DOI: 10.1148/rg.265055201
RadioGraphics 2006;26:1567-1570
© RSNA, 2006
Best Cases from the AFIP
Ascaris Pancreatitis1
Carter A. Kenamond, MD,
David M. Warshauer, MD and
Ian S. Grimm, MD
1 From the Department of Radiology (C.A.K., D.M.W.) and Division of Gastroenterology (I.S.G.), University of North Carolina School of Medicine, CB 7510, 101 Manning Dr, Chapel Hill, NC 27599-7510. Received November 16, 2005; revision requested January 11, 2006, and received February 13; accepted February 20. All authors have no financial relationships to disclose.
Address correspondence to C.A.K. (e-mail: ckenamon{at}unch.unc.edu).
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History
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An 18-year-old Hispanic man presented with a 2-week history of continuous moderate to severe epigastric pain preceded by 6 months of intermittent burning epigastric pain that worsened with eating. Past episodes typically lasted 1–2 days and then resolved spontaneously. The patient had immigrated to the United States from Mexico 1 year previously. At physical examination, he was afebrile with mild epigastric tenderness. The abdomen was soft without rebound or guarding, and bowel sounds were normal. A complete blood cell count demonstrated mild leukocytosis (12.3 x 109/L) and elevated amylase (539 U/L) and lipase (4671 U/L) levels.
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Imaging Findings
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The patient was initially evaluated at an outside hospital, where abdominal computed tomography reportedly demonstrated a dilated pancreatic duct. On referral to our facility, magnetic resonance (MR) imaging of the abdomen with MR cholangiopancreatography showed mild peripancreatic edema and a diffusely dilated pancreatic duct containing a smooth linear filling defect (Fig 1). Biliary ducts were not dilated, and there was no evidence of an ampullary mass.
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Figure 1a. (a) Axial T2-weighted (half-Fourier acquisition single-shot turbo spin-echo) MR image shows a linear filling defect (arrow) in the dilated main pancreatic duct. There is mild edema in the anterior pararenal space bilaterally (arrowheads) with a small amount of fluid about the tip of the spleen (S). (b) Coronal oblique T2-weighted source image from MR cholangiopancreatography shows the filling defect (arrow) in the dilated pancreatic duct. (c) Oblique coronal image from MR cholangiopancreatography shows linear filling defects (arrowheads) throughout the length of the dilated pancreatic duct (arrow). There is no dilatation of the bile ducts, and the gallbladder (GB) appears normal.
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Figure 1b. (a) Axial T2-weighted (half-Fourier acquisition single-shot turbo spin-echo) MR image shows a linear filling defect (arrow) in the dilated main pancreatic duct. There is mild edema in the anterior pararenal space bilaterally (arrowheads) with a small amount of fluid about the tip of the spleen (S). (b) Coronal oblique T2-weighted source image from MR cholangiopancreatography shows the filling defect (arrow) in the dilated pancreatic duct. (c) Oblique coronal image from MR cholangiopancreatography shows linear filling defects (arrowheads) throughout the length of the dilated pancreatic duct (arrow). There is no dilatation of the bile ducts, and the gallbladder (GB) appears normal.
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Figure 1c. (a) Axial T2-weighted (half-Fourier acquisition single-shot turbo spin-echo) MR image shows a linear filling defect (arrow) in the dilated main pancreatic duct. There is mild edema in the anterior pararenal space bilaterally (arrowheads) with a small amount of fluid about the tip of the spleen (S). (b) Coronal oblique T2-weighted source image from MR cholangiopancreatography shows the filling defect (arrow) in the dilated pancreatic duct. (c) Oblique coronal image from MR cholangiopancreatography shows linear filling defects (arrowheads) throughout the length of the dilated pancreatic duct (arrow). There is no dilatation of the bile ducts, and the gallbladder (GB) appears normal.
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Endoscopic retrograde cholangiopancreatography (ERCP) was performed for further evaluation. At initial inspection, the major papilla appeared dilated and contained a tubular, mucus-appearing foreign body, which was extracted in its entirety with a biopsy forceps and measured 10.5 cm in length (Fig 2). The pancreatic duct was then cannulated, and contrast material was injected. Fluoroscopic images from ERCP demonstrated a diffusely dilated main pancreatic duct containing a second tubular filling defect (Fig 3). After guidewire placement and balloon extraction, a second vermiform structure measuring 14 cm was also removed.
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Pathologic Evaluation
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The specimens removed at esophagogastroduo-denoscopy were compatible with the remnants of a dead Ascaris worm at gross inspection (Fig 4). Formal speciation with parasitology was not successful due to fragmentation of the specimens.
