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(Radiology. 2000;214:844-847.)
© RSNA, 2000


Diagnosis Please

Case 20: Biliary Ascariasis1

Ronald O. Bude, MD and Richard A. Bowerman, MD

1 From the Department of Radiology, University of Michigan Medical Center, 1500 E Medical Center Dr, Ann Arbor, MI 48109-0030. Received October 28, 1998; revision requested December 8; revision received January 28, 1999; accepted June 17. Address reprint requests to R.O.B. (e-mail: ronbude@umich.edu).

Index terms: Ascariasis, 76.2081 • Bile ducts, diseases, 76.2081 • Bile ducts, US, 76.1298, 76.12983 • Diagnosis Please • Liver, diseases, 761.2081 • Liver, US, 761.1298, 761.12983 • Parasites, 76.2081


    HISTORY
 TOP
 HISTORY
 IMAGING FINDINGS
 DISCUSSION
 References
 
A 54-year-old woman presented with a 3-month history of recurrent, intermittent abdominal pain and 15-lb (6.8-kg) weight loss without a change in appetite. Three years earlier, she had undergone endoscopic retrograde cholangiopancreatography with Oddi sphincterotomy and extraction of common duct calculi, after which laparoscopic cholecystectomy was performed several days later. Biliary drainage tubes were not left in place after surgery, and there were no subsequent surgical procedures. Her current pain was the same as that prior to cholecystectomy.

Laboratory work-up results at presentation revealed mild total hyperbilirubinemia (1.9 mg/dL [32.49 µmol/L]; normal, 0.1–1.1 mg/dL [1.71–18.81 µmol/L]) and mildly elevated liver enzymes (alkaline phosphatase [157 U/L; normal, 30–130 U/L]; aspartate aminotransferase, or AST [108 U/L; normal, 2–35 U/L]; and alanine aminotransferase, or ALT [85 U/L; normal, 0–45 U/L]). The patient was afebrile and had mild eosinophilia without overall leukocytosis.


    IMAGING FINDINGS
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 HISTORY
 IMAGING FINDINGS
 DISCUSSION
 References
 
A sagittal ultrasonographic (US) image of the porta hepatis showed a tubular, nonshadowing structure with a highly echogenic wall and a less echogenic center, within the slightly dilated common bile duct (Fig 1). Additional images (Figs 2, 3) better illustrated both the extent of the echogenic area, as it lay insinuated from the common hepatic bile duct to the head of the pancreas, and the tubular shape of the abnormality. The tubular structure is approximately 5 mm in diameter.



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Figure 1. Sagittal US image of the porta hepatis shows a tubular echogenic region (arrow) within the slightly dilated common bile duct (arrowheads).

 


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Figure 2. Oblique US image of the porta hepatis obtained in a slightly different plane than Figure 1 shows the echogenic region in lengthwise section (open arrow) in the common hepatic and common bile ducts and in cross section (solid arrow) more distally in the common bile duct. Cursors in this image were placed to measure the diameter of the intraluminal abnormality, which is approximately 5 mm. The arrowhead denotes the common bile duct. (Only a black and white image of the color Doppler image was obtained.)

 


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Figure 3. Transverse US image of the pancreas (arrowheads) shows the echogenic region within the common bile duct in cross section (arrow) at the pancreatic head. The cursors show the diameter of the common bile duct (9 mm); a cursor partially overlies the finding of interest.

 

    DISCUSSION
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The differential diagnosis for increased echogenicity within the common bile duct, either diffuse or focal, includes calculus, sludge, pus, thrombus, tumor, gas, foreign body, and parasites. Calculus or calculi are excluded in this case because the intraluminal echogenic region did not shadow and did not consist of one or multiple round or oval echogenic regions. Sludge, pus, and thrombus would not be expected to be so discretely tubular (Fig 1) yet much smaller in cross-sectional area than the common duct (Figs 2, 3) and should also appear more amorphous, lacking the prominently echogenic wall demonstrated in this case. Bacterial infection is unlikely because the patient was afebrile and without leukocytosis.

