Indian Journal of Transplantation

: 2020  |  Volume : 14  |  Issue : 4  |  Page : 352--354

Ascariasis, the uncommon cause of bile leak, postliving donor liver transplant - A case report

Nitin Gupta1, Ritu Verma1, Ethel Shangne Belho1, Suresh Kumar Singhvi2,  
1 Department of Nuclear Medicine, PET/CT Mahajan Imaging Centre, Sir Ganga Ram Hospital, New Delhi, India
2 Department of Surgical Gastroenterology, Sir Ganga Ram Hospital, New Delhi, India

Correspondence Address:
Dr. Nitin Gupta
Department of Nuclear Medicine, PET/CT Mahajan Imaging Centre, Sir Ganga Ram Hospital, New Delhi - 110 060


Ascaris lumbricoides is one of the most common parasitic infections in developing countries. History of previous biliary tract surgery risks migration of these worms to the biliary tree. Usually, 10% of patients with living donor liver transplants have biliary complications including bile leak and strictures. Here, we present an unusual case of ascariasis being a cause of biliary obstruction and bile leak in the immediate postoperative period of liver transplant.

How to cite this article:
Gupta N, Verma R, Belho ES, Singhvi SK. Ascariasis, the uncommon cause of bile leak, postliving donor liver transplant - A case report.Indian J Transplant 2020;14:352-354

How to cite this URL:
Gupta N, Verma R, Belho ES, Singhvi SK. Ascariasis, the uncommon cause of bile leak, postliving donor liver transplant - A case report. Indian J Transplant [serial online] 2020 [cited 2021 Mar 4 ];14:352-354
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Ascaris is the most common helminthic infestation in developing countries. Risk factors for this infection include poor hygiene/dietary habits. Postbiliary tract surgery or after manipulation, the parasite can migrate into the biliary tract, due to its inherent predilection toward small orifices. Migration of these worms can irritate the bile duct by their excreta, resulting in biliary colic, spasm of the sphincter of Oddi, thereby leading to partial or complete biliary obstruction.[1] Incidence of biliary complications postliver transplant is approximately 10%–15% in deceased donor transplants and maybe up to 15%–30% in living donor recipients.[2] Bile leaks have an overall incidence rate of 2% to 25% after transplantation and usually develop within 1–3 months.[3] We report an uncommon cause of bile leak after living donor liver transplant (LDLT), where re-exploration on the postoperative day 3, revealed ascariasis in the Common bile duct (CBD), causing biliary obstruction and leak.

 Case Report

A 45-year-old male patient, a known case of cryptogenic chronic liver disease with decompensation underwent LDLT. On the 3rd postoperative day, the patient was septic, and abdominal drainage devices revealed a bile leak. The patient was stable hemodynamically and a HIDA scan was requested by the operating surgeon. Hepatobiliary iminodiacetic acid (HIDA) scan dynamic images [Figure 1]a revealed inhomogeneous uptake in the transplanted liver and spot images [Figure 1]b, [Figure 1]c, [Figure 1]d demonstrated an area of tracer accumulation at the porta which depicted further build-up in delayed images. The drain bag [Figure 1]e showed tracer activity, and thus, bile leak was suspected from the anastomotic site. The patient underwent re-exploration, the anastomosis was taken down. The distal end of the recipient native duct on exploration revealed a long tubular structure similar to an Ascariasis lumbricoides worm [Figure 2]. The worm was removed and the bile duct was re-anastomosed to the liver graft. Other intraoperative findings were bile duct leak at the anastomotic site with bile collection posterior to the portal vein in the right subhepatic space and peritoneal cavity, as reported on the HIDA scan. Postoperative period was uneventful. Computed tomography (CT) scan coronal and axial views [Figure 3]c, [Figure 3]d, [Figure 3]e, [Figure 3]f, [Figure 3]g done 4 days after re-exploration revealed post-LDLT status with no evidence of any loculated collection along the cut margin of the liver. Postre-exploration HIDA scan [Figure 3]a and [Figure 3]b revealed homogeneous hepatic parenchymal tracer uptake and patent biliary outflow tract.{Figure 1}{Figure 2}{Figure 3}


A. lumbricoides (roundworm) is a commonly found human parasite and approximately 25% of the world's population is infected with this worm.[4] The infection is more commonly seen in females with a ratio of 3:1 and the reported mean age at diagnosis is 35 years. Risk factors are poor hygiene/dietary habits, living in specific regions such as the Kashmir Valley in India, subtropical and tropical climates, and poor nutritional status.[5] It is a milky white or pink roundworm, 15–50 cm long and 3–6 mm thick, transmitted by the oro-fecal route. They have a direct type of life cycle with humans as their only host. The cycle begins when embryonated eggs containing the infecting larva are ingested by a human. When in the intestine, the larvae are released from the egg and reach other organs such as lungs and heart through the bloodstream. After passing through several phases in the lungs, they migrate from the trachea to the mouth, where they are swallowed. In the small intestine, after becoming adults they mate, laying about 2 lakh eggs in a day, eliminated through the feces of the host.[6]

