure are possible and monitoring of vital signs is indicated when using sympathomimetic agents. Because of its potent and selective a1-adrenergic stimulatory properties and lack of b1-stimulatory effect, which could cause arrhythmias and angina in susceptible patients, phenylephrine is a preferred agent for achieving detumescence by intracavernosal injection and has been extensively reviewed by Lee et al [90]. These authors also have prepared a useful chart for preparation of dilutions of a-adrenergic agonists for intermittent injection or irrigation. Failing this approach, the next step in the process is irrigation with saline with or without pharmacologic agent except when contraindicated. The authors have successfully used a closed system for corporeal aspiration and irrigation as described by Futral and Witt
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[91] that has the advantages of reduced risk of body fluid exposure and corporeal contamination and the capacity for extended irrigation without repeated corporeal puncture. The authors agree with observations by Pautler and Brock [64] indicating that most cases of venoocclusive priapism treated without excessive delay (< 12 hours) respond to a-agonist therapy and that failure of resolution after 20 minutes of injection (0.1 mL/minute of a 500 1000 mg/mL phenylephrine solution for a total infused dose of 1 mg) calls for alternative strategies for management because these patients are unlikely to respond. The AFUD panel highly recommended first-line treatments (aspiration and irrigation) for low-flow priapism of more than 4-hours duration before undertaking more invasive surgical shunts and further suggested that these therapies have not shown a benefit in preserving potency when priapism has persisted beyond 72 hours [43]. Failure of resolution after conservative measures as described moves the step-care process to the surgical level. A number of different surgical shunts for diversion of blood away from the corpus cavernosum have been described. The consensus among authorities is that, in general, distal corporospongiosal shunts should be undertaken before proximal shunts; however, there is no consensus regarding the choice of percutaneous versus open surgical shunts. The authors prefer to start with a transglandular Winter shunt (corporoglandular) using a biopty gun biopsy device to create multiple channels between the corpus spongiosum and the corpora cavernosa [92]. If this technique is not successful, a larger communication between the corpora cavernosa and the corpus spongiosum may be created by a modified Al-Ghorab shunt in which the distal tunica albuginea of the corpora cavernosa is removed through a transglandular incision. Proximal shunts have been described by a number of authors and are recommended if these shunts fail and absent cavernosal artery flow is assessed by Doppler sonography [43,93]. A few authors have advocated early use of penile prostheses in cases of refractory or recurrent priapism associated with corporal fibrosis and erectile dysfunction [94]. The AFUD panel recommendations for management of priapism in patients with SCA include intravenous hydration and parenteral narcotic analgesia while preparing for aspiration and irrigation, supplemental oxygen, and exchange transfusion [43]. Initial efforts are directed at relief of pain and anxiety, and hydration with hypotonic fluids at 1.5 times maintenance. Powars and Johnson [95] state that in the static, hypoxic, and acidotic corporal environment, it is unlikely that red cells can reach the area of involve-
ment and question the use of red cell transfusion. Furthermore, they emphasize that blood volume and viscosity must be monitored closely in patients undergoing exchange transfusion or rapid single-unit transfusion, because there is an increased risk of cerebrovascular accident, coma, and intracranial hemorrhage. Low-flow infarctive priapism is uncommon. Nonetheless, adolescent patients are more likely to develop this condition compared with younger children who are more likely to respond to hydration, rest, analgesia, and warmth [95]. Failing conservative measures as described, the rest of the management algorithm for SCA patients with low-flow priapism is very similar to that described for non-SCA priapism. Stuttering or recurrent painful priapism episodes in this population have been managed successfully with instruction on sympathomimetic self-injection and gonadotropin-releasing hormone analogue injection in refractory cases [96,97]. This experience has been corroborated by the authors. Rutchik et al [98] have reported on a single case of refractory veno-occlusive priapism (failure of response to intracavernosal a-adrenergic injection or irrigation and recurrence after an Al Ghorab surgical shunt) that responded to intracavernosal injection of 15-mg tissue plasminogen activator [98]. The authors resorted to this therapy because of severe penile congestion and risk of penile necrosis with further shunting. It must be emphasized, however, that experience with this approach is very limited. A novel approach for treatment of priapism was suggested by deHoll et al [99] who described the use of methylene blue, a guanylate cyclase inhibitor, in 11 patients with priapism and reported immediate detumescence in 67%. A possible explanation for the success of this therapy is blockage of cyclic GMPinduced muscle relaxation following the initial aspiration attempts. Recently, successful treatment of recurrent idiopathic priapism with oral baclofen has been reported in two patients [100]. The treatment options for high-flow arteriogenic priapism mainly consist of conservative measures aimed at preservation of sexual function. Mechanical measures include external compression with occlusion of arterial inflow and topical application of ice. If these approaches fail, surgical, pharmacologic, or radiologic approaches may be used. Surgical and pharmacologic interventions have not had great success in resolution of highflow priapism and restoration of potency [67]. A detailed discussion of embolization therapy was presented in the previous section. There are very limited data on the safety and efficacy of surgical procedures for management of high-flow priapism and surgery was recommended as the option of last resort by the AUA Guideline panel [1].
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H. Sadeghi-Nejad et al / Radiol Clin N Am 42 (2004) 427443 [2] Papadopoulos I, Kelami A. Priapus and priapism: from mythology to medicine. Urology 1988;32:385. [3] Hinman F. Priapism: report of cases in a clinical study of the literature with reference to its pathogenesis and surgical treatments. Ann Surg 1914;60:689. [4] Taylor WN. Priapism of the corpus spongiosum and glans penis. J Urol 1980;123:961. [5] Burt FS, Scott WW. A new concept in the management of priapism. J Urol 1960;83:60. [6] Hauri D, Spycher M, Bruhlmann W. Erection and priapism: a new physiopathological concept. Urol Int 1983;38:138. [7] Dogra V, Bhatt S. Erectile dysfunction and priapism. In: Dogra V, Rubens D, editors. Ultrasound secrets. 1st edition. Philadelphia: Hanley & Belfus; 2004. p. 420 4. [8] Eland IA, van der Lei J, Stricker BH, et al. Incidence of priapism in the general population. Urology 2001; 57:970. [9] Compton MT, Miller AH. Priapism associated with conventional and atypical antipsychotic medications: a review. J Clin Psychiatry 2001;62:362. [10] Altman AL, Seftel AD, Brown SL, et al. Cocaine associated priapism. J Urol 1999;161:1817. [11] Steinhardt GF, Steinhardt E. Priapism in children with leukemia. Urology 1981;18:604. [12] Suri R, Goldman JM, Catovsky D, et al. Priapism complicating chronic granulocytic leukemia. Am J Hematol 1980;9:295. [13] Pohl J, Pott B, Kleinhans G. Priapism: a three-phase concept of management according to aetiology and prognosis. Br J Urol 1986;58:113. [14] Linet OI, Ogrinc FG. Efficacy and safety of intracavernosal alprostadil in men with erectile dysfunction. The Alprostadil Study Group. N Engl J Med 1996;334:873. [15] Ramos CE, Park JS, Ritchey ML, et al. High flow priapism associated with sickle cell disease. J Urol 1995;153:1619. [16] Fowler Jr JE, Koshy M, Strub M, et al. Priapism associated with the sickle cell hemoglobinopathies: prevalence, natural history and sequelae. J Urol 1991; 145:65. [17] Tarry WF, Duckett Jr JW, Snyder III HM. Urological complications of sickle cell disease in a pediatric population. J Urol 1987;138:592. [18] Emond AM, Holman R, Hayes RJ, et al. Priapism and impotence in homozygous sickle cell disease. Arch Intern Med 1980;140:1434. [19] Mantadakis E, Cavender JD, Rogers ZR, et al. Prevalence of priapism in children and adolescents with sickle cell anemia. J Pediatr Hematol Oncol 1999; 21:518. [20] Rubin SO. Priapism as a probable sequel to medication. Scand J Urol Nephrol 1968;2:81. [21] Ankem MK, Ferlise VJ, Han KR, et al. Risperidone-induced priapism. Scand J Urol Nephrol 2002; 36:91. [22] Abber JC, Lue TF, Luo JA, et al. Priapism induced by
Complications Early complications typically result from injection of a-adrenergic agents and include headaches, palpitation, hypertension, and cardiac arrhythmias. Vital signs should be monitored during this phase of therapy. Additional adverse events include urethral injury and urethrocutaneous or urethrocavernosal fistula from aggressive needle decompression, bleeding, and infection [101]. Rare cases of gangrene of the penis after corporospongiosal shunt have been reported [102]. Complications in high-flow states are usually secondary to the angiographic embolization used in the therapeutic stage of management. Use of angiography for diagnostic purposes is seldom necessary. Color duplex Doppler ultrasound evaluation and a thorough history and physical examination readily delineate the diagnosis in nearly all cases. Late complications are usually the sequelae of ischemic damage to cavernosal tissue and commonly manifest as corporal fibrosis and erectile dysfunction. Early decompression of the penis in the low-flow state is the most important preventive measure against these adverse events.
Summary Priapism is a relatively uncommon condition that may present as a medical emergency associated with significant pain and anxiety in the veno-occlusive or low-flow variant. Pharmacologic advances and, specifically, the availability of intracavernosal a-agonist therapy have dramatically improved the prospects of resolution for patients with low-flow priapism presenting within the first few hours of the acute episode. High-flow priapism is not considered an emergency and treatment measures are typically conservative aimed at preservation of potency. Urologists, radiologists, and other health care personnel caring for the patient with priapism must be familiar with various etiologic factors implicated in low-flow and high-flow priapism to formulate a logical stepcare approach. Differentiation of the low-flow from the high-flow state is perhaps the most critical initial diagnostic challenge that determines the sequence of further interventions including surgical shunts in lowflow priapism refractory to medical therapy.
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H. Sadeghi-Nejad et al / Radiol Clin N Am 42 (2004) 427443 chlorpromazine and trazodone: mechanism of action. J Urol 1987;137:1039. Myrick H, Markowitz JS, Henderson S. Priapism following trazodone overdose with cocaine use. Ann Clin Psychiatry 1998;10:81. Fiorelli RL, Manfrey SJ, Belkoff LH, et al. Priapism associated with intranasal cocaine abuse. J Urol 1990; 143:584. Mireku-Boateng AO, Tasie B. Priapism associated with intracavernosal injection of cocaine. Urol Int 2001;67:109. Rodriguez-Blaquez HM, Cardona PE, Rivera-Herrera JL. Priapism associated with the use of topical cocaine. J Urol 1990;143:358. Dubin NN, Razack AH. Priapism: ecstasy related? Urology 2000;56:1057. Kachhi PN, Henderson SO. Priapism after androstenedione intake for athletic performance enhancement. Ann Emerg Med 2000;35:391. Slayton W, Kedar A, Schatz D. Testosterone induced priapism in two adolescents with sickle cell disease. J Pediatr Endocrinol Metab 1995;8:199. Whalen RK, Whitcomb RW, Crowley Jr WF, et al. Priapism in hypogonadal men receiving gonadotropin releasing hormone. J Urol 1991;145:1051. Zargooshi J. Priapism as a complication of high dose testosterone therapy in a man with hypogonadism. J Urol 2000;163:907. Lapan DI, Graham AR, Bangert JL, et al. Amyloidosis presenting as priapism. Urology 1980;15:167. Bschleipfer TH, Hauck EW, Diemer TH, et al. Heparin-induced priapism. Int J Impot Res 2001;13:357. Goulding FJ. Priapism caused by glucose phosphate isomerase deficiency. J Urol 1976;116:819. Hebuterne X, Frere AM, Bayle J, et al. Priapism in a patient treated with total parenteral nutrition. JPEN J Parenter Enteral Nutr 1992;16:171. Wilson SK, Klionsky BL, Rhamy RK. A new etiology of priapism: Fabrys disease. J Urol 1973;109:646. Zimbelman J, Lefkowitz J, Schaeffer C, et al. Unusual complications of warfarin therapy: skin necrosis and priapism. J Pediatr 2000;137:266. Wilson F, Staff WG. Malignant priapism: an unexpected response to local anaesthetic infiltration of the dorsal nerves of the penis. Br J Surg 1982;69:469. Krco MJ, Jacobs SC, Lawson RK. Priapism due to solid malignancy. Urology 1984;23:264. Chan PT, Begin LR, Arnold D, et al. Priapism secondary to penile metastasis: a report of two cases and a review of the literature. J Surg Oncol 1998; 68:51. Witt MA, Goldstein I, Saenz de Tejada I, et al. Traumatic laceration of intracavernosal arteries: the pathophysiology of nonischemic, high flow, arterial priapism. J Urol 1990;143:129. Volkmer BG, Nesslauer T, Kuefer R, et al. High-flow priapism: a combined interventional approach with angiography and colour Doppler. Ultrasound Med Biol 2002;28:165.
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H. Sadeghi-Nejad et al / Radiol Clin N Am 42 (2004) 427443 [80] Langenhuijsen JF, Reisman Y, Reekers JA, et al. Highly selective embolization of bilateral cavernous arteries for post-traumatic penile arterial priapism. Int J Impot Res 2001;13:354. [81] Ravi R, Baijal SS, Roy S. Embolotherapy of priapism. Arch Esp Urol 1992;45:587. [82] Webber RJ, Thirsk I, Moffat LE, et al. Selective arterial embolization in the treatment of arterial priapism. J R Coll Surg Edinb 1998;43:61. [83] Arango O, Castro R, Dominguez J, et al. Complete resolution of post-traumatic high-flow priapism with conservative treatment. Int J Impot Res 1999;11:115. [84] Ciampalini S, Savoca G, Buttazzi L, et al. High-flow priapism: treatment and long-term follow-up. Urology 2002;59:110. [85] Sandock DS, Seftel AD, Herbener TE, et al. Perineal abscess after embolization for high-flow priapism. Urology 1996;48:308. [86] Steers WD, Selby Jr JB. Use of methylene blue and selective embolization of the pudendal artery for high flow priapism refractory to medical and surgical treatments. J Urol 1991;146:1361. [87] Colombo F, Lovaria A, Saccheri S, et al. Arterial embolization in the treatment of post-traumatic priapism. Ann Urol 1999;33:210. [88] Kerlan Jr RK, Gordon RL, LaBerge JM, et al. Superselective microcoil embolization in the management of high-flow priapism. J Vasc Interv Radiol 1998; 9:85. [89] Callewaert P, Stockx L, Bogaert G, et al. Post-traumatic high-flow priapism in a 6-year-old boy: management by percutaneous placement of bilateral vascular coils. Urology 1998;52:134. [90] Lee M, Cannon B, Sharifi R. Chart for preparation of dilutions of alpha-adrenergic agonists for intracavernous use in treatment of priapism. J Urol 1995; 153:1182. [91] Futral AA, Witt MA. A closed system for corporeal irrigation in the treatment of refractory priapism. Urology 1995;46:403. [92] Winter CC. Priapism cured by creation of fistulas between glans penis and corpora cavernosa. Trans Am Assoc Genitourin Surg 1977;69:31. [93] Sacher EC, Sayegh E, Frensilli F, et al. Cavernospongiosum shunt in the treatment of priapism. J Urol 1972;108:97. [94] Sundaram CP, Fernandes ET, Ercole C, et al. Management of refractory priapism with penile prostheses. Br J Urol 1997;79:659. [95] Powars DR, Johnson CS. Priapism. Hematol Oncol Clin North Am 1996;10:1363. [96] Levine LA, Guss SP. Gonadotropin-releasing hormone analogues in the treatment of sickle cell anemia-associated priapism. J Urol 1993;150:475. [97] Steinberg J, Eyre RC. Management of recurrent priapism with epinephrine self-injection and gonadotropin-releasing hormone analogue. J Urol 1995; 153:152.
[62] Desai KGJ. Hazards of long distance cycling. BMJ 1989;298:1072. [63] Lue TF, Hellstrom WJ, McAninch JW, et al. Priapism: a refined approach to diagnosis and treatment. J Urol 1986;136:104. [64] Pautler SE, Brock GB. Priapism: from Priapus to the present time. Urol Clin North Am 2001;28:391. [65] Koga S, Shiraishi K, Saito Y. Post-traumatic priapism treated with metaraminol bitartrate: case report. J Trauma 1990;30:1591. [66] Rudick DH. Successful treatment of arterial priapism with alpha-agonist irrigation: a rural experience. J Urol 2002;167:2132. [67] Hakim LS, Kulaksizoglu H, Mulligan R, et al. Evolving concepts in the diagnosis and treatment of arterial high flow priapism. J Urol 1996;155:541. [68] Mabjeesh NJ, Shemesh D, Abramowitz HB. Posttraumatic high flow priapism: successful management using duplex guided compression. J Urol 1999;161:215. [69] Bertolotto M, Quaia E, Mucelli FP, et al. Color Doppler imaging of posttraumatic priapism before and after selective embolization. Radiographics 2003; 23:495. [70] Kang BC, Lee DY, Byun JY, et al. Post-traumatic arterial priapism: colour Doppler examination and superselective arterial embolization. Clin Radiol 1998;53:830. [71] Wear Jr JB, Crummy AB, Munson BO. A new approach to the treatment of priapism. J Urol 1977; 117:252. [72] Belgrano E, Puppo P, Quattrini S, et al. Percutaneous temporary embolization of the internal pudendal arteries in idiopathic priapism: 2 additional cases. J Urol 1984;131:756. [73] Carmignani G, Belgrano E, Puppo P, et al. Idiopathic priapism successfully treated by unilateral embolization of internal pudendal artery. J Urol 1980;124:553. [74] Cohen GS, Braunstein L, Ball DS, et al. Selective arterial embolization of idiopathic priapism. Cardiovasc Intervent Radiol 1996;19:47. [75] Fratezi AC, Martins VM, Pereira Porta RM, et al. Endovascular therapy for priapism secondary to perineal trauma. J Trauma 2001;50:581. [76] Gorich J, Ermis C, Kramer SC, et al. Interventional treatment of traumatic priapism. J Endovasc Ther 2002;9:614. [77] Gujral S, MacDonagh RP, Cavanagh PM. Bilateral superselective arterial microcoil embolisation in delayed post-traumatic high flow priapism. Postgrad Med J 2001;77:193. [78] Kawakami M, Minagawa T, Inoue H, et al. Successful treatment of arterial priapism with radiologic selective transcatheter embolization of the internal pudendal artery. Urology 2003;61:645. [79] Kress O, Heidenreich A, Klose KJ, et al. Superselective embolization with coils in high-flow priapism. Cardiovasc Intervent Radiol 2002;25:326.
H. Sadeghi-Nejad et al / Radiol Clin N Am 42 (2004) 427443 [98] Rutchik S, Sorbera T, Rayford RW, et al. Successful treatment of recalcitrant priapism using intercorporeal injection of tissue plasminogen activator. J Urol 2001;166:628. [99] deHoll JD, Shin PA, Angle JF, et al. Alternative approaches to the management of priapism. Int J Impot Res 1998;10:11. [100] Rourke KF, Fischler AH, Jordan GH. Treatment of
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recurrent idiopathic priapism with oral baclofen. J Urol 2002;168:2552; discussion 2552. [101] De Stefani S, Savoca G, Ciampalini S, et al. Urethrocutaneous fistula as a severe complication of treatment for priapism. BJU Int 2001;88:642. [102] Fortuno RF, Carrillo R. Gangrene of the penis following cavernospongiosum shunt in a case of priapism. J Urol 1972;108:752.
Radiol Clin N Am 42 (2004) 445 456
Ultrasound evaluation of acute abdominal emergencies in infants and children

