Preface Emergency ultrasound

Preface

Emergency ultrasound

Ultrasonography has undergone many technologic changes resulting in its present state-of-the-art equip-ment that is capable of high-resolution real-time gray-scale imaging and tissue harmonics, including color and power Doppler. These advances in ultra-sound technology have resulted in improved work-up of patients undergoing evaluation in emergency de-partments because it is the first imaging performed on almost all patients presenting to an emergency facil-ity. 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 theRadiologic Clinics of North Americato 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 ultrasonog-raphy 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:[email protected]

0033-8389/04/$ – see front matterD2004 Elsevier Inc. All rights reserved. doi:10.1016/j.rcl.2004.01.004

Vikram Dogra, MD Guest Editor

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 approxi-mately 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 his-tory of right upper quadrant pain diminishes further. Specific criteria for the diagnosis of acute cholecys-titis are important, because many patients have gall-stones but may not have acute cholecystitis. The primary diagnostic criterion is a positive sonographic Murphy’s sign in the presence of gallstones. Second-ary 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 Murphy’s sign

The sonographic Murphy’s sign is defined as specific reproducible point tenderness over the gall-bladder 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 Mur-phy’s sign was 87% specific for the diagnosis of acute cholecystitis. When a positive sonographic Murphy’s sign is used in conjunction with the pres-ence of gallstones, it has a positive predictive value of 92% for diagnosing acute cholecystitis. Persons in whom a sonographic Murphy’s sign may be absent include persons who are medicated; therefore, careful attention to a patient’s clinical status is important. Denervated gallbladders in patients who have diabe-tes or gangrenous cholecystitis may result in the loss of a sonographic Murphy’s 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 accu-racy ( > 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 im-pacted in the gallbladder neck or in the cystic duct and may not be as readily visible (seeFig. 1)[5]. If the gallbladder is focally tender but no gallstones are appreciated, the patient should be examined from 0033-8389/04/$ – see front matterD2004 Elsevier Inc. All rights reserved.

doi:10.1016/j.rcl.2003.12.004

multiple positions, including prone position or up-right 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 (seeFig. 1).

Echogenicity of stones may be decreased in soft pigment stones. These stones are commonly associ-ated 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 shad-ows. 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 gener-ated 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 (seeFig. 1A). A calcium bile salt precipi-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).

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 inAshows 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).

tate may form with the use of Ceftriaxone and mimic gallstones on sonographic examination. These precip-itates 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 gall-bladder or acalculous cholecystitis).

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

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 (seeFig. 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]

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 post-trauma and postsurgical patients and other hospital-ized patients and occurs because of conditions that lead to ischemia, hypotension, or sepsis[12]. These critically ill patients are often medicated with nar-cotics, are on ventilators, and receive hyperalimenta-tion, 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 Murphy’s sign. This is a difficult clinical and ultrasonic diagnosis, because gallstones are absent and the sonographic Murphy’s sign may be limited because of other illnesses and medication. The diagnosis is made by gallblad-der tengallblad-derness (if present) and is associated with gallbladder distension, intraluminal debris, and gall-bladder 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].

Complicated cholecystitis

Complications of acute cholecystitis include gan-grenous cholecystitis, emphysematous cholecystitis, Fig. 3. Acute cholecystitis. This patient presented with right

upper quadrant pain and a positive sonographic Murphy’s sign. Longitudinal US shows stones (arrows) and diffuse gallbladder wall thickening (cursors) that measures 5 mm.

and gallbladder perforation. These complications oc-cur 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 proce-dure 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 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 peri-cholecystic fluid (arrows), free air (arrowheads), and extraluminal accumulated air (paired arrowheads) in perforated duo-denal ulcer.

diagnosis of gangrenous cholecystitis because a sono-graphic Murphy’s sign is absent in two thirds of patients [15]. A relatively specific finding is intra-luminal 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 character-ized 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 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).

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]; how-ever, no specific US features predict which gallblad-ders 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 gallblad-der lumen or in the gallbladgallblad-der wall. As many as 40% of patients with emphysematous cholecystitis have diabetes [2]. The clinical course is rapidly progres-sive, 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 loca-tion 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 hypo-echoic layers. This patient had right upper quadrant pain, fever, abnormal liver function tests, and a negative sono-graphic Murphy’s 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).

uncertain, either CT or plain film radiography can be used to differentiate between gas and calcification.

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

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.

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 ap-proaches 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 symptoms—elevated bilirubin, pain, sepsis, or elevated liver enzymes, including alkaline phosphatase—the dilated ducts are unlikely to be clinically relevant. Similar to the presence of gall-stones, when assessing the ducts for biliary disease, the clinical scenario is of prime importance. Intra-hepatic 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 possi-ble 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-Fig. 7 (continued).

Fig. 8. Acalculous cholecystitis. Longitudinal US of a debris-filled (asterisk) gallbladder with a thick, striated wall (ar-rows). No stones are visualized. At surgery, this was acute acalculous cholecystitis.

