|
 
 |
| REVIEW ARTICLE |
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| Year : 2022 | Volume
: 9
| Issue : 4 | Page : 145-151 |
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Intrabiliary rupture of hepatic echinococcosis
Sardar Muhammad Adil Farooq, Wenya Liu
Department of Radiology Xinjing Medical University, First Affiliated Hospital of Xinjiang Medical University, Urumqi, China
| Date of Submission | 19-Dec-2022 |
| Date of Decision | 02-Feb-2023 |
| Date of Acceptance | 08-Feb-2023 |
| Date of Web Publication | 21-Mar-2023 |
Correspondence Address:
Wenya Liu
First Affiliated Hospital of Xinjiang Medical University, Urumqi
China
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/RID.RID_46_22
Echinococcosis is a zoonotic parasitic disease caused by the larval stages of the Taeniid cestode species within the genus echinococcosis. The most commonly affected organ is the liver. Hepatic hydatid cysts have various complications, including superinfection and biliary, intrathoracic, and abdominal rupture. Intrabiliary rupture is the most common complication of hepatic hydatid cysts and is associated with high morbidity and mortality. Urgent imaging diagnosis and surgical management are required in these cases.
Keywords: Echinococcoses, imaging diagnosis, intrabiliary rupture
How to cite this article:
Farooq SM, Liu W. Intrabiliary rupture of hepatic echinococcosis. Radiol Infect Dis 2022;9:145-51 |
| Introduction | |  |
Echinococcosis is a zoonotic parasitic disease caused by the larvae of Taeniid cestode species within the genus Echinococcus. Nine species are recognized, but only six cause infection in humans, namely Echinococcus granulosus, Echinococcus multilocularis, Echinococcus oligarthrus, Echinococcus vogeli, Echinococcus canadensis, and Echinococcus ortleppi.[1],[2] The main species of major public health and global significance are E. granulosus, which is the main etiological agent in cystic echinococcosis, and E. multilocularis, which is the causative agent in alveolar echinococcosis.[3],[4] Both of these diseases have a worldwide geographic distribution and may be fatal if untreated.
The clinical presentation of echinococcosis depends on various factors, including growth rate, cyst size, and the organ involved. In general, symptoms appear as a result of either rupture of a cyst into the bile duct or the peritoneal cavity or compression of adjacent structures or the viscera by surrounding inflammation.[5]
In most cases, hydatid cysts have an uncomplicated course, and their diagnosis and management are not challenging. However, a complicated course requires input by an experienced surgeon and interventional radiologist. Commonly encountered complications of hydatid cysts include intrabiliary rupture (IBR) or rupture into the peritoneal cavity, compression of the biliary tree and nearby structures, invasion of other organs, and infection. Among these, IBR is considered the most common and severe complication, occurring in 2%–42% of cases.[6] The clinical presentation of IBR may include jaundice, cholangitis, cholecystitis, liver abscess, pancreatitis, and septicemia. However, undiagnosed rupture can lead to a biliary leak, cavity infection, and obstructive jaundice.[7] Rare complications include invasion of the abdominal wall, cyst rupture into hollow viscera, hepatic complications (e.g., portal vein thrombosis), and Budd-–Chiari syndrome.