Pauravi Vasavada, MD
Department of Pediatric Radiology, University Hospitals of Cleveland, 11100 Euclid Avenue, Cleveland, OH 44106, USA
Ultrasonography is an essential component in the evaluation of acute abdominal pain and vomiting in children. Radiation exposure is a prime consideration in the pediatric population. Ultrasonography, unlike CT or fluoroscopy, allows the radiologist to acquire diagnostic information without the use of ionizing radiation. Ultrasound (US) can be performed in any imaging plane, which is advantageous when evaluating such structures as the pylorus and appendix, which may not be fixed in their orientation. Small children with abdominal pain often are not able to lie down quietly for a CT or MR image without the use of sedation. US, however, is able to obtain diagnostic images in nonsedated children. It is also cost effective, being far less expensive than CT or MR imaging. Real-time ultrasonography can be performed in the radiology department or at bedside in the emergency department [1,2].
Hypertrophic pyloric stenosis Hypertrophic pyloric stenosis (HPS) is the most common surgical disorder producing emesis in infancy [1,3]. The incidence of HPS is approximately 2 to 5 per 1000 births per year and it varies with the geographic area. HPS is less common in India, and among black and Asian population, with a frequency that is one third to one fifth compared with that in the white population [3]. Boys are four times more likely to be affected than girls, with the incidence significantly higher in first-born boys [2 4]. Although its etiology remains unknown, there is a familial predis-
E-mail address: vasavada@uhrad.com
position. Close to 7% of children with HPS have parents with the same condition [2,4]. Hypertrophic pyloric stenosis is characterized by a defect in contractility or relaxation of the circular muscle of the pylorus that results in hypertrophy of the pyloric circular muscle and narrowing of the pyloric channel [3,4]. This leads to stomach dilation and gastric outlet obstruction of variable severity. Pyloric stenosis should be suspected in neonates 3 to 6 weeks old with postprandial nonbilious vomiting. Symptoms, however, can be present in the first week of life or as late as 5 months of age. The patient classically presents with nonbilious vomiting that is projectile secondary to the pressures generated by the hypertrophied gastric muscles [5]. Persistent vomiting results in large losses of gastric secretions. Because only gastric secretions are lost, prolonged vomiting leads to hypokalemic, hypochloremic metabolic alkalosis. If uncorrected the condition can lead to malnutrition, weight loss, dehydration, and death. More recent evidence suggests, however, that more than 90% of infants with HPS present without any metabolic disorders. This lower incidence has been linked to proper diagnosis before protracted vomiting is allowed to occur, and it has been suggested that easy access to ultrasonography may be contributing to earlier diagnosis [6]. Nonbilious vomiting can present in several other conditions including gastroesophageal reflux disease and pylorospasm [4]. The clinical diagnosis of HPS has traditionally been made by palpation of an olive-shaped mass in the epigastrium representing the hypertrophic pyloric muscle. Palpation of a tumor-like mass in the right upper quadrant by an experienced examiner is usually considered specific and diagnostic without further testing [3,4,7]. In those infants in whom a mass is
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P. Vasavada / Radiol Clin N Am 42 (2004) 445456
Fig. 1. Fluoroscopic image from an upper gastrointestinal study in a patient with HPS. The double track sign (arrows) is formed by contrast material coming through the mucosal interstices of the canal.
not palpated unequivocally, an imaging examination is required. The diagnosis of HPS can be established by imaging upper gastrointestinal tract with the help of a radiographic contrast, such as barium, or by sonography. An upper gastrointestinal tract reveals a beak or a string sign because of the narrow opening of the pylorus or the double tract sign (Fig. 1) [2]. In patients with pyloric stenosis the muscle is hypertrophied and the intervening mucosa is crowded and
thickened and protrudes into the distended portion of the antrum resulting in the nipple sign. The upper gastrointestinal tract provides indirect information about the status of the pyloric channel based on the morphology of the canal lumen as outlined by contrast material. Secondary to this fact, failure of relaxation of the pyloric channel, known as pylorospasm, may be confused with pyloric stenosis. Upper gastrointestinal tract can be time consuming, because the radiologist has to wait for contrast to pass through the high-grade obstruction. Fluoroscopy time and radiation exposure may be prolonged. Upper gastrointestinal tract sensitivity rate has been reported to be approximately 95% but error rate as high as 11% has also been reported [3,7]. Sonography has become the modality of choice for the diagnosis of HPS. Sonography is documented to be a highly sensitive (90% 96%) and specific modality for the diagnosis of HPS [4]. US avoids radiation and allows direct visualization of the pyloric muscle as opposed to the upper gastrointestinal tract where the morphology of the muscle is inferred by the thinness and length of the barium through the area [1 3]. The sonographic examination is typically performed with a 5- to 7.5-MHz linear array transducer. A transducer up to 10 MHz can be used adjusted to the size of the infant and the depth of the pylorus [3,4]. The patient is placed in the right posterior oblique position, which allows fluid in the stomach to distend the antrum and pyloric region.
Fig. 2. (A,B) Sonograms in a patient with a normal pylorus. Longitudinal views demonstrate normal measurement of the pyloric muscle. The pyloric channel is not elongated measuring 1.1 cm, and the muscle wall is not thickened measuring 2.6 mm.
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Because the stomach in infants with pyloric stenosis is normally distended it is usually not necessary to introduce more fluid. If the antrum does not contain adequate fluid, a glucose solution or water can be given orally or through a nasogastric tube [3,4,7]. Occasionally, the stomach may become so distended and displace the duodenal cap caudally and medially rendering the pylorus difficult to visualize. In these cases, if the patient is placed in the supine or left posterior oblique (LPO) position, the pylorus is able to rise anteriorly for more optimal evaluation.
The pylorus is viewed in longitudinal and transverse planes. The examination begins by placing the transducer in the transverse plane, beginning at the gastroesophageal junction and following the contour of the stomach to its antrum. The duodenal cap is recognized by its arrowhead shape. By positively identifying the gastric antrum and the duodenal cap, the interposed pyloric channel can be imaged [7]. A negative study hinges on the diagnosis of a normal pyloric ring and a distensible pyloric portion of the stomach (Fig. 2) [3,7].
Fig. 3. Hypertrophic pyloric stenosis. (A,B) Longitudinal sonographic views demonstrate the hypertrophied pyloric muscle measuring 5.8 mm. The pyloric channel is elongated measuring 23 mm. (C) Cross-sectional view shows the thickened hypoechoic muscle surrounding the echogenic mucosa.
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On longitudinal views the muscle has a uniformly hypoechoic appearance. In the short axis view, the hypertrophic pyloric muscle has a target or bulls eye appearance reflecting the thickened hypoechoic muscle surrounding the echogenic mucosa. The sonographic hallmark of HPS is the thickened pyloric muscle (Fig. 3). The numeric value for the diagnostic muscle thickness has varied greatly. The exact recommended measurement includes a range of numbers with a broad range of sensitivities and specifications [8]. Controversy persists regarding the significance of muscle thickness between 3 and 4 mm. Some authors consider 3 mm as diagnostic, whereas others believe that this diagnosis cannot be made reliably until a muscle thickness of 3.5 to 4 mm has been attained [3,8]. The length of the hypertrophic canal is variable and may range from as little as 14 mm to more than 20 mm. Despite this variability in numbers in the literature, a patient with HPS has an examination and overall morphology of the pylorus that is characteristic of pyloric stenosis. The muscle thickness is at least 3 mm or more during the examination and the intervening lumen is filled with crowded or redundant mucosa through the center of the canal. Additionally, gastric peristaltic activity fails to distend the preduodenal portion of the stomach [3]. In patients without HPS the muscle does not measure more than 3 mm at any given time. Thick-
ening of the pyloric channel may be a transient phenomenon because of peristaltic activity or pylorospasm. During a normal examination, one can document the pyloric canal changing from a rigid linear morphology to a relaxed canal that permits pockets of fluid within the lumen. If the stomach is empty and the antrum is collapsed a small amount of fluid may be fed to the infant to document a normal fluid-filled antrum (Fig. 4). Patients in whom the pyloric canal relaxes to a normal morphology do not have pyloric stenosis. Patients in whom the muscle is 2 to 3 mm thick during the examination and does not relax warrant monitoring and follow-up examination. Because the cause and evolution of HPS are unknown, it is uncertain whether a young infant in whom the canal fails to relax completely will go on to develop HPS requiring surgery or whether the changes will be arrested and resolve with sequelae [3]. Potential causes of errors in the diagnosis of HPS are overdistention of the stomach, which may lead to displacement of the pylorus posteriorly making identification and measurement of the pyloric thickness more difficult. Additionally, offmidline or tangential images can lead to erroneous diagnosis of a thickened muscle [3,4]. The treatment of HPS is pyloromyotomy in which the hypertrophic muscle is split longitudinally. A study by Yoshizawa et al [9] showed that although
Fig. 4. (A, B) Sonographic images of the pylorus after the infant was given a small amount of fluid. Both images show fluid within the antrum passing through a normal pylorus (P, arrow) into the duodenum (D, arrow).
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the pyloric muscle thickness remains abnormal after surgery, by 5 months the dimensions gradually return to less than or equal to normal values.
Intussusception Intussusception is one of the most common causes of acute abdomen in infancy. The condition occurs when a segment of intestine (the intussusceptum) prolapses into a more caudal segment of intestine (the intussuscipiens). This condition usually occurs in children between 5 months to 2 years of age. In this age group most intussusceptions are idiopathic with no pathologic lead point demonstrated. More than 90% of intussusceptions are believed to be secondary to enlarged lymphoid follicles in the terminal ileum. Intussusception is more common in boys and the condition is rare in children younger than 3 months. The peak incidence is between 5 and 9 months of age. Lead points are noted in children younger than 3 months of age or greater than 2 years of age. Lead points include such entities as Meckels diverticulum, duplication cysts, intestinal polyps, lymphoma, and intramural hematomas [4]. Transient intussusception is seen in patients with celiac disease (sprue). Most intussusceptions involve the ileocolic region (75%), where the ileum becomes telescoped into the colon. This is followed in decreasing frequency by ileoileocolic, ileoileal, and colocolic intussusceptions. The classic clinical triad of acute abdominal pain (colic), currant jelly stools or hematochezia, and a palpable abdominal mass is present in less than 50% of children with intussusception [10,11]. Up to 20% of patients may be pain free at presentation. Additionally, in some instances lethargy or convulsion is the predominant sign or symptom. This situation results in consideration of a neurologic disorder rather than intussusception. Given the uncertainty of achieving an accurate clinical diagnosis, imaging is required in most cases to achieve an early and quick diagnosis to reduce morbidity and mortality. Delay may be lifethreatening because of the development of bowel necrosis and its complications [12]. Much controversy exists in the literature related to the diagnosis and management of intussusception. Realistically speaking children with intussusception can be managed successfully in a number of different ways. It is best to use diagnostic tools that are as benign as possible, however, to avoid potential harm to these children and to lessen the discomfort to the children who are not shown to have intussusception. Conventional radiography and the contrast enema examination have been the principal methods used for
Fig. 5. Intussusception. Plain radiograph demonstrates a round soft tissue density mass (arrows) in the right upper quadrant protruding into the gas-filled transverse colon.
the diagnosis and treatment of intussusception. Radiographs of the abdomen are useful and can suggest the diagnosis by showing a mass usually located in the right upper quadrant effacing the adjacent hepatic contour (Fig. 5). Other signs include reduced air in the small intestine, gasless abdomen, or obstruction of the small intestine [13 15]. Identification of a cecum filled with gas or feces in the normal location is the finding that allows exclusion of intussusception with most confidence [10,13]. In the presence of intussusception, plain radiography allows exclusion of bowel perforation, a major complication of intussusception. The accuracy of plain radiography in diagnosis on exclusion of intussusception ranges from 40% to 90% [13,16,17]. Barium enema examination has been the standard of reference for the diagnosis of intussusception for many years. At many institutions liquid enema or air enema examination is the principal diagnostic tool.
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Fig. 6. Meniscus sign. Image from barium enema reduction shows the rounded apex of the intussusception protruding into the column of contrast material.
transducer, 5 to 10 MHz, can be used to improve the definition of the image. The abdomen and the pelvis should be scanned in both longitudinal and transverse planes [1]. The intussusception mass is a large structure, usually greater than 5 cm. Most intussusception occurs in the subhepatic region often displacing adjacent bowel loops (Fig. 7). Even inexperienced operators can readily identify the intussusception on sonography. An intussusception is a complex structure. The intussuscipiens (the receiving loop) contains the folded intussusceptum (the donor loop), which has two components: the entering limb and the returning limb. The attached mesentery is dragged between the entering and returning limbs. Sonographically, the intussusception may demonstrate an outer hypoechoic region surrounding an echogenic center, referred to as a target or doughnut appearance (Fig. 8) [20]. The hypoechoic outer ring seen on axial scans is formed by the everted returning limb, which is the thickest component of the intussusception and the thin intussuscipiens. The echogenic center of intussusception contains the central or entering limb, which is of normal thickness and is eccentrically surrounded by hyperechoic mesentery [20]. Another pattern of imaging that has been described is that of multiple con-
The classic signs of intussusception at enema examination are the meniscus sign and the coiled spring sign. The meniscus sign is produced by the rounded apex of the intussusception (the intussusceptum) protruding into the column of contrast material (Fig. 6). The coiled spring sign is produced when the edematous mucosal folds of the returning limb of the intussusception are outlined by contrast material in the lumen of the colon. The enema examination, however, can be a very unpleasant experience for both the parent and child and is also associated with radiation. The role of sonography in the diagnosis of intussusception is well established with a sensitivity of 98% to 100% and a specificity of 88% to 100% [18]. It has been suggested that sonography should be the initial imaging modality and that the enema examination should only be performed for therapeutic reasons [11,18,19]. Sonography not only aids in the diagnosis of intussusception but it also allows the identification of patients who are candidates for therapeutic reduction. Sonography may also detect other abnormalities that are overlooked by the enema examination [4]. In addition, there is a high level of patient comfort and safety with US. A technique of graded compression is used for the sonographic evaluation of suspected intussusception. Because deep penetration of the US beam is not necessary in small children, a linear high-resolution
Fig. 7. Intestinal intussusception. Transverse sonographic image demonstrates a soft tissue mass in the right upper quadrant adjacent to the gallbladder (GB).
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Fig. 8. Target appearance. Transverse sonographic view demonstrates the intussusception. The hypoechoic outer layer represents the intussuscipiens and the central echogenic layer represents the intussusceptum (arrow).
centric rings. Within the bowel wall the mucosa and submucosa are echogenic, whereas the muscularis layer is hypoechoic. Multiple hypoechoic and hyperechoic layers are identified when there is little bowel edema present. This represents the mucosa, submucosa, and muscularis layers of the intussusceptum and intussuscipiens. With increasing degrees of bowel edema, the hyperechoic mucosal and submucosal echoes are obliterated in the intussusceptum resulting in fewer layers. On long axis scans the hypoechoic layers on each side of the echogenic center may result in a reniform or pseudokidney appearance (Fig. 9).
The pseudokidney sign is seen if the intussusception is curved or imaged obliquely [1]. Although the target and pseudokidney signs are the most common ultrasonographic signs used, they are not pathognomic because they have also been seen in normal or pathologic intestinal loops. Differential consideration for the US findings includes other causes of bowel wall thickening, such as neoplasm, edema, and hematomas. An inexperienced operator may mistake stool or psoas muscle for an intussusception. In addition to diagnosing the intussusception US has other advantages. US may detect the presence of a lead point, which is present in approximately 5% of intussusception. Various sonographic findings have been reported to be predictive of success of hydrostatic reduction. A study by Koumanidou et al [18] shows that the sonographic presence of enlarged mesenteric lymph node in the intussusception is a prediction of hydrostatic irreducibility. Small amounts of free peritoneal fluid are seen in up to 50% of cases. The presence of trapped peritoneal fluid within an intussusception correlates significantly with ischemia and irreducibility, however, because it reflects vascular compromise of the everted limb.
Fig. 9. Long-axis sonographic view shows an elongated appearance resulting in a pseudokidney appearance (arrow).
Fig. 10. Use of Doppler ultrasound to evaluate intussusception. Doppler ultrasound shows blood flow within the intussusception, suggesting its reducibility.
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Additionally, the absence of flow within the intussusception on color Doppler sonography correlates with a decreased success of reduction and a higher likelihood of bowel ischemia [21 23], and presence of color flow within the intussusception correlates with higher success rate of its reduction (Fig. 10). There are many different techniques used to reduce intussusception described in the literature. Water-soluble contrast material, barium, air enema guided by fluoroscopy, and physiologic saline solution combined with US have all been used [24,25]. The use of sonography to guide hydrostatic reduction has been predominately performed in the eastern hemisphere and is increasingly being used in Europe. The reduction rate is high (76% 95%), with only 1 perforation in 825 cases reported [25,26]. The procedure may be performed with water, saline solution, or Hartmann solution. The instilled fluid is followed as it courses through the large bowel until the intussusception is no longer visualized and the terminal ileum and distal small bowel are filled with fluid or air. There has been little experience with US-guided air enema therapy. Because air prevents the passage of the US beam, it may be difficult to visualize the ileocecal valve; therefore, small residual ileoileal intussusception can be observed. Additionally, it is difficult to detect perforation resulting in pneumoperitoneum [24]. Sonography has been shown to be highly successful in the diagnoses and reduction of intussusception. The appropriate use of US in children with suspected intussusception obviates the necessity for diagnostic enema, and the use of enema should be limited to therapeutic purposes [27].
Acute appendicitis Acute appendicitis is one of the major causes of hospitalization in children and it is the most common condition requiring emergency abdominal surgery in the pediatric population. The condition typically develops in older children and young adults with the diagnosis being rare under the age of 2. Clinical signs and symptoms associated with acute appendicitis include crampy, periumbilical, or right lower quadrant pain; nausea; vomiting; point tenderness in the right lower quadrant; rebound tenderness; and leukocytosis with a left shift [28]. When the history and clinical findings are classic, the diagnosis of acute appendicitis is often straightforward [29]. Not only do one-third of children with acute appendicitis have atypical findings, however, but also the presenting signs and symptoms of many nonsurgical conditions may mimic those of acute appendicitis. Most children
with acute abdominal pain have self-limited nonsurgical disease. Upper respiratory tract infections, pharyngitis, viral syndrome, gastroenteritis, and constipation are the most common associated conditions noted in these children. The actual prevalence of acute appendicitis in children presenting in the outpatient setting with acute abdominal pain ranges from 1% to 4% [28,30]. The delayed diagnosis of acute appendicitis can carry serious consequences. Perforation, abscess formation, peritonitis, wound infection, sepsis, infertility, adhesions, bowel obstruction, and death have been reported. Morbidity and mortality in acute appendicitis are related almost entirely to appendiceal perforation. The prevalence of appendiceal perforation in various pediatric series has ranged from 23% to 73%, with the perforation rate even higher in young children [28,31 33]. Up to half of children with perforated appendicitis may experience a complication, with nearly all deaths associated with perforated appendix [28]. For fear of missing the diagnosis and allowing the development of perforation, peritonitis, and sepsis, a low index of suspicion and early operative intervention have been recommended. As a result, negative laboratory rates as high as 20% have been reported with rates of 10% to 15% widely accepted [29,34,35]. Unnecessary appendectomy carries potentially major risks and substantial costs, however, prompting many to advocate increased efforts to avoid unnecessary appendectomy [36]. The goal of imaging in a child with suspected appendicitis should be to identify the presence of disease in patients with equivocal clinical findings. Used correctly, imaging should reduce the negative laparotomy and perforation rates and reduce the intensity and cost of care. The ideal diagnostic test should be fast, noninvasive, highly accurate, and readily available [37]. The primary imaging technique over the past decade for evaluating children with suspected appendicitis has been graded-compression US because it is widely available, noninvasive, and does not involve radiation [28,38 40]. The reported diagnostic accuracy of US in the diagnosis of acute appendicitis has varied greatly. The sensitivity of US has ranged from 44% to 94% and the specificity has ranged from 47% to 95% [28]. The clinical use of US lies primarily in the subgroup of children in whom the clinical findings are equivocal. Not only can it establish the diagnosis of appendicitis but also it can identify other abdominal and pelvic conditions, especially gynecologic, that present as right lower quadrant pain [28,41]. The graded-compression technique of US is performed with a high-resolution, linear-array transducer
453
of 5 to 10 MHz. Graded-compression sonography primarily consists of anterior forced compression to reduce the distance between the pathologic process and the transducer and to displace or compress bowel structures to eliminate gas artifacts. Reducing the abdominal cavity by compression enables clear visualization of the retroperitoneal structures [42]. Anterior compression is considered adequate when the iliac vessels and psoas muscles are visualized because the appendix is anterior to these structures. Scanning is performed in both longitudinal and transverse planes. The examination begins with the identification of the cecum and the terminal ileum. The ascending colon is a nonperistaltic structure containing gas and fluid. The terminal ileum is compressible easily and displays active peristalsis. The cecal tip where the appendix arises is approximately 1 to 2 cm below the terminal ileum. The examination can be expedited by asking the patient to point to the area of maximal tenderness. This can also aid in locating a retrocecal appendix [28]. In early nonperforated appendicitis, an inner echogenic lining representing submucosa can be identified. The inflamed, nonperforated appendix appears as a fluid-filled, noncompressible, blind-ending
tubular structure on longitudinal US image. The maximal appendiceal diameter from outside wall to outside wall is greater than 6 mm in an inflamed appendix. A noncompressible enlarged appendix measuring greater than 6 mm in maximal diameter is the only US sign that is specific for appendicitis (Fig. 11). Other findings of appendicitis include an appendicolith, which appears as an echogenic focus with acoustic shadowing; pericecal or periappendiceal fluid; and enlarged mesenteric lymph nodes. On transverse imaging a target appearance is delineated. This is characterized by a fluid-filled appendiceal lumen, which is surrounded by the echogenic mucosa and submucosa and hypoechoic muscularis layer. The US features of perforation include loss of the echogenic submucosal layer and presence of a loculated periappendiceal or pelvic fluid collection or abscess (Fig. 12) [43,44]. The appendix is visible in 50% to 70% of patients with perforated appendicitis [44]. The use of color Doppler has also been described in the evaluation of appendicitis. Color Doppler US of nonperforated appendicitis demonstrates peripheral wall hyperemia reflecting inflammatory hyperperfusion. Color flow may be absent in gangrenous
Fig. 11. Acute appendicitis. Longitudinal (A) and transverse (B) ultrasound images show an inflamed appendix (between the calipers), which is enlarged.
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secondary to causes other than appendicitis, such as Crohns disease or pelvic inflammatory disease. The use of US in patients with acute appendicitis is a subject of controversy in the literature [42]. Many studies have been performed to evaluate the use of US in the ultimate outcome of children with suspected appendicitis. Some studies have suggested that the use of US has not improved outcome in children with suspected appendicitis. A study by Roosevelt and Reynolds [49] showed no significant differences in the perforation rate or cost of care in children who underwent US compared with those who did not. A study by Lessin et al [29], however, suggests that the early and selective US in clinically equivocal cases could rapidly allow an accurate diagnosis, without the need for prolonged observation or hospitalization. There are several other tests that have been used to facilitate the diagnosis of acute appendicitis but the advantage of ultrasonography is its low cost, lack of radiation exposure, easy availability, and noninvasive nature [38].
Fig. 12. Right lower quadrant abscess. Two-year-old girl presented with abdominal pain. A complex mass in the right lower quadrant consistent with an appendiceal abscess was demonstrated on ultrasound.
Summary Ultrasound is extremely beneficial in the evaluation of acute pediatric abdominal disease, such as HPS, intussusception, and acute appendicitis. As techniques and equipment improve, its role in the evaluation of infants and children continues to increase.
appendicitis or early inflammation [45]. Color Doppler findings of appendiceal perforation include hyperemia in the periappendiceal soft tissue or within a well-defined abscess [46]. Color Doppler US does not increase the sensitivity of the examination but it does make interpretation of the gray-scale US findings easier and can increase observer confidence in the diagnosis of acute appendicitis. Most false-negative diagnosis results from failure to visualize the appendix. This may be secondary to operator dependency, inability to compress the right lower quadrant adequately, a retrocecal position of the appendix, or appendiceal perforation [37,42]. In patients with obesity the high-frequency transducer may fail to reach the necessary depth, which makes accurate diagnosis difficult because of decreased spatial resolution. Another pitfall is early inflammation limited to the appendiceal tip, which can be missed if only the proximal appendix is imaged [47,48]. False-positive diagnosis has also been reported. The normal appendix, which may be visible in 10% to 50% of children and adolescents, may be mistaken for appendicitis. The normal appendix measures 6 mm or less, is compressible, and lacks adjacent inflammatory changes. Periappendiceal changes may also be
References
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P. Vasavada / Radiol Clin N Am 42 (2004) 445456 in the diagnosis of hypertrophic pyloric stenosis. J Ultrasound Med 1999;18:773 7. Yoshizawa J, Eto T, Higashimoto Y, Saitou T, Maie M. Ultrasonographic features of normalization of the pylorus after pyloromyotomy for hypertrophic pyloric stenosis. J Pediatr Surg 2001;36:582 6. del-Pozo G, Albillos JC, Tejedor D, Calero R, Rasero M, de-la-Calle U. Intussusception in children: current concepts in diagnosis and enema reduction. Radiographics 1999;19:299 319. Shanbhogue RL, Hussain SM, Meradji M, Robben SG, Vernooij JE, Molenaar JC. Ultrasonography is accurate enough for the diagnosis of intussusception. J Pediatr Surg 1994;29:324 8. Kim MC, Strouse PJ, Peh WC. Clinics in diagnostic imaging (80). Ileocolic intussusception. Singapore Med J 2002;43:645 8. Sargent MA, Babyn P, Alton DJ. Plain abdominal radiography in suspected intussusception: a reassessment. Pediatr Radiol 1994;24:17 20. Bisset III GS, Kirks DR. Intussusception in infants and children: diagnosis and therapy. Radiology 1988; 168:141 3. Ratcliffe JF, Fong S, Cheong I, OConnell P. Plain film diagnoses of intussusception: prevalence of the target sign. AJR Am J Roentgenol 1992;158:619 21. Eklof O, Hartelius H. Reliability of the abdominal plain film diagnosis in pediatric patients with suspected intussusception. Pediatr Radiol 1980;9:199 206. Meradji M, Hussain SM, Robben SG, Hop WC. Plain film diagnosis in intussusception. Br J Radiol 1994;67: 147 9. Koumanidou C, Vakaki M, Pitsoulakis G, Kakavakis K, Mirilas P. Sonographic detection of lymph nodes in the intussusception of infants and young children: clinical evaluation and hydrostatic reduction. AJR Am J Roentgenol 2002;178:445 50. Verschelden P, Filiatrault D, Garel L, Grignon A, Perreault G, Boisvert J. Intussusception in children: reliability of US in diagnosis a prospective study. Radiology 1992;184:741 4. del Pozo G, Albillos JC, Tejedor D. Intussusception: US findings with pathologic correlation-the crescentin-doughnut sign. Radiology 1996;199:688 92. Lim HK, Bae SH, Lee KH, Seo GS, Yoon GS. Assessment of reducibility of ileocolic intussusception in children: usefulness of color Doppler sonography. Radiology 1994;191:781 5. Lam AH, Firman K. Value of sonography including color Doppler in the diagnosis and management of long standing intussusception. Pediatr Radiol 1992; 22:112 4. Lagalla R, Caruso G, Novara V, Derchi LE, Cardinale AE. Color Doppler ultrasonography in pediatric intussusception. J Ultrasound Med 1994;13:171 4. Rubi I, Vera R, Rubi SC, Torres EE, Luna A, Arcos J, et al. Air reduction of intussusception. Eur J Pediatr Surg 2002;12:387 90. Riebel TW, Nasir R, Weber K. US-guided hydrostatic
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Radiol Clin N Am 42 (2004) 457 478
Emergent ultrasound interventions