Fig. 9. Gallbladder gangrene/mucosal sloughing. Longitu-dinal US of patient with acute cholecystitis secondary to stone (arrow) impacted in the gallbladder neck. Note the intraluminal membranes (arrowheads), which are associ-ated with gallbladder gangrene.

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.

tation can be diagnosed by irregular angular branch-ing, 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.

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 duode-num and using transverse scans to follow the duct accurately [1]. Additional technical improvements sometimes can be achieved by having the patient

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 be-cause 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 (seeFig. 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 situa-tions 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.

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, Fig. 11 (continued).

most often the liver parenchyma is normal[20,21]. Rarely, the liver may have diffusely decreased echo-genicity with relatively increased echoecho-genicity of the portal triads—the ‘‘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, includ-ing gallbladder wall thickeninclud-ing (see Fig. 6) and sometimes a contracted gallbladder [20,21]. When 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.

the patient recovers from hepatitis, the gallbladder wall and distention return to normal. Other viral infections that involve the liver, such as mononucleo-sis, 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 diver-ticulosis or Crohn’s 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 conspicu-ous than on contrasted CT scans. This is particularly true in small clustered microabscesses(Fig. 17A, B). Predominately abscesses are hypoechoic (seeFig. 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 transmis-sion. Because of this variable appearance, the differ-ential 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 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 patient’s symptoms.

confirm that these are not solid tumors; however, necrotic neoplasm remains in the differential diagno-sis. 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 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).

thrombosis. If a transplant patient presents with a hepatic abscess, the patency of the hepatic arteries should be assessed (seeFig. 12).

Noninfectious diffuse enlargement of the liver Patients with diffuse metastatic disease may pres-ent 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, meta-static disease may be of any type from cystic metas-tases of carcinoid to echogenic metasmetas-tases 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, how-ever, 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 hemo-lysis, elevated liver enzymes and low platelets (HELLP) syndrome[23]. Patients present with vari-ous symptoms, most commonly nausea, vomiting, abdominal pain, fever, and jaundice [23,24]. Symp-toms commonly mimic hepatitis. Laboratory ab-normalities 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. 15. Acute hepatitis. Transverse image shows a

hypo-echoic liver relative to the kidney (K) and bright portal triads (arrowheads), the ‘‘Starry Sky’’ appearance. Although strik-ing, this appearance is rare. Most often the hepatic echo-genicity is normal.

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.

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 asympto-matic 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 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.

steroid therapy, does have a predisposition for bleed-ing[25]. The rate of intratumoral or intra-abdominal hemorrhage with adenomas is reported as high 50% to 65%[26]. Contrary to focal nodular hyper-plasia 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 cor-respond 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. 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 thick-walled 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).

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.

most likely to correspond to hemorrhagic necrosis; however, it cannot be distinguished from other tu-mors 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 malig-nancy 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

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 emer-gent 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], as-sociated pancreatitis, and hypercoagulable states,

including stem cell transplantation[28]. Septic throm-bophlebitis has a mortality rate as high as 50%[27]. The most common cause is diverticulitis, with inflam-matory bowel disease, bowel perforation, and suppu-rative 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 hyperbilirubi-nemia[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 throm-bosis. 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 hyper-echoic and recanalizes, or the patient forms collater-als. 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).

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 trans-plant status, and other malignancies, including hepa-toma, 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 inter-ruption 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]. Ob-struction of the suprahepatic IVC also can be docu-mented 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 Valsalva’s 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 enhance-ment of the hepatic parenchyma with edema and relative caudate sparing because the caudate drains di-rectly into the IVC and does not go through the hepa-tic 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).

diagnosis consists of color Doppler and spectral Doppler examination. Absent hepatic arteries indicate thrombosis, although vessels may be small and diffi-cult 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 find-ings is usually performed angiographically. Prompt revascularization or retransplantation is desirable be-cause asymptomatic patients may achieve up to an 80% graft salvage rate versus 43% on symptomatic patients [37]. Massive acute hepatic arterial throm-bosis may result in liver infarction(Fig. 22).

Acute right upper quadrant pain, outside the hepatobiliary system

The differential diagnosis for patients with right upper quadrant pain is extensive and includes pneu-monia, 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

renal infarction, renal obstruction, and renal or adre-nal hemorrhage(Fig. 23), also can present occasion-ally 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, duode-nal 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 incom-plete 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.

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.

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Venous protocols, techniques, and interpretations of the

upper and lower extremities

James D. Fraser, MD

*, David R. Anderson, MD

a

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

Deep venous thrombosis (DVT) and pulmonary embolism (PE), collectively known as venous throm-boembolism, are common problems and are frequent-ly in the differential diagnosis of patients presenting to the emergency department and in the acute care setting. In the United States, the annual combined cidence of DVT and PE is at least 70 per 100,000 in-dividuals[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. Com-pression ultrasonography (CUS) is the diagnostic pro-cedure of choice for the assessment of patients with suspected DVT. It has been shown to be highly sen-sitive and specific for the diagnosis of DVT, particu-larly 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 pul-monary angiography in patients with suspected PE.