Various imaging modalities have been used for the detection of hydatid cysts and their complications. Ultrasonography (US) is particularly helpful for the detection of cyst membranes, septa, and hydatid sand. However, wall calcification and infection are better revealed by computed tomography (CT). CT and magnetic resonance imaging (MRI) may reveal defects in the cyst wall and the passage of contents through a defect. Chest radiography, US, CT, and MRI are all valuable for showing transdiaphragmatic herniation of hydatid disease. CT is the study of choice for peritoneal seeding. US and CT reveal rupture in most cases that involve extensive communication. High echogenicity in the US with a fluid level and changes in signal intensity on MRI are indirect signs of biliary communication. CT allows exact calculation of osseous lesions, whereas MRI is superior for detecting neural involvement.[8]
| Life Cycle of Echinococcus granulosus | | |
E. granulosus is a tapeworm that is approximately 2–7 mm in length.[4] The life cycle consists of both a definitive canine host and an intermediate host. The definitive hosts are dogs and canids, whereas the intermediate hosts are sheep, goats, pigs, and horses. The eggs are expelled in the host feces. Humans become infected by the consumption of food or water containing the eggs of the parasite. On reaching the intestinal tract, larvae hatch from the eggs and travel through the intestinal mucosa to the portal vessel and enter the liver. Approximately 75% of hydatid infections involve the liver. After evading filtering in the liver, the larvae infect the lungs in about 15% of cases. From the lungs, the larvae can affect any part of the body via the hematogenous route.[9]
If the larvae can escape host defense, they then form small cysts with a surrounding fibrous capsule. During the initial 6 months, they can grow to 1 cm, with later growth dependent on the resistance of the host tissue. The cyst can rupture suddenly during the initial early growth phase when hydrostatic pressure exceeds the nearby pericyst resistance. Scolices and daughter cysts are produced after the early hydatid growth phase when the hydatid cyst enters a phase of aging and progressive involution. During this phase, the cyst fluid is changed by scolices and membranes. Progressive calcification of the wall occurs as a result of the host reaction.[8],[10]
Complications of hepatic hydatid cysts are usually linked to their growth and a pressure effect on nearby structures, secondary infection, or cyst rupture.[8] Cyst rupture is the most common complication of hydatid disease. It can be silent, but the antigenic properties of the cyst fluid may progress to an anaphylactic reaction.[10],[11]
Cyst rupture can be categorized as contained, communicating, or direct.[10],[12] The contained type entails rupture of an endocyst with a complete pericyst; the hydatid cyst generally retains its size and shape on cross-sectional imaging, and the detached endocyst is generally seen as an intracystic floating membrane displaying the “water lily sign,” “snake sign,” or “serpent sign.”[13],[14] A communicating rupture occurs when a pericyst enters the biliary tree and the hydatid cyst empties its contents into the biliary system, and a direct rupture occurs when a pericyst or endocyst ruptures and spills the contents of the cyst.[10],[13]
| Epidemiology | | |
The worldwide picture of echinococcus infection is still incomplete. A recent study has shown that this infection occurs in at least 100 countries and in all regions. A high prevalence is found in Eurasia, the Mediterranean region, China, Russia, Australia, Africa, and South America. The annual incidence of human cystic echinococcosis requiring hospitalization varies between <1 and >8/100,000 population in some European countries. Echinococcosis is considered to be a major health problem in China.[15] The annual incidence of Echinococcus infection was reported to be 8.7/100,000 in Xinjiang in 1990, and a rate of 2.1% (85/3998) was found in Sichuan in 1997–1998.[16] A high prevalence has also been documented in countries in South America and in Northern and Eastern Africa (prevalence >3%). Some island nations, including Iceland and Greenland, are considered free of echinococcosis infection. In contrast, others, including New Zealand, Tasmania, and southern Cyprus, have reported sporadic cases in household animals. Sporadic cases of E. granulosus have not been documented in Northern or Central Europe, the Pacific region, Northern or Central America, or in the Caribbean.
| Complications | | |
Complications of hydatid cysts are not rare and have been reported to occur in one-third to approximately 60% of all diagnosed and treated cases of hydatid disease.[9] Commonly encountered complications are intrahepatic bile duct rupture, abdominal rupture, intrathoracic rupture, compression of the biliary tree and adjacent structures, invasion of other organs, and superinfection. The most commonly encountered problems are rupture and superinfection.[17],[18]
| Superinfection | | |
Superinfection is a common complication of communicating rupture. Secondary bacterial infection has been reported to occur in only 5%–8% of cases.[10] However, hydatid cyst superinfection in the liver was found in 24% of cases in a large group of patients who were managed surgically.[18],[19] Patients with clinical findings of pain, fever, and leukocytosis and a clinical history of known hydatid cysts are considered the most likely candidates for cyst infection.