Dean A. Nakamoto, MD*, John R. Haaga, MD
Department of Radiology, Case Western Reserve University, 11100 Euclid Avenue, Cleveland, OH 44106, USA
Interventional radiologists are frequently asked to perform emergent diagnostic and therapeutic procedures. The choice of image guidance depends on user preference; availability of CT, ultrasound, and MR imaging; and the ability of the modality to visualize the target. Ultrasound is the most preferred modality and has many advantages including real-time imaging of the needle tip during the procedure; multiplanar imaging capabilities; its relatively low cost; and the equipment is mobile, so procedures can be performed at the bedside of critically ill patients in the intensive care unit. Ultrasound-guided interventions have become very common in many institutions [1,2]. Emergent procedures frequently performed with ultrasound guidance include thoracentesis, paracentesis, percutaneous nephrostomy, and percutaneous cholecystostomy. The role of ultrasound guidance has also expanded to include abscess drainage, particularly in the pelvis, and chest tube placement. This article discusses various emergent interventions performed with ultrasound imaging guidance.
effusion. Ultrasound evaluation before the procedure confirms the presence of fluid and distinguishes pleural fluid from atelectasis, mass, or elevated diaphragm. Typically, the patient is seated upright. Pleural fluid is generally anechoic, although debris or septations may be present. The diaphragm must be identified, and the underlying liver or spleen. A 3- to 4-MHz sector or vector probe is usually sufficient to survey the hemithorax quickly. Technique Most diagnostic and therapeutic thoracenteses are performed with ultrasound guidance. Typically, the patient is seated upright with his or her back to the interventionalist. To perform the procedure safely, there should be at least one rib interspace of fluid above and below the puncture site. If there is less fluid, the procedure may be deferred depending on the clinical urgency and the ability of the patient to cooperate. Very small pleural fluid collections can be aspirated safely, however, if the patient can cooperate with breath-holding. Patients who cannot sit upright are placed either supine or in a lateral decubitus position. In either of the latter two positions, there must be a larger amount of fluid to attempt thoracentesis. Because ultrasound can be performed portably, ultrasound-guided thoracenteses can be performed in an ICU, even on mechanically ventilated patients [3]. If visualization is difficult because of patient body habitus, air in the pleural fluid, or the patients inability to be positioned adequately, CT guidance may be helpful. Initial scanning should be performed with a sector, vector, or curvilinear probe. This is to document the amount of fluid and quickly to find the largest pocket of fluid. At this time, it is important to verify the location of the diaphragm. Scanning can then be performed with a linear probe of 6 MHz. This enables
Ultrasound-guided chest interventions Thoracentesis Ultrasound-guided thoracentesis is usually performed easily because most pleural fluid collections are accessible using percutaneous methods. In the septic patient, a diagnostic thoracentesis is usually performed to evaluate for empyema. Other indications include evaluation for chylous, bloody, or malignant
* Corresponding author. E-mail address: Nakamoto@uhrad.com (D.A. Nakamoto).
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D.A. Nakamoto, J.R. Haaga / Radiol Clin N Am 42 (2004) 457478
Fig. 1. Aberrant intercostal artery. This sagittal color Doppler scan performed with a 6-MHz linear probe demonstrates an aberrant, tortuous course of the intercostal artery (arrow). Here the artery is situated close to the midpoint of the rib interspace. In this location, the artery is more susceptible to injury from a needle.
accurate localization of the rib interspace, particularly in obese patients. The location of the intercostal artery (Fig. 1) also is verified at this time. Although the artery is usually directly adjacent to the inferior aspect of the rib, it can be located more inferiorly and in the rib interspace. If the patient has a malignancy, pleuralbased metastases can also be visualized at this time and avoided (Fig. 2). It is important to be able to recognize hypoechoic, consolidated lung and not mistake it for pleural fluid. Sometimes consolidated
lung may mimic complex fluid (Fig. 3) and color Doppler may be helpful to verify the presence of pulmonary vessels in consolidated lung. Following sterile preparation of the skin, local anesthesia should be administered from the skin surface to the pleural surface. Although one could use ultrasound to visualize needle insertion directly, typically a site is marked on the skin surface and the needle is advanced until fluid is obtained. A variety of needles and catheters are available for thoracenteses. The simplest method is to use an 18- or 20-gauge angiocatheter. The angiocatheter with puncture needle is advanced into the pleural space until fluid is aspirated, and then the angiocatheter is advanced into the pleural space over the puncture needle. Single-step 6F trocar-based catheters (Skater, Medical Device Technologies, Gainesville, Florida) are also available, particularly if the procedure is both diagnostic and therapeutic. These are used in a similar fashion. After a thoracentesis, the authors obtain a chest radiograph in posteroanterior view to evaluate for pneumothorax. The chance of pneumothorax is small and generally ranges from 2.5% to 7.5% [4 7], although rates up to 13.9% have been reported [8]. Symptoms caused by pneumothorax include shortness of breath and shoulder pain on the affected side. Some investigators do not advocate routine postprocedure chest radiograph for the asymptomatic patient, because of the low complication rate [4,9,10]; however, because sizable pneumothoraces may be asymptomatic, the authors routinely obtain a chest radiograph. The mechanisms of postthoracentesis pneumothorax
Fig. 2. Pleural-based metastases. This patient with metastatic lung cancer was referred for therapeutic thoracentesis. The pleuralbased mass was noted (cursors); a different location was used.
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Fig. 3. Consolidated lung mimicking complex pleural fluid. This patient was referred for possible thoracenteses. Longitudinal vector scan of the left hemithorax demonstrates complex-appearing mixed solid and cystic foci in the hemithorax (arrowheads) consistent with consolidation of the lung.
include (1) inadvertent introduction of air into the pleural space, usually by leaving the needle or catheter open to the air after the tip is in the pleural space; (2) puncture of the lung; and (3) rupture of the visceral pleura because of a decrease in pleural pressure [4,11]. If the pneumothorax is large, is symptomatic, or increases with time, the patient may require a chest tube placement. Other significant complications of thoracentesis include pain, vasovagal reaction, bleeding, and reexpansion pulmonary edema. Pleuritic pain may be caused by the rubbing of the visceral and parietal pleural surfaces after the fluid has been removed. Pain during the procedure may also be caused by the inability of the patients collapsed lung to re-expand as the fluid is removed. This may be an indication to stop the procedure [4,7]. Vasovagal reactions may occur during any interventional procedure. The patient may become transiently bradycardic, hypotensive, and may then lose consciousness. Predisposing factors include volume depletion. A quick physical examination of these patients shows bradycardia, diaphoresis, dilated pupils, and hypotension. These vasovagal reactions are usually minor and temporary. Placing the patient in the Trendelenburg position to improve venous return to the heart usually resolves the problem. If the patient improves within a few minutes, no other action is needed. If significant, the patient may require atropine. Typical atropine doses are as follows: adult 1 mg intravenously; children0.02 mg/kg to 0.60 mg (maximum) intravenously. The treatment interval is every 3 to 5 minutes to a total of 3 mg for adults or 2 mg for children. If the atropine does not improve the
situation, then urgent consultation with the resuscitation team is appropriate. Re-expansion pulmonary edema is an uncommon complication of uncertain etiology. It may be asymptomatic; however, it can cause various degrees of hypoxia and can even be life-threatening [12,13]. It presents as unilateral pulmonary edema, which may progress to bilateral edema [4,12]. Re-expansion pulmonary edema is believed to be more likely if a large volume (ie, greater than 1 L) of pleural fluid is aspirated at one time. Some investigators have removed up to 2 L at one time, however, without adverse consequences [4,7]. Bleeding is an uncommon complication. The risk is higher in patients with coagulopathies. It also may occur with inadvertent laceration of the intercostal artery [14]. The authors typically check platelets, prothrombin time and partial thromboplastin time, and International Normalized Ratio (INR) before any procedure and adjust accordingly. They prefer platelet counts over 50,000, and the prothrombin time to be within 2 seconds of normal, or INR less than 1.5. Fine-needle aspirations may be performed outside of these ranges. Every case, however, should be individually tailored. Ultrasound-guided chest tube insertion Pleural effusions can occur in a variety of settings, including pneumonia (parapneumonic effusion); malignancy; bleeding; and fluid overload. The pleural fluid can be classified as transudative or exudative, depending on the laboratory analysis as described in Box 1. Parapneumonic effusions are generally
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Box 1. Lights criteria for diagnosis of exudative effusions