Many tumors may involve the common hepatic bile duct or the common bile duct, including cholangiocarcinoma, local adenopathy, and direct spread from gallbladder carcinoma (1); papilloma, adenoma, lipoma, fibroma, granular cell tumor, and intraductal metastases (2); and biliary cystadenoma and cystadenocarcinoma, as well as hepatocellular carcinoma (3). Cholangiocarcinoma usually manifests as an infiltrating process and produces mural thickening (84% of patients), which often appears as a small mass owing to apposition of the opposing, thickened walls of the duct, although it less often appears in nodular or papillary forms (1,4). Hepatocellular carcinoma, if it obstructs bile ducts, usually does so by direct compression; it rarely manifests as a bulky intraluminal mass (3). Local adenopathy usually obstructs the bile duct by means of extrinsic compression. Gallbladder carcinoma involves the bile duct by means of direct extension, with a gallbladder mass (1). Biliary cystadenoma and cystadenocarcinoma are at least partially cystic (3). The other very uncommon neoplasms manifest as sessile or polypoid masses. None of these tumors has an appearance that simulates the long, well-defined, tubular, constant-diameter, intraluminal abnormality surrounded by bile that is present in this case.

Intraluminal gas would not manifest in nondependent portions of the common duct as in this case; furthermore, if a collection of gas were as large as the abnormality in this case, it would be expected to shadow, and distal acoustic shadowing was not present in this case. A foreign body such as an indwelling biliary catheter could conceivably give this appearance, but this is excluded by the history.

Clonorchis sinensis flukes are much smaller than the lesion in this case, are 8–15 mm long, and are flat in cross section (5); therefore, they do not mimic the findings in this case. Fasciola hepatica, another fluke, is larger than C sinensis but still smaller than Ascaris lumbricoides and grows 15–40 mm long (6). However, it is much smaller in diameter than A lumbricoides, and therefore does not present a US appearance similar to that in this case (7). Ascariasis is the most likely diagnosis and was confirmed by both the presence of A lumbricoides eggs in the feces and by the patient vomiting a 20-cm-long A lumbricoides worm 1 day after antihelminthic therapy with albendazole.

Since treatment, the patient's abdominal pain has completely resolved, and she has regained some of her lost weight. Of interest is that the patient vacationed in her native India several months before the onset of symptoms, but this history was not available at the time the US images were interpreted.

A lumbricoides infects approximately 1 billion people worldwide (8). It is distributed throughout the tropics and subtropics and is also present in other humid regions such as the rural southeastern United States (8). Approximately 4 million people in the United States are infected, many of whom are immigrants (9). Most cases occur where there is poor fecal sanitation (8).

The human infection life cycle begins by ingestion of an egg, with the larvae hatching in the small intestine. The larvae invade the small-bowel mucosa, migrate through the circulatory system to the lungs, invade the alveoli, ascend the tracheobronchial tree, and then are swallowed into the small intestine where they mature into adult worms (8). Ascarids may reach 40 cm in length (8) with a width of 3–6 mm (10). Intestinal infestation is often asymptomatic. Migration of worms into the biliary tree is a well-known complication, which may result in biliary colic, cholecystitis, cholangitis, intrahepatic abscesses, or pancreatitis (8). After cholelithiasis, it is the second most common cause of acute biliary symptoms worldwide (11).

There is evidence to suggest that sphincterotomy predisposes a patient to biliary ascariasis (12). Jaundice (10) and elevated liver enzymes (13) may occur. The diagnosis is established by means of microscopic identification of A lumbricoides eggs in fecal samples. An A lumbricoides worm occasionally is identified in stool or vomitus (8). US readily depicts the worm in the bile ducts or gallbladder (11,12,1419). Mebendazole (3 days of twice daily oral therapy) or albendazole (a single oral dose of medication) are the treatments of choice (8).

At US, A lumbricoides in the biliary ducts usually manifests as an echogenic tubular structure, compared with bile, and has a diameter of approximately 3–6 mm, a relatively hypoechoic center, and a more echogenic wall. It may exhibit slow movement. Ascarids typically lie parallel with the long axis of the bile duct (11,15,17). They may be coiled. If multiple, they may completely fill the bile duct, producing either the "spaghetti sign" (11), or if they are very densely packed in the bile ducts, they may appear amorphous and manifest as hyperechoic pseudotumors (19).