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Discussion
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Ascariasis is the most common helminthic disease in humans. Infection by Ascaris lumbricoides occurs when Ascaris eggs are ingested from infected soil, food, or water. Larvae emerge in the duodenum and then migrate to the cecum, where they access veins of the portal system and are transported to the liver. From the hepatic veins, larvae pass to the heart and lungs. Transport to the lungs can also occur via the bowel lymphatics and thoracic duct. After migrating up the tracheo-bronchial tree, the larvae are swallowed. Mature worms develop in the small intestine over several months, and eggs are passed in the feces (1).
Ascariasis has a global distribution, with more than 1 billion people infected worldwide (1–3). Ascariasis is highly endemic in China, Southeast Asia, Africa, and Latin America (1,4). In 1993, an estimated 4 million people in the United States were infected, with immigrants from developing countries constituting a large percentage (1). The highest prevalence of Ascaris infection is in children between the ages of 4 and 14 years (1). Pulmonary, intestinal, peritoneal, appendiceal, hepatobiliary, and pancreatic disease can occur, although most Ascaris infections are clinically asymptomatic (1).
Hepatobiliary and pancreatic ascariasis (HPA) is common. Mature Ascaris worms can enter and exit the biliary tree or pancreatic duct via the ampulla. Five distinct clinical presentations of HPA have been reported including biliary colic, acalculous cholecystitis, acute cholangitis, acute pancreatitis, and hepatic abscess (1). Bile peritonitis has also been reported (4). HPA affects women more than men with a ratio of 3:1. Adults are more commonly involved than children with a mean age of 35–42 years, a fact that may reflect the inability of the worms to invade the small-caliber childhood ducts. Many patients with HPA have had previous surgery involving the biliary system including cholecystectomy or sphincterotomy (1,3). Pregnancy and fasting have also been implicated as risk factors for HPA in endemic areas (1,3).
Ascaris lumbricoides is the most common parasite that causes pancreatitis (5). In certain parts of India, ascariasis is second only to cholelithiasis as a cause of pancreatitis (5). Ascaris pancreatitis can be caused by invasion of the biliary tree, pancreatic duct, or both (6). However, invasion of the pancreatic duct is rare, presumably secondary to its smaller caliber (6). Nearly all patients with Ascaris-related pancreatitis present with abdominal pain, and many also report back pain, nausea, vomiting, and worm emesis (3,6). Most cases of Ascaris-related pancreatitis are mild (6), although a small group of patients with severe Ascaris infection and pancreatitis die (1).
The diagnosis of HPA is most commonly made by using ultrasonography (US) and ERCP. US is a sensitive and specific method for detection of worms in the biliary tree, and it can be repeated frequently to monitor response to therapy and worm movement (2,4,7,8). Sensitivity for detection of pancreatic duct involvement, as in this case, is thought to be less (9). Similarly, detection of a single worm is more difficult than detection of multiple worms (8).
Sonographic findings reflect the worm morphology and include single or multiple, long, linear echogenic strips without acoustic shadowing in the biliary or pancreatic ducts (the "strip" sign) (4,8). Characteristic movement is occasionally observed, and a central, longitudinal, anechoic tube may be observed within the worm, probably representing its digestive tract (the "inner tube" sign) (4,8). A spaghetti-like appearance can be seen with infestation with multiple worms (4). Associated findings of HPA include biliary or pancreatic duct dilatation, pancreatic edema or gallbladder wall thickening, air in the biliary or pancreatic ducts, and intrahepatic abscess (4,8).
Endoscopic imaging can demonstrate active worms within the duodenal lumen and ampulla. At ERCP, Ascaris worms can be identified as smooth, linear filling defects within the ducts (1). ERCP images may also show the worms as parallel smooth filling defects or as curves or loops traversing the ducts (10). Reversible biliary and pancreatic duct dilatation is common and proportional to the number of infecting worms (10). All patients demonstrate ova of Ascaris lumbricoides in the stool (6).
MR imaging and MR cholangiopancreatographic findings of pancreatic Ascaris have not been previously described, to our knowledge. In the present case, worms were best demonstrated on T2-weighted images as linear filling defects within a dilated pancreatic duct.
The differential diagnosis for pancreatic ductal dilatation with intraductal filling defects would include both intraductal papillary-mucinous neoplasm (IPMN) as well as chronic pancreatitis with intraductal stones. Although mucinous threads can appear linear, IPMN would more commonly appear globular or masslike, as would stones associated with chronic pancreatitis. The internal structure of Ascaris, when visible, would also distinguish it from intraductal mucin or stones.