Pleural fluid protein to serum protein
ratio > 0.5

Pleural fluid to serum L-lactate
dehydrogenase ratio > 0.6

Pleural L-lactate dehydrogenase con-
centration more than two thirds of the normal upper limit for serum L-lactate dehydrogenase *satisfying any one of these criteria suggests exudative nature Data from reference [16].
either radiologic or surgical. The third stage usually requires surgical decortication, although there are some data suggesting that the pleural peels may resolve with closed-tube drainage [17]. Anechoic pleural collections or collections with fine linear septations on ultrasound respond best to catheter drainage, whereas those with a complex honeycomb pattern usually fail catheter drainage and require decortication. Patients showing parietal pleural thickness greater than 5 mm are unlikely to respond to catheter drainage. Indications for chest tubes and technique The primary indication for chest tube placement is to drain an empyema and prevent progression to the organized stage. This can be accomplished with surgical drainage or closed-tube drainage. Closedtube drainage can be performed with blind insertion of a large-bore (22 34F catheter) chest tube placed by a surgeon or with image-guided chest tube placement using CT or ultrasound. Typically, smaller-bore, 8 to 14F catheters are used with the image-guided methods. The smaller tubes placed by imaging methods are usually better tolerated by the patients than the larger, surgically placed tubes. Therapeutic options for infected pleural collections are summarized in Box 3. Large pleural fluid collections are amenable to single-step trocar catheters. The patient can be positioned either upright or in a lateral decubitus position with the affected side up. As with a thoracentesis, initial scanning should confirm the location of the diaphragm and the overall size of the effusion. Once a site is marked and the skin is sterilely prepared, adequate local anesthesia should be used from the skin surface to the pleural surface. A small incision should be made with a scalpel, and the tract should be dilated with a small hemostat. An initial aspiration can be performed with a 19-gauge sheath needle with a disposable 5F tetra-fluoro-ethylene (TFE) catheter (Yueh centesis disposable catheter needle, Cook,
divided into complicated and uncomplicated effusions. The uncomplicated effusions are transudative effusions and small free-flowing exudative effusions. These effusions can resolve spontaneously with antibiotic treatment. The complicated effusions are exudative effusions that do not respond to medical treatment and require drainage. Empyema, hemothorax, and malignant effusions are all complicated effusions. Indications for drainage of pleural fluid are given in Box 2. Regarding parapneumonic effusions, there are three stages in the evolution of empyema [15,16]. The first stage is a free-flowing exudative effusion. The second stage is the fibrinopurulent stage during which the cellularity and protein content of the effusion increase. Fibrin is deposited on the visceral and parietal surfaces. The third stage is the organization stage; fibroblasts and capillaries grow into exudates and form a pleural peel. If untreated, this stage can result in lung entrapment and subsequent fluid drainage into the chest wall or into the lung. Empyema requires emergent drainage to control sepsis. The first two stages should be drained by closed-tube drainage,
Box 2. Indications for drainage of pleural fluid

A very large pleural effusion causing
Box 3. Therapeutic options for infected pleural collections

cardiorespiratory embarrassment
Grossly purulent or hemorrhagic
pleural fluid Positive Gram stain pH > 7.2 Glucose < 40 mg/dL L-lactate dehydrogenase > 1000 U/L
Antibiotics Tube thoracotomy Intrapleural fibrinolytics (urokinase) Thoracoscopy with lysis of adhesions Decortication Open surgical drainage
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Bloomington, Indiana) to determine the viscosity of the fluid. A trocar based, self-retaining catheter can then be inserted blindly or under ultrasound visualization, depending on the size of the effusion. If the effusion is thin, a single-step, 6 to 8F catheter (Skater, Medical Technologies, Gainesville, Florida) can be placed. Although 10F and larger catheters are avail-
able on single-step trocars, the authors have found that these larger catheters can be difficult to insert in a single-step procedure. If a 10F or larger catheter is needed, the Seldinger technique can make catheter insertion easier (Fig. 4). A standard 0.035-inch angiographic guidewire can be placed through the 5F Yueh catheter and the tract can then be dilated.
Fig. 4. Complex left pleural effusion in heart transplant patient, left chest tube placement. (A) Longitudinal vector scan demonstrates a large loculated left pleural effusion, which inverts the left hemidiaphragm. (B) Schematic representation illustrating the procedure. Under ultrasound guidance, a 19-gauge disposable sheath needle (Yueh centesis needle) is placed into the effusion at the level of the midaxillary line. The needle is withdrawn, a small amount of fluid is aspirated, and a standard 7.5-mm J 0.035-inch angiographic guidewire is placed. (C) The tract is sequentially dilated to 10F catheter, and a 10F catheter self-retaining nephrostomy-type tube is placed. Arrows point to nephrostomy tube.
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Box 4. Indications for external drainage of lung abscess