This article reviews the clinical indications, diag-nostic techniques, and interpretation of CUS for the assessment of DVT in the upper and lower extrem-ities 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 pres-ent 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 calf-popliteal vein thrombosis experience pain and swell-ing 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 lower-extremity 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-0033-8389/04/$ – see front matterD2004 Elsevier Inc. All rights reserved.

doi:10.1016/j.rcl.2004.01.001 * Corresponding author.

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.

moral DVT is associated with pelvic masses, recent pelvic surgery, oral contraceptive use, and the anti-phospholipid antibody syndrome.

In contrast, patients presenting with upper-extrem-ity 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 ve-nous catheters. It occasionally occurs in otherwise healthy individuals or following strenuous upper-extremity exercise, such as weight lifting[8].

Patients with acute PE may present with dyspnea, pleuritic chest pain, dizziness, and loss of conscious-ness with or without symptoms of DVT. Tachypnea, tachycardia, and hypotension may be noted on phys-ical examination. The range of presentation of PE is great, from minimal chest symptoms to life-threaten-ing shock.

The role of ultrasound in the evaluation of thromboembolic disease

Because of the nonspecific nature of the presen-tation 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 diag-nosis of DVT isolated to the calf to be 73%[11]. The rate of technically inadequate studies has been re-ported 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 estab-lished. 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 determin-ing 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 pro-spective study published in 2002 comparing color Doppler with contrast venography in 126 patients, Baarslag et al[15] reported a sensitivity and speci-ficity 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-Fig. 1 (continued).

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 partic-ularly 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 ex-clusion 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 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.

extend into the proximal deep venous system. Eighty percent of clots isolated to the calf are asympto-matic; 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 unreli-able, 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 Fig. 2 (continued).

alternate diagnosis as the cause for the patient’s 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 con-firmed 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 valu-able 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 Fig. 2 (continued).

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.

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 (seeFigs. 4 – 6). D-dimer is less useful for excluding venous throm-boembolism 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.

Ultrasound technique for the evaluation of deep venous thrombosis of the extremities

Lower extremities

The venous anatomy of the lower extremity is shown inFig. 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 Fig. 3 (continued).

Non-diagnostic Ventilation Perfusion (VQ)/ Computerized axial Tomography (CT) Scan Bilateral Compression Ultrasound (CUS) Pretest Probability (PTP) + D-dimer (DD) Low PTP or - DD Mod/High PTP and + DD PE excluded Pulmonary angiogram

or 1 wk CUS

Treat for PE +

+ -

Fig. 4. Algorithm for investigation of patients with sus-pected PE. CUS, compression ultrasound; DD, D-dimer; PE, pulmonary embolism; PTP, pretest probability.

Table 1

Clinical evaluation table for predicting pretest probability of deep vein thrombosis

Clinical characteristics Score Active cancer (treatment ongoing, within

previous 6 mo or palliative)

1 Paralysis, paresis, or recent plaster

immobilization of the lower extremities

1 Recently bedridden > 3 d or major surgery

within 12 wk requiring general or regional anesthesia

1

Localized tenderness along the distribution of the deep venous system

1

Entire leg swollen 1

Calf swelling 3 cm larger than asymptomatic side (measured 10 cm below tibial tuberosity)

1 Pitting edema confined to the symptomatic leg 1 Collateral superficial veins (nonvaricose) 1 Alternative diagnosis at least as likely as deep

vein thrombosis

2 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.

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 (seeFig. 1C, D). In the presence of DVT, the lumen does not collapse completely even with enough pres-sure 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 (Hunter’s) 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 ad-vantageous for following the course of the vein and for assessing flow (seeFigs. 2A, 3D). It is important, however, to confirm compressibility in the transverse

plane; compression in the longitudinal plane is unre-liable 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 (seeFig. 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 iso-lated to the calf veins of, which 20% to 30% eventu-ally 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 non-diagnostic or inadequate. Reported rates of nondiag-nostic 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 out-comes 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) Compression Ultrasound (CUS) DD/PTP DVT Excluded Low PTP or - DD Mod/High PTP and + DD

Venogram Treat for DVT

- + + -+ Moderate/High

Fig. 6. Algorithm for suspected DVT in the upper extremity. CUS, compression ultrasound; DD, D-dimer; DVT, deep vein thrombosis; PTP, pretest probability.

Clinically Suspected Deep Vein Thrombosis (DVT)

Pretest Probability (PTP) Low D-dimer (DD) Compression Ultrasound (CUS) DD/PTP DVT Excluded Low PTP or - DD Mod/High PTP and + DD

1 wk CUS Treat for DVT - + + + -Moderate/High

Fig. 5. Algorithm for clinically suspected DVT. CUS, compression ultrasound; DD, D-dimer; DVT, deep vein thrombosis; PTP, pretest probability.