For the treatment of HPA, some authors recommend initial conservative therapy consisting of bowel rest, intravenous fluids, analgesic-antispasmodics, and antibiotics followed by mebendazole once acute symptoms subside. In these cases, endoscopic intervention is reserved for patients who (a) fail conservative therapy or (b) have worms in the ducts after 3 weeks of observation (1,2). Other authors advocate emergent ERCP if HPA is suspected in an attempt to clear the pancreatic and biliary ducts of all roundworms and prevent serious complications (3,11). Worm extraction by using a basket or forceps without sphincterotomy results in rapid relief of signs and symptoms and is successful in 90%–98% of patients (2,3,6,9, 11). Extraction of worms from the pancreatic duct can also be performed with a "whirlpool jet" technique if the worms are otherwise inaccessible (3).
Complications related to endoscopic procedures are rare (2,6,9,11). It is not uncommon to find dead and macerated or fragmented worms at endoscopy. Such debris may serve as a nidus for intrahepatic biliary stone formation if not removed (1,2,4,9). Worm remnants in the pancreatic duct may calcify and contribute to recurrent pancreatitis (12). Surgery is occasionally required for definitive therapy of HPA (2,9,12). All patients should receive antihelminthic therapy (9).
The patient in the present case experienced resolution of his abdominal pain following worm removal. He was treated with a single 400-mg dose of albendazole and discharged from the hospital 1 day later. He has not returned for follow-up.
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Footnotes
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Abbreviations: ERCP = endoscopic retrograde cholangiopancreatography, HPA = hepatobiliary and pancreatic ascariasis
Editor’s Note.—Everyone who has taken the course in radiologic pathology at the Armed Forces Institute of Pathology (AFIP) remembers bringing beautifully illustrated cases for accession to the Institute. In recent years, the staff of the Department of Radiologic Pathology has judged the "best cases" by organ system, and recognition is given to the winners on the last day of the class. With each issue of RadioGraphics, one or more of these cases are published, written by the winning resident. Radiologic-pathologic correlation is emphasized, and the causes of the imaging signs of various diseases are illustrated.
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References
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- Khuroo MS. Ascariasis. Gastroenterol Clin North Am 1996;25:553–577.[CrossRef][Medline]
- Khuroo MS, Zargar SA, Yattoo GN, et al. Worm extraction and biliary drainage in hepatobiliary and pancreatic ascariasis. Gastrointest Endosc 1993;39:680–685.[Medline]
- Sandouk F, Haffar S, Zada MM, Graham DY, Anand BS. Pancreatic-biliary ascariasis: experience of 300 cases. Am J Gastroenterol 1997;92: 2264–2267.[Medline]
- Ferreyra NP, Cerri GG. Ascariasis of the alimentary tract, liver, pancreas and biliary system: its diagnosis by ultrasonography. Hepatogastroenterology 1998;45:932–937.[Medline]
- Parenti DM, Steinberg W, Kang P. Infectious causes of acute pancreatitis. Pancreas 1996;13: 356–371.[Medline]
- Khuroo MS, Zargar SA, Yattoo GN, et al. Ascaris-induced acute pancreatitis. Br J Surg 1992; 79:1335–1338.[Medline]
- Grover SB, Pati NK, Rattan SK. Sonographic diagnosis of Ascaris-induced cholecystitis and pancreatitis in a child. J Clin Ultrasound 2001;29: 254–259.[CrossRef][Medline]
- Khuroo MS, Zargar SA, Mahajan R, Bhat RL, Javid G. Sonographic appearances in biliary ascariasis. Gastroenterology 1987;93:267–272.[Medline]
- Leung JW, Chung SC. Endoscopic management of biliary ascariasis. Gastrointest Endosc 1988;34: 318–320.[Medline]
- Bhushan B, Watal G, Mahajan R, Khuroo MS. Endoscopic retrograde cholangiopancreaticographic features of pancreaticobiliary ascariasis. Gastrointest Radiol 1988;13:327–330.[CrossRef][Medline]
- Chen YS, Den BX, Huang BI, Xu LZ. Endoscopic diagnosis and management of Ascaris-induced acute pancreatitis. Endoscopy 1986;18: 127–128.[Medline]
- Krige JE, Lewis G, Bornman PC. Recurrent pancreatitis caused by a calcified Ascaris in the duct of Wirsung. Am J Gastroenterol 1987;82:256–257.[Medline]
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History
Imaging Findings