Persistent sepsis after 5 to 7 days of
for such patients should not be delayed. Complications from chest tube insertion include sepsis, inappropriate pathway of chest tube, bleeding, and injury to adjacent organs. Lung abscesses Most lung abscesses are caused by oropharyngeal aspiration of bacteria as can occur with alcoholic stupor, general anesthesia, seizures, or cerebral vascular accidents [28,29]. Other causes include malignancy, septic emboli, foreign bodies, and lung cysts [28,29]. It is important to distinguish between lung abscess and empyema because empyema requires external drainage, whereas most lung abscesses resolve with medical management [30]. The distinction between lung abscess and empyema is best made with contrast-enhanced CT. A lung abscess appears round and if it contacts the pleural surface, it forms an acute angle with the pleura. Empyema is more biconvex in shape and forms obtuse angles with the pleura. The wall of an abscess may have thick and irregular enhancement, whereas the enhancing pleura with empyema has a smooth curvilinear appearance (ie, the split pleura sign) [31]. Indications for external drainage of lung abscess [32] are summarized in Box 4. Relative contraindications for external drainage of lung abscess are given in Box 5. The abscess-pleural symphysis occurs when a lung abscess is continuous with the pleura. It is important to have a needle traverse the abscess-pleural symphysis to decrease the chances of complications, such as leak of abscess fluid into the pleural space and bronchopleural fistula. Catheter drainage is usually performed by CT; however, ultrasound can be used in selected cases. If the abscess-pleural symphysis is small, CT is the modality of choice because it is easier to place the needle accurately under CT guidance. Because lung abscesses may have fine strands of residual normal parenchyma, which can bleed, one should not be too aggressive with catheter insertions or guidewire manipulations [32].
antibiotic therapy
Abscesses 4 cm or more in diameter
that are under tension

Abscesses 4 cm or more in diameter
that are enlarging

Failure to wean from a ventilator
because of a large abscess
CT is the preferred method for smaller effusions or effusions close to vital structures, such as the heart or major vessels. When placing the chest tube, a lateral approach is preferred rather than a direct posterior approach, if possible. The ideal site for catheter placement is usually at the level of the midaxillary line; the authors try to avoid a direct posterior approach so that the patient does not lay on the tube. Once the tube is placed, some of the fluid should be withdrawn to confirm the location of the tube. Direct visualization with ultrasound should also document the location. The tube should be secured to the skin and placed to a water-seal pleural drainage system (Pleur-Evac, Deknatel, Fall River, Massachusetts) with suction at 20 cm H2O. Patients are monitored daily to ensure proper tube functioning and to record the amount of drained fluid. Once the fluid becomes serous, the tube output has decreased to 20 mL or less per 24 hours, and the patient has defervesced, the tube may be removed. A CT scan should be performed before tube removal to ensure that there are no undrained collections. Additional drainage tubes may be placed for any separate collections not being drained. Many empyemas are loculated, which can make chest tube drainage difficult. Fibrinolytic agents, such as streptokinase and urokinase, have been used successfully to lyse septations [18 20]. Because urokinase is not always available, the authors have been using streptokinase, 125,000 IU every 12 hours for up to 2 days. Success rates range from 70% to 94%, with a cumulative success rate of approximately 85% in various radiologic studies [19 27]. Not all empyema are amenable to percutaneous drainage. Patients who develop a pleural peel or who have persistent fevers and elevated white blood cell counts despite adequate drainage and appropriate antibiotics may require surgical drainage and decortication. Surgical treatment
Box 5. Relative contraindications for external drainage of lung abscess