Our congratulations to the 117 individuals who submitted the most likely diagnosis (biliary ascariasis) for Diagnosis Please, Case 20. The names and locations of the individuals, as submitted, are as follows:


    References
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 HISTORY
 IMAGING FINDINGS
 DISCUSSION
 References
 

  1. Robledo R, Muro A, Prieto ML. Extrahepatic bile duct carcinoma: US characteristics and accuracy in demonstration of tumors. Radiology 1996; 198:869-873.[Abstract/Free Full Text]
  2. Friedman AC, Sachs L, Birns MT. Radiology of jaundice includingcholedocholithiasis and biliary neoplasms. In: Friedman AC, eds. Radiology of the liver, biliary tract, pancreas and spleen. Baltimore, Md: Williams & Wilkins, 1987; 544-548.
  3. Friedman AC, Fishman EK, Radecki PD, et al. Focal diseases. In: Friedman AC, eds. Radiology of the liver, biliary tract, pancreas and spleen. Baltimore, Md: Williams & Wilkins, 1987; 151-264.
  4. Cohen SM, Kurtz AB. Biliary sonography. In: Bernardino ME, eds. The Radiologic Clinics of North America: imaging of the liver and biliary tree, vol 29, no 6. Philadelphia, Pa: Saunders, 1991; 1171-1198.
  5. Lim JH, Ko YT, Lee DH, Kim SY. Clonorchiasis: sonographic findings in 59 proved cases. AJR Am J Roentgenol 1989; 152:761-764.[Abstract/Free Full Text]
  6. Laing FC. The gallbladder and bile ducts. In: Rumack CM, Wilson SR, Charboneau JW, eds. Diagnostic ultrasound. 2nd ed. St Louis, Mo: Mosby–Year Book, 1998; 175-223.
  7. Van Beers B, Pringot J, Geubel A, Trigaux JP, Bigaignon G, Dooms G. Hepatobiliary fascioliasis: noninvasive imaging findings (case report). Radiology 1990; 174:809-810.[Free Full Text]
  8. Liu LX, Weller PF. Intestinal nematodes. In: Fauci AS, Braunwald E, Isselbacher KJ, et al., eds. Harrison's principles of internal medicine. 14th ed. New York, NY: McGraw-Hill, 1998; 1208-1209.
  9. Bratton RL, Nesse RE. Ascariasis: an infection to watch for in immigrants. Postgrad Med 1993; 93:171-173.
  10. Hoffman H, Kawooya M, Esterre P, et al. In vivo and in vitro studies on the sonographical detection of Ascaris lumbricoides. Pediatr Radiol 1997; 27:226-229.[Medline]
  11. Mani S, Merchant H, Sachdev R, Rananavare R, Cunha N. Sonographic evaluation of biliary ascariasis. Australas Radiol 1997; 41:204-206.[Medline]
  12. Khuroo MS, Zargar SA, Mahajan R. Hepatobiliary and pancreatic ascariasis in India. Lancet 1990; 335:1503-1506.[Medline]
  13. Louw JH. Biliary ascariasis in childhood. S Afr J Surg 1974; 12:219-225.[Medline]
  14. Schulman A, Loxton AJ, Heydenrych JJ, Abdurahman KE. Sonographic diagnosis of biliary ascariasis. AJR Am J Roentgenol 1982; 139:485-489.[Abstract/Free Full Text]
  15. Cerri GG, Leite GJ, Simões JB, et al. Ultrasonographic evaluation of ascaris in the biliary tract (case report). Radiology 1983; 146:753-754.[Abstract/Free Full Text]
  16. Kolt SD, Wirth PD, Speer AG. Biliary ascariasis: a worm in the duct (case report). Med J Aust 1991; 154:629-630.[Medline]
  17. Aslam M, Dore SP, Verbanck JJ, De Soete CJ, Ghillebert GG. Ultrasonographic diagnosis of hepatobiliary ascariasis. J Ultrasound Med 1993; 12:573-576.[Abstract]
  18. Filice C, Marchi L, Meloni C, Patruno SFA, Capellini R, Bruno R. Ultrasound in the diagnosis of gallbladder ascariasis. Abdom Imaging 1995; 20:320-322.[Medline]
  19. Schulman A. Ultrasound appearances of intra- and extrahepatic biliary ascariasis. Abdom Imaging 1998; 23:60-66.[Medline]



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