The worm usually resides in the jejunum. However, increasing pressure and concomitant intestinal infection by viruses or bacteria may stimulate parasite motility. The worms usually have a predilection for small openings. Various factors that influence the migration of this worm into the biliary tract include prior cholecystectomy (due to an increase in the secretion of cholecystokinin which in turn leads to relaxation of the sphincter of Oddi), history of manipulation, like dilation of the sphincter of Oddi to examine the bile duct, leading to the later dysfunction with diminished pressure, pregnancy (increasing the concentration of progesterone, thus relaxing smooth muscles, and including the sphincter of Oddi).[7] Roundworms also secret polypeptides causing allergic reactions and thus leading to the spasm of the sphincter of Oddi. This helps them to migrate into the bile duct and triggers biliary stasis and subsequent pyogenic cholangitis, biliary stricture, cholecystitis, and pancreatitis.[8] Their migration into the bile duct irritates the latter, by their excreta, resulting in biliary colic, spasm of the sphincter of Oddi, and leading to partial of complete biliary obstruction.[1] Few case reports have been published describing ascariasis in the biliary tract.[9],[10],[11],[12]

Biliary complications postliver transplant can be early (within 30 days) or late. Up to 1/3 of these complications occur within the 1st month of the procedure. Types of early biliary complications are strictures, leaks, bile duct stone/cast, and ischemic biliary strictures. In the early postoperative period, leaks are predominant and late strictures account for up to 40% of all biliary complications. Bile leaks frequently occur at the biliary anastomosis but can also occur at cystic duct remnant or a T-tube site. Anastomotic leaks occur due to technical issues or due to ischemic necrosis at the bile duct anastomosis. Nonanastomotic leaks develop due to vascular insufficiency or inadvertent T-tube removal. Bile leaks may cause abdominal pain, fever, peritonitis, sepsis, or even death. It may unnecessarily prolong hospital stay, increase financial burden, and may ultimately impair graft survival. HIDA scan is an important test for the detection of bile leaks in the postoperative abdomen and has been discussed in detail in the literature.[13] As seen in our case, HIDA scan helped in detecting bile leak and its site. Postsurgery, HIDA scan confirmed patent biliary tract. Ascariasis causing bile leak in the postliver transplant period is a rare finding as seen in our report.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understands that their names and initials will not be published, and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.


1Khuroo MS, Zargar SA, Mahajan R. Hepatobiliary and pancreatic ascariasis in India. Lancet 1990;335:1503-6.
2Hampe T, Dogan A, Encke J, Mehrabi A, Schemmer P, Schmidt J, et al. Biliary complications after liver transplantation. Clin Transplant 2006;20 Suppl 17:93-6.
3Greif F, Bronsther OL, Van Thiel DH, Casavilla A, Iwatsuki S, Tzakis A, et al. The incidence, timing, and management of biliary tract complications after orthotopic liver transplantation. Ann Surg 1994;219:40-5.
4Crompton DW. Ascaris and ascariasis. Adv Parasitol 2001;48:285-375.
5Khuroo MS, Mahajan R, Zargar SA, Javid G, Sapru S. Prevalence of biliary tract disease in India: A sonographic study in adult population in Kashmir. Gut 1989;30:201-5.
6Holland CV. Predisposition to ascariasis: Patterns, mechanisms and implications. Parasitology 2009;136:1537-47.
7Ochoa B. Surgical complications of ascariasis. World J Surg 1991;15:222-7.
8Shah OJ, Robanni I, Khan F, Zargar SA, Javid G. Management of biliary ascariasis in pregnancy. World J Surg 2005;29:1294-8.
9Paganelli M, Taglietti L, Di Flumeri G, Giovanetti M. Rare cause of biliary obstruction by ascariasis associated with choledocholithiasis. Chir Ital 2008;60:733-8.
10Vagholkar K, Suryawanshi S, Subudhi S, Vagholkar S. Hepatobiliary ascariasis. Int Surg J 2017;4:1087-9.
11Jethwani U, Singh GJ, Sarangi P, Kandwal V. Laproscopic management of wandering biliary ascariasis. Case Rep Surg 2012;2012:561-3.
12Sanai FM, Al-Karawi MA. Biliary ascariasis: Report of a complicated case and literature review. Saudi J Gastroenterol 2007;13:25-32.
13Matesan, M, Bermo M, Cruite I, Shih CH, Elojeimy S, Behnia F, et al. Biliary Leak in the Postsurgical Abdomen: A Primer to HIDA Scan Interpretation. Semin Nucl Med 2017;47:618-29.