Noncompliant patient Lack of an abscess-pleural
symphysis
Coagulopathy
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Ultrasound-guided abdominal interventions Paracentesis Ultrasound-guided paracentesis is a commonly performed procedure. Typically, the procedure is performed emergently in a septic patient as a diagnostic procedure to evaluate for spontaneous bacterial peritonitis [33] or for hemoperitoneum in the setting of trauma [34]. More commonly, this procedure is performed urgently as a therapeutic measure for symptomatic relief of tense ascites. Initial scanning is performed with a sector or curvilinear probe to find the largest pocket. Attention is then made to the abdominal wall to ensure that there are no vessels at the site of subsequent needle puncture, such as the epigastric artery or collateral vessels in a patient with cirrhosis. In patients with malignancy, one should ensure that there are no peritoneal metastases at the needle insertion site. This can be performed with a linear transducer, usually of 6 MHz or greater. The preferred site for large-volume paracentesis is chosen in the dependent position, such as right or left lower quadrants. The site of puncture is chosen usually lateral to the rectus muscle to avoid the accidental puncture of the inferior epigastric artery. The inferior epigastric artery normally travels at the junction of the medial two thirds and lateral one third of the rectus or approximately 5 cm laterally from the midline (Fig. 5). After standard sterile skin preparation, 1% lidocaine is injected into the abdominal wall for local anesthesia. The authors anesthetize all the
way to the parietal peritoneum. Then they perform the aspiration with a standard 18-gauge angiocatheter. If the patient is obese, the authors use a 15- or 20-cmlong, 19-gauge sheath needle (Yueh centesis disposable catheter needle; Cook, Bloomington, Indiana). For smaller collections or collections adjacent to major vessels or to the spleen, the authors use direct ultrasound guidance with either the freehand technique or the needle guide. Large-volume paracentesis provides rapid resolution of symptoms with minimal complications and is well tolerated by most patients. Complications from paracentesis have rarely been reported, and include inferior epigastric artery pseudoaneurysm [35], hemorrhage after large-volume paracentesis [36 38], bowel perforation [38], hypotension [39], and a fragment of the catheter left in the abdominal wall or peritoneum [38]. Postparacentesis circulatory dysfunction has been reported and is characterized by hyponatremia, azotemia, and an increase in plasma renin activity. Postparacentesis circulatory dysfunction is associated with an increased mortality and may be prevented by administration of albumin intravenously (6 to 8 g/L of ascites removed) along with large volume parasynthesis (LVP). Percutaneous cholecystostomy Acute cholecystitis in high-risk patients in the ICU is difficult to manage. In critically ill, oftentimes septic patients with possible acalculous or gangrenous cholecystitis, percutaneous cholecystostomy may be
Fig. 5. Paracentesis, epigastric artery. (A) Color Doppler transverse image of the anterior abdominal wall with a 6-MHz linear transducer was used to localize the location of the inferior epigastric artery (arrow) before paracentesis. This is the typical location along the lateral aspect of the rectus abdominis muscle. (B) CT scan on a different patient demonstrates the location of the epigastric arteries (arrowheads).
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both diagnostic and therapeutic. These patients are not suitable candidates for surgery. Percutaneous cholecystostomy is used as a diagnostic and therapeutic procedure in these critically ill and difficult to manage patients [26,40 43]. In unstable patients with calculous cholecystitis, percutaneous cholecystostomy permits stabilization so that cholecystectomy can be performed electively. Indications Percutaneous cholecystostomy may be performed in critically ill septic patients to exclude acute cholecystitis, because of the difficulties of establishing the diagnosis of acute cholecystitis in these patients [26,44,45]. The findings on the various diagnostic tests can be nonspecific. A sonographically normal gallbladder virtually excludes cholecystitis in an ICU patient, and a positive sonographic Murphys sign may be the most specific finding of acute cholecystitis in these patients [46]. Other findings, such as sludge, distention, pericholecystic fluid, wall thickening, and striations, are nonspecific in this setting [46,47]. The presence of gallstones, distention, and pericholecystic fluid, however, have been described as findings that may predict a more favorable response to percutaneous cholecystostomy [41,47] Technique Two access routes are used. The transhepatic route approaches from the right midaxillary line and aims for the bare area of the gallbladder. This route is preferred by most investigators and theoretically reduces the risk of bile peritonitis [26,41,42,48]. The transperitoneal approach is from the anterior abdomen and is aimed at the gallbladder fundus [41,49 51]. Because of the risks of bile peritonitis and inadvertent perforation of the colon, the transperitoneal approach is probably best reserved for patients with very distended gallbladder in which the gallbladder fundus abuts the anterior abdominal wall. This approach is also useful in patients with coagulopathy or underlying liver disease [41,43,49 51]. The transhepatic route for percutaneous cholecystostomy does not always result in a puncture of the bare area of the gallbladder and the free peritoneal surface of the gallbladder may still be punctured [52]. Some investigators have also used simple aspiration of the gallbladder contents without placement of a drainage tube [45,53]. The authors typically use the transhepatic approach and ultrasound guidance. Sometimes CT guidance may be necessary, however, particularly for a liver in a high subcostal location. Typically, a small 6F single-step trocar catheter (Skater, Medical Device Technologies, Gainesville, Florida) is used. If
the trocar-based catheter buckles against the liver or gallbladder wall, the Seldinger technique can be used (Fig. 6). The acutely inflamed gallbladder wall can be friable and catheter and wire manipulations should not be too aggressive. If the Seldinger technique is used, the authors use a 5F catheter on a 19-gauge needle (Yueh centesis disposable catheter needle, Cook, Bloomington, Indiana) to puncture the gallbladder lumen. They then use a standard 0.035-inch guidewire; carefully dilate the tract to 8F catheter; and then place an 8F catheter, self-retaining nephrostomy tube. The authors recommend not using a super-stiff guidewire, such as an Amplatz, because it may perforate the gallbladder wall. If the transperitoneal approach is used, a small 8F catheter or less, single-step trocar catheter is recommended. The gallbladder lumen should be punctured with a sharp jab, and the gallbladder should be emptied once the catheter is within [49]. The Seldinger technique is not favored with this technique, because there is a theoretical risk of bile leakage into the peritoneum. Once the self-retaining tube is within the gallbladder, it is recommended that it remain there for at least 2 to 3 weeks to allow formation of a mature tract along the catheter; otherwise, there may be bile leakage once the catheter is removed [42,48]. It also is recommended that a cholangiogram be performed before catheter removal to ensure patency of the cystic duct and common bile duct [26,48,54]. Some investigators also advise imaging the tract at the time of tube removal [26,43,44], although other investigators disagree [41,49] even if the transperitoneal approach is used [49]. Complication rates generally range from 5% to 13.8% [41,43,45,49,51,55]. Complications include bleeding, bile leakage, catheter dislodgement, and vasovagal events. Bile leakage has been reported with both the transhepatic and transperitoneal approaches. Technical success rates (ie, adequate placement of a drain in the gallbladder) are high (ie, as great as 97% 100%) [26,41 43,45,47 49,56]. Overall patient response is lower, however, because of the relatively low threshold of clinicians to request the procedure and the nonspecificity of the diagnostic tests; no clinical response to the procedure can be found in up to 42% of the patients [26,42]. Placement of a cholecystostomy tube is still helpful in these circumstances, however, because it does reassure the clinicians that cholecystitis is not a cause of a patients sepsis. Some investigators have used simple gallbladder aspiration in patients with suspected acute cholecystitis [45,53]. Simple percutaneous gallbladder aspiration does seem to be beneficial in patients with acute cholecystitis and comorbid conditions. Chopras et al
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Fig. 6. Ultrasound-guided percutaneous cholecystostomy in a patient status-post recent myocardial infarction. (A) Longitudinal vector scan demonstrates distended gallbladder with sludge and a thick wall. Initial attempts with a 6F catheter one-step trocarbased catheter were not successful, because of the thickened gallbladder wall. The catheter buckled on the trocar. The Seldinger technique was used. A 19-gauge disposable sheath needle (Yueh centesis needle) was used to enter the gallbladder lumen. A standard 0.035-inch angiographic guidewire was placed, the tract was carefully dilated to 8F catheter, and a self-retaining 8F catheter nephrostomy-type tube (arrowhead) was placed. (B) Schematic representation of the procedure described in Fig. 6A.
[45] patient population, although at high surgical risk, consisted of noncritically ill patients. As stated in their article, they excluded patients who had had prolonged admission to the ICU. Intra-abdominal abscess drainage Image-guided percutaneous abscess drainage is a well-established technique, which has become the
primary method of treatment for many patients with intra-abdominal abscess [18,57 60]. In many hospitals in the United States, CT is the imaging modality of choice to detect abscesses. Once detected, an abscess can be drained using either CT or ultrasound guidance depending on which modality best delineates the abscess and its surrounding structures. In general, CT is used for abscesses inaccessible to ultrasound, such as abscesses in deep locations adjacent to vital
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structures (eg, major vessels or those adjacent to bone), which may block the ultrasound beam. These abscesses include pancreatic, interloop, and deep retroperitoneal abscesses. Abscesses in more superficial locations of the peritoneum or visceral organs are usually amenable to ultrasound guidance. Ultrasound has many advantages, including its lower cost, its ability to be performed portably at the patients bedside, and its multiplanar imaging capabilities.
Indications In general, intraperitoneal abscesses adjacent to the abdominal wall and abscesses in the periphery of visceral organs, such as the liver or kidney, are amenable to ultrasound-guided aspiration and drainage. The authors always avoid traversing uninvolved spaces or organs, such as the liver or bowel, when performing any interventional procedure. The exceptions are traversing the stomach for pancreatic procedures and traversing the rectum or vagina for pelvic abscess drainages. Other investigators have reported success without significant complications from traversing uninvolved spaces or organs while performing interventional procedures [61 63]. If a loop of bowel is inadvertently traversed with a catheter, the catheter should be left in place for 2 to 3 weeks so a tract can form. After this period the catheter can usually be removed safely without spillage of bowel contents into the peritoneum [64,65]. This assumes that the underlying bowel is otherwise normal and that there is no distal bowel obstruction. Relative contraindications common to all percutaneous procedures include coagulopathy, the patients inability to cooperate, and lack of safe access to the abscess.
Technique Simple, uncomplicated abscess drainage is described next. Management of more complex abscesses, such as infected hematomas, abscesses associated with fistulae, and fungal abscesses, is also discussed. Pelvic abscesses, particularly those caused by gynecologic sources, are discussed separately. Preprocedure imaging is best performed with CT because the size of the fluid collection, its location, and extent can be well-delineated. The authors typically review the patients CT before the procedure and if possible have a copy of the CT in the ultrasound suite when performing the procedure. The CT provides an excellent roadmap to help plan the needle trajectory. The authors frequently use a commercially available needle guide, although for superficial abscesses they use the freehand technique. For most
abscesses, the Seldinger technique is favored unless the abscess is very large and superficial. After obtaining informed consent, the fluid is localized and the needle trajectory planned. The site for needle insertion is marked, and the skin is prepared and draped in a sterile manner. The ultrasound probe is then covered with a sterile cover, and the needle guide is attached unless the procedure is performed freehand. A skin wheal is raised with local 1% lidocaine, and a skin nick is made with a scalpel. Using a 19-gauge sheath needle (Yueh centesis disposable catheter needle; Cook, Bloomington, Indiana), the projected needle tract is anesthetized to the fluid collection. The fluid collection is then punctured with the 19-gauge sheath needle, the 5F disposable sheath catheter is advanced over the needle, the sharp needle is then removed, and the fluid is aspirated through the 5F disposable catheter sheath. If the fluid is purulent, a standard 0.035-inch angiographic guidewire can be advanced into the abscess. After confirming the location of the guidewire, the tract can be dilated and an appropriate-sized, self-retaining nephrostomy tube can be placed. For thin pus, 8 to 10F catheters are usually sufficient. Catheters up to 14F can be used for more viscous pus. The tube position should then be verified so that additional purulent fluid can be aspirated. The catheter is then secured to the skin either with sutures or adhesive fixation devices (Percu-Stay Percutaneous Catheter Fastener, Derma Sciences, Princeton, New Jersey). Routine catheter care is then performed. The authors place catheters to gravity drainage. Daily tube rounds are made to evaluate the drainage progress. Once the fluid becomes serous, the tube output has decreased to less than 20 mL per 24 hours, the patient has defervesced, and the white blood cell count is normal, the tube may be removed. The authors typically repeat a CT scan before tube removal to ensure that there are no residual fluid collections.
Liver abscess Pyogenic liver abscesses located in the periphery are amenable to ultrasound aspiration and drainage. Those located more centrally are better approached with CT guidance. Typically, a cuff of normal parenchyma should be included within the needle trajectory to prevent spillage of the abscess contents into the peritoneum (Fig. 7). The pleural space, loops of bowel, and large intrahepatic vessels should be avoided. Multilocular abscesses may be drained; however, close follow-up and additional catheters may be necessary [62]. The cure rate for liver abscess
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Fig. 7. Ultrasound-guided liver abscess drainage in a septic patient whose previous catheter was inadvertently pulled out. (A) CT scan demonstrates residual abscess in the dome of the right lobe of the liver (arrows). (B) Transverse ultrasound of the liver demonstrates the 8F pigtail catheter (arrowhead) placed by the Seldinger technique into the abscess by a subphrenic approach.
is about 80% to 90%. Causes of failures of percutaneous drainage of liver abscess are given in Box 6.
Percutaneous nephrostomy The main emergent indication for percutaneous nephrostomy is pyohydronephrosis, which can occur in native or a transplant kidney. Other urgent indications include a rapidly rising creatinine level or recent endourologic complication. Indications of percutaneous nephrostomy are summarized in Box 7. Ultrasound is an excellent method to guide the initial needle placement for percutaneous nephrostomy. These procedures are typically performed in the angiography suite using a portable ultrasound unit. Although the entire procedure can be performed with fluoroscopic guidance only, ultrasound is very
Renal and perinephric abscess Renal and perirenal abscesses may be drained using ultrasound guidance; however, such abscesses are usually better detected and delineated by CT [66]. This is particularly important for abscesses in the pararenal space because they can extend from the pelvis to the diaphragm. A posterolateral approach is preferred because it avoids the erector spinal muscles, colon, liver, and spleen.
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Box 6. Causes of failures of percutaneous drainage of liver abscess Preprocedure Unable to access the abscess safely Improper pathway to abscess Inability to place the catheter appropriately within the abscess Postprocedure Premature withdrawal of catheter Dislodged catheter Catheter kinked or occluded High-output fistula to gastrointestinal tract Fungal abscess Infected necrotic tumor Viscous pus or multiple septations, resistant to fibrinolytic therapy Sepsis or death
their numbers were small. Green [68] described successful percutaneous drainage in only one of four patients. Lucey et al [67] successfully drained five of six splenic abscesses; the one failure required a splenectomy. The authors believe that splenic abscess drainage should only be performed in rare circumstances and should generally be reserved for select patients. Close consultation with the surgical service is recommended so that an emergent splenectomy can be performed if needed. If percutaneous drainage of a splenic abscess is to be attempted, the abscess ideally should be peripheral so that the least amount of normal splenic parenchyma is traversed. Thanos et al [69], however, have performed drainages in two patients where the needle and catheter traversed 2.3 cm of normal splenic parenchyma. Fistulae Uncomplicated abscesses have gradually decreasing output following percutaneous drainage. In those abscesses with persistently elevated output (ie, greater than 100 mL per 24 hours) more than 3 to 4 days after
useful for obtaining initial access to the renal collecting system [20,67], particularly in cases where the hydronephrosis is mild, or for renal transplants where the renal axis can vary. For a native kidney, the authors target a posterior calyx using a posterolateral approach to avoid most of the erector spinus muscles. For transplant kidneys, the authors target an anterior calyx. Typically, they use a 20-gauge Chiba needle for initial access, followed by instillation of contrast and a small amount of air (3 5 mL) to confirm the needle position (Fig. 8). The air rises to the nondependent calices. If the needle position is satisfactory, the tract can be dilated with a micropuncture set through the 20-gauge Chiba needle. If there is a better site to access the collecting system, a second needle can then be placed under fluoroscopic guidance using either a 20-gauge Chiba needle or 19-gauge sheath needle (Yueh centesis needle). The tract is dilated using the Seldinger technique, and an 8 to 14F catheter selfretaining nephrostomy tube can be placed. Splenic abscess Splenic abscess if untreated have a mortality rate of 80% to 100% and mortality rate of 14% to 30% with surgical drainage. Experience with percutaneous drainage is limited [59,68 70]. Although no major complications were reported in these series [59,70],
Box 7. Indications for percutaneous nephrostomy 1. Relief of urinary obstruction Improve renal function Evacuate pyonephrosis Assess recoverable renal function in chronic obstruction 2. Diversion of urine in case of urinary leakage Traumatic or iatrogenic urinary tract injury Inflammatory or malignant urinary fistula 3. Provide access for urinary manipulation Perform dynamic flow-pressure studies (Whitaker test) Biopsy Stone therapy Benign stricture dilatation Ureteral stent placement Foreign body retrieval Nephroscopic surgery (eg, endopyelotomy) Administration of antifungal agents
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Fig. 8. Ultrasound-guided percutaneous nephrostomy in a renal transplant with pyohydronephrosis caused by ureteral calculus. (A) Initial ultrasound demonstrates complex-appearing urine within the hydronephrotic transplant, which is consistent with pyohydronephrosis. The indwelling stent is noted (arrows). (B) Longitudinal ultrasound of the dilated distal transplant ureter demonstrates an obstructing calculus in the cursors. Note the twinkle artifact from the calculus with the color Doppler. (C) Longitudinal image during placement of a nephrostomy tube (arrowhead). (D) Schematic representation of the kidney and positioning of the catheter.
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twice a day-for 2 days, may improve drainage from such hematomas. Fungal abscess Fungal abscesses are difficult to treat with percutaneous drainage and may require surgical drainage and debridement [18,73]. This is probably caused by the extensive tissue invasion, necrosis, and mycotic plaque formation in the wall of the cavity [18]. Echinococcal abscess A number of investigators have described successful treatment of hydatid cysts using percutaneous aspiration and drainage [74 79]. The technique is similar to routine abscess aspiration and drainage. Various catheter irrigants are used, such as hypertonic saline [74,79], scolicidal agent [75], or alcohol [76,77,79]. Anaphylaxis is a potential complication, which can be severe or even fatal [78]. Many of the patients were given prophylaxis with albendazole. Some investigators perform single-step aspiration [74,77], whereas others aspirate the smaller cysts and leave catheters in larger (> 6 cm) cysts [75,78,79]. Pelvic abscesses Image-guided percutaneous drainage (Fig. 9) is commonly performed for pelvic abscesses. Typically, pelvic abscesses arise from gastrointestinal sources, such as diverticulitis, ruptured appendicitis, and Crohns disease, and from postoperative fluid collections. In female patients, pelvic abscesses may also arise from gynecologic sources, such as tubo-ovarian abscess from pelvic inflammatory disease. Such pelvic abscesses are traditionally treated with medical therapy and if drainage of abscess is required many investigators prefer image-guided interventional techniques [80 87]. Pelvic abscesses in a female secondary to gynecologic causes are a special category and usually have acute presentation. Imaging-guided pelvic abscess drainage offers several advantages to traditional surgical drainage. The imaging-directed methods are less invasive and do not require general anesthesia. The indications for surgical drainage include ruptured tubo-ovarian abscess, when diagnosis is uncertain; pelvic abscess secondary to appendicitis or ruptured viscus [88]; and failed percutaneous drainage. The imaging-guided methods include transabdominal, transgluteal, transrectal, and transvaginal approaches. The transperineal approach has also been described [89]. In general, the transabdominal approach is preferred,
Fig. 8 (continued ).
initial catheter placement, especially drainage consisting of bilious or enteric material, a gastrointestinal fistula is likely [71,72]. At this point a sinogram confirms the communication to the gastrointestinal tract. The cause of the fistula should then be determined so that appropriate treatment may be initiated. Fistulae caused by distal obstruction, neoplastic involvement, or ongoing infection must have these underlying conditions corrected or the abscess does not heal. Low-output fistulae (ie, less than 320 mL per day) usually close spontaneously without additional therapy [18]. High-output fistulae may require additional treatment, including suction on the abscess catheter, and bowel rest often with nasogastric tube placement. Hyperalimentation may be necessary, and surgical intervention may be required [18]. Infected hematomas Most infected hematomas do not drain with simple catheter placement because of their extensive amount of fibrin and the protective effects of fibrin on bacteria [18]. For patients with a suspected infected hematoma, the authors perform an initial aspiration. If the fluid is bloody but not grossly infected, they only take a sample for laboratory analysis and do not place a catheter for the fear of secondary infection. If the fluid is grossly purulent or if the cultures subsequently come back positive for infection, a drainage catheter is placed. Sometimes local instillation of fibrinolytic agents, such as streptokinase, 125,000 IU
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Fig. 9. Ultrasound-guided pelvic abscess drainage, transabdominal, in a postsurgical patient. (A) Initial CT scan demonstrates abscesses in the right and left lower quadrants of the pelvis (arrows). (B) Under ultrasound guidance the abscess in the right lower quadrant was localized and punctured with a 19-gauge sheath needle. After confirming pus, a standard 0.035-inch angiographic guidewire (Rosen) was advanced into the abscess. The tract was dilated to 10F catheter, and a self-retaining 10F catheter nephrostomy tube (arrowhead) was placed. (C) The left lower quadrant abscess was then localized. Initial attempts were made with a 12F one-step catheter; however, the patient complained of too much discomfort. This abscess was also punctured with a 19-gauge sheath needle. After confirming pus, the tract was dilated and a 12F catheter nephrostomy tube was placed (arrowhead). (D) Schematic representation of the procedure.
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abscess drainage and may be a viable alternative for patients who have undergone abdominoperineal resection [89]. Technique The transvaginal approach is best performed with ultrasound guidance (Fig. 10). First, the abscess should be localized by endovaginal ultrasound. The abscess should be directly adjacent to the vaginal vault with no intervening structures. The ultrasound probe then is removed and the perineum and vagina are prepared with a standard povidone-iodine solution. A vaginal speculum is then inserted and the vaginal vault is prepared using sponges soaked in iodine-iodine solution. The speculum is then removed. Despite the iodine-iodine preparation, the vagina is still semi-sterile. If the patient is not already receiving intravenous antibiotics, she should be given an appropriate antibiotic before beginning the procedure. Because it can be difficult to hold the ultrasound probe while doing the various catheter manipulations, the procedure generally requires two people. The endovaginal ultrasound probe is then fitted with a modified guide to allow catheter insertion. The commercially available needle guides typically do not allow placement of trocar-based catheters. Various methods can be used [80,88], although the authors prefer using the plastic sheath that comes with the catheter, as described by ONeill et al [79]. The endovaginal probe is initially placed in a sterile probe cover with coupling gel. A modified guide then is made from the plastic catheter protector. The plastic protector is cut so that approximately 5 cm of the catheter protrudes beyond the end of the guide; a slit is then made along the length of the guide, which facilitates subsequent removal of the guide from the catheter. This modified guide is then attached to the sterilely prepared endovaginal probe with sterile rubber bands along the groove intended for the metal probe guide. The 6 to 8F trocar-based catheter (Skater, Medical Device Technologies, Gainesville, Florida) is then placed into the modified guide and a second sterile probe cover is placed over the catheter and guide. The catheter punctures the outer sterile probe cover before puncturing the vaginal wall. One can attempt to use local lidocaine at the vaginal wall but this can be difficult because there are no landmarks to ensure that the same area is traversed with the catheter. Before placing a catheter, an initial aspiration should be performed using an 18- to 20-gauge needle to document infection. Initial scanning should be done to place the abscess centrally within the scan plane and to visualize where the catheter enters the abscess. The tip of the trocar-based catheter should indent the
Fig. 9 (continued ).
using CT or ultrasound, because it is very welltolerated by patients. Pelvic abscesses may not be accessible using the transabdominal approach, however, because of the presence of intervening loops of bowel, urinary bladder, major blood vessels, or the uterus. The transgluteal approach has several disadvantages, including patient discomfort, injury to the sciatic nerve, and an increased chance of catheter kinking and subsequent malfunction [84,90]. Although initially underused, some investigators have recently been successful using the transgluteal approach [90 93]. The transrectal [94 97] and transvaginal approaches are well established [60,80 84,88,98]. The transrectal approach can be guided using CT [94], ultrasound [95 97,99], or ultrasound combined with fluoroscopy [100]. The transvaginal approach is usually guided with ultrasound. Most patients with tubo-ovarian abscesses respond to intravenous antibiotic therapy. As expected, the response to antibiotics is inversely related to the size of the abscess [82]. In unruptured tubo-ovarian abscesses not responding to antibiotics, image-guided drainage is indicated. The decision to proceed with drainage is usually made in conjunction with the gynecologic service. The authors prefer the transabdominal approach, if possible, followed by the transrectal approach with CT guidance, and finally the transvaginal approach with ultrasound. Female patients tolerate transrectal catheter placement better as compared with transvaginal placement [99]. The authors use the transgluteal approach only when necessary (ie, a deep pelvic abscess in a patient with underlying rectal mucosal disease or in premenarchal or sexually inactive females). The transperineal approach provides an additional option for deep pelvic
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Fig. 10. Ultrasound-guided transvaginal pelvic abscess drainage. (A) Photograph shows the trocar catheter advanced through the guide and projecting approximately 5 cm past the end of the probe (arrow). Note that the guide (plastic sheath) needs to be cut to a length such that it allows at least 5 cm of catheter advancement so that the catheter can be advanced through the vaginal vault. (B) Photograph shows the catheter has been fed off and the pigtail has been formed. The inner needle has been removed, but the outer metal cannula stiffener is left in the straight portion of the catheter to stiffen it and ease the peeling away of the guide from the catheter. (C) CT scan shows a complex right adnexal fluid collection (straight arrow). An incidentally noted right-sided fundal fibroid is noted (curved arrow). (D) Transvaginal ultrasound scan shows trocar-catheter assembly (arrow) in the right adnexal collection along the guide. (From ONeill MJ, Rafferty EA, Lee SI, et al. Transvaginal interventional procedures: aspiration, biopsy, and catheter drainage. Radiographics 2001;21:657 72; with permission.)
wall of the abscess during light palpation. Assuming there are no intervening structures and the trajectory is appropriate, the abscess wall is punctured using a sharp thrust of 1 to 2 cm. This is the most difficult part of the procedure. It is helpful to apply enough pressure with the endovaginal ultrasound probe so that the vaginal wall is taut before being punctured with the trocar. The sharp needle of the trocar is removed and a diagnostic aspiration is performed. Once pus is aspirated, the catheter is advanced over the metal stiffener of the trocar until the self-retaining loop is formed and locked. The endovaginal probe is then removed carefully and the rubber bands and outer sterile cover gradually are cut. The modified guide is then removed
from the catheter. This is easier to perform if the metal stiffener is placed partially within the catheter. The stiffener is then removed and more pus is aspirated. Because of difficulties in penetrating the vaginal wall, the authors have found that 10F or smaller catheters are easier to insert. Although the single-step trocar-based catheter is in general easier to perform, the authors find the Seldinger technique useful for inserting larger catheters into abscesses with thick pus [84,101,102]. For experienced operators, ultrasound alone can be used. Alternatively, a combination of ultrasound and fluoroscopy can be performed. With the Seldinger technique, the abscess is punctured with a 19-gauge sheath
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needle with a disposable 5F TFE catheter (Yueh centesis disposable catheter needle; Cook, Bloomington, Inidana). After aspirating pus to confirm its location, the 19-gauge needle is removed, leaving the 5F catheter in the abscess, and a standard 0.035inch angiographic guidewire is advanced into the abscess. The 5F TFE catheter is then removed and a standard 5F pigtail catheter is placed over the guidewire and coiled into the abscess. Placement should be confirmed with ultrasound. The disposable 5F TFE catheter is not long enough to allow a guidewire to coil within the abscess. The 0.035-inch guidewire is removed, and a 0.035-inch Amplatz wire (Amplatz Super Stiff, Boston Scientific, Medi-Tech, Miami, Florida) is advanced into the 5F pigtail catheter. The 5F pigtail catheter is then removed, the tract can be dilated up to 14F catheter, and an appropriate size of self-retaining nephrostomy-type tube can be placed. If the abscess is large enough, an Amplatz wire can be introduced initially; however, this must be done carefully to avoid perforating the wall of the abscess with the super-stiff wire. The stiffness of the Amplatz wire (Amplatz Super Stiff, Boston Scientific, Medi-Tech, Miami, Florida) allows the tract to be dilated despite the distance between the operators hands and the point of wire insertion in the vaginal wall. Less stiff guidewires may kink. All of the dilatations can be performed through the modified guide on the endovaginal probe. Some investigators perform simple needle aspiration of an abscess without catheter placement [81,103 106]. Although large, multiloculated collections can be treated this way, this method may be most useful for small, unilocular collections. Nelson et al [80] found no correlation between the size of an abscess and the success rates for simple aspiration. The advantages of this method are that it is safe, easier to perform than catheter drainage, and there is no problem with catheter misplacement or dislodging. The disadvantages include multiple punctures for multiloculated abscesses, an extended period of antibiotic coverage to control residual infection, and repeat aspiration for recurrent abscess [81,88]. For this method, a standard needle guide attached to an endovaginal probe can be used with an 18- to 20-gauge needle. The needle must be at least 18 to 20 cm long to fit through the needle guide. Contraindications include diffuse multifocal abscesses or abscess with peritonitis, abscesses associated with fistulas, foreign bodies, or abscesses caused by pancreatitis. After the catheter is placed in the abscess and locked in position, the authors tape the catheter to the patients leg. Routine catheter care is then used. The catheters are left to gravity drainage. The authors do
not routinely flush the catheters unless they are using fibrinolytic agents, such as streptokinase. Success rates for transvaginal drainage range from 78% to 100% [60,81,82,84,98,106]. Similar success rates are noted for the other methods (ie, transabdominal, transrectal, and transgluteal) of pelvic abscess drainage, ranging from 94% to 100% [83,91,94,96]. Complications from transvaginal drainage are infrequent and include bleeding, infection, underlying organ damage, and vaginal fistula formation. Catheter dislodgement may occur following any drainage procedure; however, this did not adversely affect patient outcome in three of four patients in the study of Ryan et al [94].
Summary The interventionist can perform many emergent procedures with ultrasound guidance, because of its real-time, multiplanar imaging capability and portability. With the use of color Doppler, additional important information, such as aberrant vessels, can be ascertained to help plan needle trajectory. Ultrasound is also useful for nonemergent procedures, such as biopsies. All interventionists are encouraged to be facile with the use of ultrasound.
Acknowledgment The authors thank Elena DuPont of the radiology department at University Hospitals of Cleveland for the line drawings and Joe Molter for assisting in the preparation of images.
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Radiol Clin N Am 42 (2004) 479 486
Index
Note: Page numbers of article titles are in boldface type.
A
Abdomen, interventional ultrasonography in. See Interventional ultrasonography. Abdominal aortic aneurysms, aortic endografting for, 372 373 complications of, 369 370 CT of, 373 Ehlers-Danlos syndrome and, 370 risk factors for, 368 ultrasonography of, 365 373 anatomy and histology in, 365 366 as screening tool, 370 false aneurysms, 370 371 flow characteristics in, 366 for aortic dissection, 371 372 inflammatory aneurysms, 371 limitations of, 370 mycotic aneurysms, 371 technique for, 366 368 Abdominal ectopic pregnancy, ultrasonography of, 333 Abdominal injuries, emergency ultrasonography of, 421 Abdominal surgery, during pregnancy, ultrasonography in, 323 Abortion, spontaneous, and first-trimester bleeding, 301 303, 306 ultrasonography of, 322 Abruption, placental, ultrasonography of, 319 Abscesses, abdominal, interventional ultrasonography for. See Interventional ultrasonography. intratesticular, ultrasonography of, 353 354 liver, diagnosis of, 268 270 lung, interventional ultrasonography for, 462 tubo-ovarian, ultrasonography of, 338 339 Abscess-pleural symphysis, lung abscesses and, 462
Acalculous cholecystitis, acute, ultrasonography of, 260 Acute painful scrotum, ultrasonography of, 349 363 anatomy in, 349 350 for appendageal torsion, 356 357 for cellulitis, 353 for epididymo-orchitis, 351 353 for Fourniers gangrene, 351 for idiopathic varicocele, 357 358 for inguinal hernia, 360 361 for intratesticular abscess, 353 354 for intratesticular arteriovenous malformation, 359 for intratesticular varicocele, 358 359 for primary orchitis, 353 for secondary varicocele, 358 for testicular torsion, 354 356 for testicular trauma, 359 360 for testicular tumor, 361 technique for, 350 351 Adenomas, hepatic, ultrasonography of, 271 273 Adnexal masses, ultrasonography of, 329 348 corpus luteal cysts, 329 331 cystadenocarcinoma, 342 cystic teratomas, 341 diverticulitis, 344 ectopic pregnancy, 331 334 abdominal, 333 adnexal ring sign in, 332 cervical, 333 double decidual sac sign in, 332 b-human chorionic gonadotropin in, 334 interstitial, 333 intradecidual sign in, 331 332 management of, 333 334 endometriomas, 339 340 epiploic appendages, 345 follicular cysts, 329 leiomyomata, 340 341 luteoma of pregnancy, 338 ovarian hyperstimulation syndrome, 334 336
0033-8389/04/$ see front matter D 2004 Elsevier Inc. All rights reserved. doi:10.1016/S0033-8389(04)00032-6
480
Index / Radiol Clin N Am 42 (2004) 479486
ovarian neoplasms, 341 ovarian torsion, 336 338 pelvic inflammatory disease and tubo-ovarian abscess, 338 339 perforated appendicitis, 343 344 serous and mucinous cystadenomas, 341 342 theca lutein cysts, 334 Adnexal ring sign, in ectopic pregnancy, 332 Amniotic sac, ultrasonography of, 301 Androgens, and priapism, 430 431 Aneurysms, ultrasonography of, abdominal aortic. See Abdominal aortic aneurysms. iliac artery, 377 379 peripheral artery, 379 popliteal, 379 splanchnic artery, 377 splenic artery, 377 in pregnancy, 325 Ankle-brachial index, in arterial injuries, 383 384 Antipsychotic drugs, and priapism, 430 Aortic dissection, ultrasonography of, 371 372 Aortic endografting, for abdominal aortic aneurysms, 372 373 Appendageal torsion, scrotal, ultrasonography of, 356 357 Appendicitis, acute, in infants and children, 452 454 ultrasonography of, 453 454 perforated, ultrasonography of, 343 344 Arterial embolization, for acute limb ischemia, 392 394 for priapism, 436 437 Arterial injuries, ankle-brachial index in, 383 384 pathologic validation of, 383 ultrasonography of, 383 396 acute limb ischemia, 392 394 arteriovenous fistulas, 388 389 craniocervical dissections, 389 391 diabetic foot, 394 hematomas, 386 388 pseudoaneurysms, 384 386 stroke and carotid artery stenosis, 391 392 upper limb ischemia, 394 395 Arteriovenous fistulas, renal, ultrasonography of, 406 407 ultrasonography of, 388 389 Arteriovenous malformations, and first-trimester bleeding, 309 311 intratesticular, ultrasonography of, 359
B
Barium enema examination, of intussusception, in infants and children, 449 450 Bell-clapper deformity, scrotal, ultrasonography of, 354 Biliary duct dilatation, diagnosis of, 264 266 Biliary obstruction, diagnosis of, 266 Biopsy, renal, complications of, 406 407, 410 Bleeding, first-trimester. See First-trimester bleeding. Bowel strangulation, inguinal hernias and, 360 361 Budd-Chiari syndrome, ultrasonography of, 275
C
Calf veins, ultrasonography of, for thromboembolic disease, 287 288 Carotid artery dissection, ultrasonography of, 389 390 Carotid artery stenosis, and stroke, ultrasonography of, 391 392 Cellulitis, scrotal, ultrasonography of, 353 Cervical ectopic pregnancy, ultrasonography of, 333 Chest, interventional ultrasonography in. See Interventional ultrasonography. Chest injuries, emergency ultrasonography of, 421 424 Chest tube insertion, ultrasonography in, 459 462 Chlorpromazine, and priapism, 430 Cholecystitis, ultrasonography of, acute, 257 acute acalculous, 260 complicated, 260 261 emphysematous, 263 264 gangrenous, 261 262 Cholecystostomy, percutaneous, ultrasonography in, 463 465 Choriocarcinoma, and first-trimester bleeding, 309 Chronic intestinal ischemia, ultrasonography of, 373 377 Cirrhotic native liver, ultrasonography of. See Liver. Cocaine, and priapism, 430 Compression ultrasonography, of thromboembolic disease, 281, 283, 286, 287, 291, 294 Computed tomography, in trauma patients, versus ultrasonography, 420
481
of of of of
abdominal aortic aneurysms, 373 acute hepatic vein thrombosis, 275 diverticulitis, 344 intra-abdominal abscesses, 465 466
Empyema, chest tubes for, 460 462 versus lung abscesses, 462 Endoluminal repair, of abdominal aortic aneurysms, 372 373 Endometriomas, ultrasonography of, 339 340 Endometrium, sonographic anatomy of, 297 Endovaginal ultrasonography, of ectopic pregnancy, 331 Epididymo-orchitis, ultrasonography of, 351 353 Epiploic appendages, ultrasonography of, 345
Corpus luteal cysts, ultrasonography of, 329 331 Craniocervical dissections, ultrasonography of, 389 391 Crown-rump length, of embryo, 301, 305 Cystadenocarcinoma, ultrasonography of, 342 Cystadenomas, ultrasonography of, 341 342 Cystic teratomas, ultrasonography of, 341 Cysts, corpus luteal, ultrasonography of, 329 331 follicular, ultrasonography of, 329 theca lutein, ultrasonography of, 334 Cytotec, and spontaneous abortion, 322
F
Fatty infiltration of liver, and liver enlargement, 270 Fatty liver of pregnancy, and liver enlargement, 270 271 Fibroids, uterine, ultrasonography of, 322 323 First-trimester bleeding. See also Pregnancy. ultrasonography of, 297 314 anatomy in, 297 298 for absent intrauterine gestational sac, 303 304 for arteriovenous malformations, 309 311 for choriocarcinoma, 309 for gestational sac with embryo, 305 for gestational trophoblastic disease, 306 309 for hydatidiform mole, 307 309 for intrauterine growth restriction, 305 for retained products of conception, 306 for spontaneous abortion, 301 303 for subchorionic hematoma, 305 306 for trophoblastic tumors, 309 technique for, 298 versus normal ultrasonography, 298 301 amniotic sac in, 301 embryo in, 300 301 gestational sac in, 298 300 yolk sac in, 300 yolk sac criteria for, 304 305 Fistulas, abdominal, interventional ultrasonography for, 468, 470 arteriovenous, renal, ultrasonography of, 406 407 ultrasonography of, 388 389 Focal hemorrhagic lesions, hepatic, diagnosis of, 271 274 Focused abdominal sonography for trauma technique. See Trauma patients, emergency ultrasonography in.
D
Deep venous thrombosis, ultrasonography of, 286 294 Diabetic foot, ultrasonography of, 394 D-dimer test, for thromboembolic disease, 284, 286 Diverticulitis, CT of, 344 ultrasonography of, 344 Double decidual sac sign, in ectopic pregnancy, 332 in transvaginal ultrasonography, 299
E
Echinococcal abscesses, interventional ultrasonography for, 470 Ectopic pregnancy, ultrasonography of. See Adnexal masses. Edema, re-expansion pulmonary, thoracentesis and, 459 Ehlers-Danlos syndrome, and abdominal aortic aneurysms, 370 Embolization, arterial, for acute limb ischemia, 392 394 for priapism, 436 437 transcatheter, for priapism, 437 438 Embryo, ultrasonography of, 300 301, 305 Emphysematous cholecystitis, ultrasonography of, 263 264
482
Follicular cysts, ultrasonography of, 329 Foot, diabetic, ultrasonography of, 394 Fourniers gangrene, ultrasonography of, 351 Fungal abscesses, interventional ultrasonography for, 470
G
Gallbladder disease, in pregnancy, ultrasonography of, 324 Gallbladder perforation, ultrasonography of, 262 263 Gallbladder wall thickening, ultrasonography of, 260 Gallstones, ultrasonography of, 257 260 Gangrene, Fourniers, ultrasonography of, 351 Gangrenous cholecystitis, ultrasonography of, 261 262 Gestational sac, ultrasonography of, 298 300, 303 305 Gestational trophoblastic disease, and first-trimester bleeding, 306 309
of acute cholecystitis, 257 of acute right upper quadrant pain, 276 of biliary duct dilatation, 264 266 of biliary obstruction, 266 of complicated cholecystitis, 260 261 of emphysematous cholecystitis, 263 264 of focal hemorrhagic lesions, 271 274 of gallbladder perforation, 262 263 of gallbladder wall thickening and pericholecystic fluid, 260 of gallstones, 257 260 of gangrenous cholecystitis, 261 262 of hepatic artery stenosis, 398, 399 of hepatic artery thrombosis, 275 276, 398 of hepatic vascular abnormalities, 274 276 of hepatic vein thrombosis, 275 of hepatitis, 266 268 of liver abscesses, 268 270 of noninfectious liver enlargement, 270 271 of portal vein thrombosis, 274 275, 399, 401 402, 405 Hepatocellular carcinoma, ultrasonography of, 273 274 Hepatofugal flow, ultrasonography of, 402 Hernias, inguinal, ultrasonography of, 360 361 b-Human chorionic gonadotropin, in ectopic pregnancy, 334 in molar pregnancy, 308 309 in ovarian hyperstimulation syndrome, 334 in pregnancy, 299 300 Hydatidiform mole, and first-trimester bleeding, 307 309 Hydronephrosis, in pregnancy, ultrasonography of, 325 Hydrosalpinx, ultrasonography of, 339 Hypertension, in pregnancy, ultrasonography of, 316 317 portal, ultrasonography of, 402 Hypertrophic pyloric stenosis, in infants and children, 445 449 clinical features of, 445 incidence of, 445 management of, 448 449
H
HELLP syndrome, ultrasonography of, 316 317 Hematoceles, ultrasonography of, 359 Hematomas, infected, interventional ultrasonography for, 470 scrotal, ultrasonography of, 359 360 subchorionic, and first-trimester bleeding, 305 306 ultrasonography of, 386 388 Hemorrhage, postpartum, ultrasonography of, 321 thoracentesis and, 459 Hemorrhagic lesions, hepatic, diagnosis of, 271 274 Hepatic abscesses, interventional ultrasonography for, 466 467 Hepatic artery stenosis, ultrasonography of, 398, 399 Hepatic artery thrombosis, ultrasonography of, 275 276, 398 Hepatic vein thrombosis, ultrasonography of, 275 Hepatic veins, ultrasonography of, 399 400 Hepatitis, diagnosis of, 266 268 Hepatobiliary ultrasonography, 257 278 Murphys sign in, 257 of acute acalculous cholecystitis, 260
I
Iliac artery aneurysms, ultrasonography of, 377 379 Inferior vena cava, ultrasonography of, 399 400 Inflammatory aneurysms, ultrasonography of, 371
483
Inguinal hernias, ultrasonography of, 360 361 Interstitial ectopic pregnancy, ultrasonography of, 333 Interventional ultrasonography, 457 478 abdominal, 463 474 for echinococcal abscesses, 470 for fistulas, 468, 470 for fungal abscesses, 470 for hepatic abscesses, 466 467 for infected hematomas, 470 for pelvic abscesses, 470, 472 474 for renal and perinephric abscesses, 467 for splenic abscesses, 468 in intra-abdominal abscess drainage, 465 466 in paracentesis, 463 in percutaneous cholecystostomy, 463 465 in percutaneous nephrostomy, 467 468 of chest, 457 462 for lung abscesses, 462 in chest tube insertion, 459 462 in thoracentesis, 457 459 Intestinal ischemia, chronic, ultrasonography of, 373 377 Intracavernosal arteries, laceration of, and priapism, 431 Intracorporeal injection therapy, and priapism, 430 Intradecidual sign, in ectopic pregnancy, 331 332 in transvaginal ultrasonography, 299 Intratesticular abscesses, ultrasonography of, 353 354 Intratesticular arteriovenous malformations, ultrasonography of, 359 Intratesticular varicoceles, ultrasonography of, 358 359 Intrauterine growth restriction, ultrasonography of, 305 Intussusception, in infants and children, 449 452 barium enema examination for, 449 450 diagnosis of, 449 450 management of, 452 plain films of, 449
K
Kidneys, ultrasonography of, 405 412 after transplantation, 405 409 allograft dysfunction, 408 409 arteriovenous fistulas, 406 407 pseudoaneurysms, 406 renal artery stenosis, 407 renal vein thrombosis, 408 anatomy and appearance in, 405 during transplantation, 407 native kidney, 409 412 for biopsy complications, 410 for pyelonephritis, 410 for renal artery stenosis, 411 412 for renal trauma, 411 for renal vein thrombosis, 411 for urinary obstruction, 410
L
Leiomyomata, ultrasonography of, 340 341 Limb ischemia, ultrasonography of, 392 395 Liver, ultrasonography of, 397 405 after transplantation, 398 400 hepatic artery stenosis, 398, 399 hepatic artery thrombosis, 398 hepatic veins and inferior vena cava, 399 400 portal vein thrombosis, 399 pseudoaneurysms, 400 anatomy and appearance in, 397 398 native cirrhotic liver, 400 404 after transjugular intrahepatic portosystemic shunt, 400 404 for portal hypertension, 402 for portal vein aneurysmal ectasia, 404 for portal vein thrombosis, 401 402 noncirrhotic native liver, 404 405 Liver abscesses, diagnosis of, 268 270 interventional ultrasonography for, 466 467 Liver enlargement, noninfectious, diagnosis of, 270 272 Lower extremities, thromboembolic disease in, ultrasonography of, 286 288, 291, 293 294
J
Jugular vein, ultrasonography of, for thromboembolic disease, 289 290
Lung abscesses, interventional ultrasonography for, 462 Luteoma of pregnancy, ultrasonography of, 338
484
M
Magnetic resonance imaging, of acute hepatic vein thrombosis, 275 Mesenteric vasculature, ultrasonography of, 373 377 Metastatic disease, and liver enlargement, 270 Methotrexate, for ectopic pregnancy, 333 334 Mifepristone, and spontaneous abortion, 322 Molar pregnancy, and first-trimester bleeding, 307 309 Mucinous cystadenomas, ultrasonography of, 341 342 Murphys sign, in hepatobiliary ultrasonography, 257 Mycotic aneurysms, ultrasonography of, 371 Myometrium, sonographic anatomy of, 297
Percutaneous cholecystostomy, ultrasonography in, 463 465 Percutaneous nephrostomy, interventional ultrasonography in, 467 468 Pericholecystic fluid, ultrasonography of, 260 Perinephric abscesses, interventional ultrasonography for, 467 Peripheral artery aneurysms, ultrasonography of, 379 Placentation, abnormal, ultrasonography of, 317 319 Plain films, in trauma patients, versus ultrasonography, 422 424 of intussusception, in infants and children, 449 Pleural effusions, chest tubes for, 459 462 emergency ultrasonography of, 421 Pleuritic pain, thoracentesis and, 459 Pneumothorax, emergency ultrasonography of, 421 423 thoracentesis and, 458 459 Popliteal aneurysms, ultrasonography of, 379 Popliteal vein, ultrasonography of, for thromboembolic disease, 287 Portal hypertension, ultrasonography of, 402
N
Nephrostomy, percutaneous, interventional ultrasonography in, 467 468 Neurologic disease, and priapism, 431
O
Orchitis, ultrasonography of, 353 Ovarian hyperstimulation syndrome, ultrasonography of, 334 336 Ovarian neoplasms, ultrasonography of, 341 Ovarian torsion, ultrasonography of, 336 338 Ovaries, sonographic anatomy of, 297 Ovulation induction therapy, and ovarian hyperstimulation syndrome, 335
Portal vein aneurysmal ectasia, ultrasonography of, 404 Portal vein thrombosis, ultrasonography of, 274 275, 399, 401 402, 405 Pregnancy. See also First-trimester bleeding. ectopic, ultrasonography of. See Adnexal masses. molar, and first-trimester bleeding, 307 309 ultrasonography in, 315 327 during abdominal surgery and trauma, 323 for abnormal placentation, 317 318 for acute renal disorders, 324 325 for gallbladder disease, 324 for pelvic thrombophlebitis, 324 for placenta previa, 318 319 for placental abruption, 319 for postpartum hemorrhage, 321 for pregnancy-induced hypertension, 316 317 for retained products of conception, 321 322 for splenic artery aneurysms, 325 for spontaneous abortion, 322 for uterine fibroids, 322 323 for uterine rupture, 317 for vasa previa, 320 321 for venous thromboembolism, 323 324 technique for, 315 316
P
Paracentesis, ultrasonography in, 463 Parapneumonic effusions, chest tubes for, 459 460 Pelvic abscesses, interventional ultrasonography for, 470, 472 474 Pelvic inflammatory disease, ultrasonography of, 338 339 Pelvic pain, adnexal masses and. See Adnexal masses. Pelvic thrombophlebitis, in pregnancy, ultrasonography of, 324
485
Priapism, 427 443 arterial embolization for, 436 437 definition of, 427 428 diagnosis of, 434 436 epidemiology of, 428, 430 etiology of, 430 431 management of, 438 439 complications of, 439 440 pathophysiology of, 431 434 sickle cell anemia and, 430, 433, 439 transcatheter embolization for, 437 438 ultrasonography of, 436, 438 anatomy in, 428 technique for, 428 Pseudoaneurysms, hepatic, ultrasonography of, 400 renal, ultrasonography of, 406 ultrasonography of, 384 386 Pulmonary edema, re-expansion, thoracentesis and, 459 Pulmonary embolism, ultrasonography of, 294 Pyelonephritis, ultrasonography of, 410 Pyogenic liver abscesses, interventional ultrasonography for, 466 467
Shunts, for priapism, 439 Sickle cell anemia, and priapism, 430, 433, 439 Solid organ injuries, emergency ultrasonography of, 420 421 Splanchnic artery aneurysms, ultrasonography of, 377 Splenic abscesses, interventional ultrasonography for, 468 Splenic artery aneurysms, ultrasonography of, 377 in pregnancy, 325 Spontaneous abortion, and first-trimester bleeding, 301 303, 306 ultrasonography of, 322 Stroke, carotid artery stenosis and, ultrasonography of, 391 392 Subchorionic hematomas, and first-trimester bleeding, 305 306
T
Testicular torsion, ultrasonography of, 354 356 Testicular trauma, ultrasonography of, 359 360
R
Raynauds phenomenon, ultrasonography of, 394 395 Renal abscesses, interventional ultrasonography for, 467 Renal artery stenosis, ultrasonography of, 407, 411 412 Renal disorders, in pregnancy, ultrasonography of, 324 325 Renal trauma, ultrasonography of, 411 Renal vein thrombosis, ultrasonography of, 408, 411 Retained products of conception, and first-trimester bleeding, 306 ultrasonography of, 321 322 RU 486, and spontaneous abortion, 322
Testicular tumors, ultrasonography of, 361 Theca lutein cysts, ultrasonography of, 334 Thioridazine, and priapism, 430 Thoracentesis, ultrasonography in, 457 459 Thrombin injection, for pseudoaneurysms, 386 Thromboembolic disease, clinical evaluation of, 283 284 clinical features of, 279 281 D-dimer test for, 284, 286 ultrasonography of, 279 296 adjuncts to, 291 deep venous thrombosis, 286 294 in lower extremities, 286 288, 293 294 in pregnancy, 323 324 in upper extremities, 288 290, 294 pitfalls of, 291 pulmonary embolism, 294 Thrombophlebitis, pelvic, in pregnancy, ultrasonography of, 324 Transabdominal ultrasonography, technique for, 298 Transcatheter embolization, for priapism, 437 438 Transhepatic approach, to percutaneous cholecystostomy, 464
S
Scrotum, acute painful. See Acute painful scrotum. Seldinger technique, for percutaneous cholecystostomy, 464 Serous cystadenomas, ultrasonography of, 341 342
486
Transjugular intrahepatic portosystemic shunt, ultrasonography after, 400 404 Transplantation, kidney, ultrasonography after. See Kidneys. liver, ultrasonography after. See Liver. Transvaginal approach, to pelvic abscess drainage, 472 474 Transvaginal ultrasonography, of embryo, 300 301 of gestational sac, 298 300 of molar pregnancy, 308 309 of yolk sac, 300 technique for, 298 Trauma, during pregnancy, ultrasonography of, 323 renal, ultrasonography of, 411 testicular, ultrasonography of, 359 360 Trauma patients, emergency ultrasonography in, 417 425 for chest injuries, 421 424 for solid organ injuries, 420 421 free fluid in, 417 418 free fluid scoring systems in, 419 420 pitfalls in, 418 419 sensitivity of, 420 versus CT, 420 versus plain films, 422 424 Trazodone, and priapism, 430 Trophoblastic tumors, and first-trimester bleeding, 309 Tubo-ovarian abscesses, ultrasonography of, 338 339
of adnexal masses. See Adnexal masses. of arterial injuries. See Arterial injuries. of first-trimester bleeding. See First-trimester bleeding. of hypertrophic pyloric stenosis, in infants and children. See Hypertrophic pyloric stenosis. of intussusception, in infants and children. See Intussusception. of kidneys. See Kidneys. of liver. See Liver. of mesenteric vasculature, 373 377 of pregnancy-related emergencies. See Pregnancy. of priapism, 428, 436, 438 of thromboembolic disease. See Thromboembolic disease. transvaginal. See Transvaginal ultrasonography. Upper extremities, thromboembolic disease in, ultrasonography of, 288 290, 294 Urinary obstruction, ultrasonography of, 410 Urolithiasis, in pregnancy, ultrasonography of, 325 Uterine fibroids, ultrasonography of, 322 323 Uterine rupture, in pregnancy, ultrasonography of, 317 Uterus, sonographic anatomy of, 297
V
Varicoceles, ultrasonography of. See Acute painful scrotum. Vasa previa, in pregnancy, ultrasonography of, 320 321 Vasovagal reactions, thoracentesis and, 459 Venous thromboembolism, in pregnancy, ultrasonography of, 323 324
U
Ultrasonography, endovaginal, of ectopic pregnancy, 331 hepatobiliary. See Hepatobiliary ultrasonography. in trauma patients. See Trauma patients. interventional. See Interventional ultrasonography. of abdominal aortic aneurysms. See Abdominal aortic aneurysms.
Y
Yolk sac, ultrasonography of, 300, 304 305

2004 Vol.42 Issues 2 Emergency Ultrasound

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2004 Vol.42 Issues 2 Emergency Ultrasound

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Radiol Clin N Am 42 (2004) xi

Vikram Dogra, MD Guest Editor

Radiol Clin N Am 42 (2004) 257 278

Hepatobiliary imaging and its pitfalls

E-mail address: Deborah_Rubens@urmc.rochester.edu

D.J. Rubens / Radiol Clin N Am 42 (2004) 257278

D.J. Rubens / Radiol Clin N Am 42 (2004) 257278

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Radiol Clin N Am 42 (2004) 279 296

* Corresponding author. E-mail address: J.D.Fraser@Dal.Ca (J.D. Fraser).

J.D. Fraser, D.R. Anderson / Radiol Clin N Am 42 (2004) 279296

J.D. Fraser, D.R. Anderson / Radiol Clin N Am 42 (2004) 279296

J.D. Fraser, D.R. Anderson / Radiol Clin N Am 42 (2004) 279296

J.D. Fraser, D.R. Anderson / Radiol Clin N Am 42 (2004) 279296

J.D. Fraser, D.R. Anderson / Radiol Clin N Am 42 (2004) 279296

J.D. Fraser, D.R. Anderson / Radiol Clin N Am 42 (2004) 279296

J.D. Fraser, D.R. Anderson / Radiol Clin N Am 42 (2004) 279296

Pulmonary angiogram or 1 wk CUS

J.D. Fraser, D.R. Anderson / Radiol Clin N Am 42 (2004) 279296

Treat for DVT

Treat for DVT

J.D. Fraser, D.R. Anderson / Radiol Clin N Am 42 (2004) 279296

Superficial femoral vein Great saphenous vein (superficial)

Fig. 7. Diagrammatic representation of the veins of the lower extremity.

J.D. Fraser, D.R. Anderson / Radiol Clin N Am 42 (2004) 279296

J.D. Fraser, D.R. Anderson / Radiol Clin N Am 42 (2004) 279296

Median cubital vein

J.D. Fraser, D.R. Anderson / Radiol Clin N Am 42 (2004) 279296

J.D. Fraser, D.R. Anderson / Radiol Clin N Am 42 (2004) 279296

J.D. Fraser, D.R. Anderson / Radiol Clin N Am 42 (2004) 279296

J.D. Fraser, D.R. Anderson / Radiol Clin N Am 42 (2004) 279296

ography, particularly if the clinical pretest probability is high.

Radiol Clin N Am 42 (2004) 297 314

Sonographic evaluation of first-trimester bleeding

* Corresponding author. E-mail address: paspulati@uhrad.com (R.M. Paspulati).

R.M. Paspulati et al / Radiol Clin N Am 42 (2004) 297314

fallopian tubes cannot be visualized with current US imaging equipment

Always present if GS > 20 mm Cardiac activity GS > 2.5 cm

Abbreviations: GS, gestational sac; US, ultrasound.

Embryo Embryonic cardiac activity

R.M. Paspulati et al / Radiol Clin N Am 42 (2004) 297314

R.M. Paspulati et al / Radiol Clin N Am 42 (2004) 297314

R.M. Paspulati et al / Radiol Clin N Am 42 (2004) 297314

First Trimester Ultrasound

MSD > 18MM

MSD < 18MM

MSD < 10MM