| Biliary Communication | | |
IBR is a common complication in patients with hydatid cysts in the liver and can occur as an internal breach secondary to high intracystic pressure or as an external breach as a result of trauma or sudden rupture. The incidence of this complication in surgically treated patients was 26% in one case series and 34% in another.[18],[19] The frequency varies in the radiology literature from 3% to 17%. IBR usually involves the right hepatic duct, with the left hepatic duct and confluence less frequently affected. Three types of hepatic hydatid cyst have been reported.[20] Communicating rupture is the first type and is the most common; when the rupture is contained, hydatid cyst fluid seeps between the endocyst and pericyst but with no outflow from the cyst. In a communicating rupture, there is spillage of material to the adjacent bile ducts; this type of rupture may be simple or obvious. Simple rupture is frequently asymptomatic and does not involve movement of hydatid material into bile ducts but can progress to obvious rupture. In obvious rupture, sufficient hydatid material moves into the bile ducts to produce signs of obstruction. In direct rupture, which is the third type, cyst material may move into the pleural or peritoneal cavity.[21]
Jaundice, cholecystitis, cholangitis, liver abscess, pancreatitis, and septicemia can occur as a consequence of the rupture of a cyst in the bile duct. Presenting signs include fever, nausea, and vomiting, loss of appetite, abdominal swelling, pain in the right hypochondrium, tachycardia, and jaundice and can progress to sepsis or even death if diagnosis and management is delayed.[22],[23]
| Intrathoracic Rupture | | |
Involvement of the diaphragm or thoracic cavity is seen in 0.16%–16% of cases of hepatic hydatid disease.[24] The most common route of transdiaphragmatic spread is via the bare area of the liver and the posterior segment of the right hepatic lobe. Transdiaphragmatic spread is best detected by CT. However, although not definitive, the presence of air inside a hydatid cyst indicates linkage with the bronchial tree, particularly if associated with findings in the lung parenchyma. Atelectasis, pleural effusion, and pulmonary consolidation are common indicators of thoracic involvement.[11]
Depending on the degree and association of cyst changes, five surgical grades of thoracic association in hydatid disease have been identified.[24] In grade 1, there is a strong linkage between the diaphragm and the cyst surface but without diaphragmatic rupture. In grade 2, the cyst ruptures the diaphragm with limited involvement of the chest cavity. In grade 3, the formation of daughter vesicles or spread of cysts inside the chest cavity is seen as cyst rupture through the diaphragm. In grade 4, there is a spread in the lung parenchyma accompanied by a connection with the bronchial tree or atelectasis. In grade 5, there is complete rupture and transdiaphragmatic spread with the expulsion of contents in sputum. Expectoration of bile is a warning sign of bronchobiliary fistula, which requires an urgent surgical procedure, including ligation of the fistula, lobectomy, decortication, and finally, repair of the diaphragm.[9]
| Abdominal Rupture | | |
Abdominal rupture of a hydatid cyst occurs along the thin-walled anterior or inferior surface of the liver. Blunt abdominal trauma or even minor injury can lead to spontaneous rupture. The clinical presentation may include the acute abdomen, anaphylactic shock, or both.[25],[26] Peritoneal involvement in hydatid disease is seen in up to 13% of patients. Most of these cases are the result of hepatic hydatid disease. Surgically treated cases are most likely to have this presentation, which leads to sudden micro-rupture into the peritoneal cavity in approximately 12% of cases.[27] Hydatid cyst rupture on CT appears as a decrease in cyst size, detached membranes, a wall defect, and a structural change in the cyst. CT can also demonstrate intraperitoneal daughter cysts.
Most peritoneal hydatid cysts are silent and remain undetected until they become large enough to produce symptoms. Direct rupture of a hydatid cyst can be enclosed in the subscapular space.[11] Although, peritoneal disease can be widespread; peritoneal hydatidosis is a term that refers to hydatid disease covering most of the peritoneal cavity as a multiloculated mass. Metastatic hydatidosis indicates the implantation of scolices in most of the abdominal organs, followed by intraperitoneal implanting of hepatic hydatid disease.[13] Surgical management includes the removal of all cysts, followed by peritoneal lavage with a scolicidal agent.[18],[19]
The incidence of pelvic involvement in hydatid disease has been reported to be 2.2%.[28] These hydatid cysts may lead to a pressure effect on nearby structures and urinary obstruction. In complicated cases, a pelvic hydatid cyst can become attached to the urinary bladder and create problems during a surgical procedure.[29],[30]
| Rare Complications | | |
Cyst rupture into hollow viscera is seen in about 0.5% of cases.[8] Hydatid emesis with or without hydatidorrhea may be the presenting feature. Hepatic hydatid cysts may spread in an exophytic fashion and probably via the bare area of the liver or the gastrohepatic ligament. This can result in complications in structures adjacent to the liver. Anterior abdominal wall involvement is a very rare complication of hydatid cysts.[11] Hepatic hydatid cysts can also result in portal vein thrombosis, portal hypertension, cavernous transformation, and Budd-Chiari syndrome as a result of a mass effect on the hepatic or portal vein.[9]
| Imaging Findings | | |
Hepatic hydatid cysts and their complications are managed according to the patient's clinical history, findings on physical examination, blood tests, serologic examinations, and imaging results. Abdominal US, CT, endoscopic retrograde cholangiopancreatography (ERCP), MRI, and magnetic resonance cholangiopancreatography (MRCP) are useful tools for the preoperative diagnosis of IBR.[31]
| Ultrasonography | | |
The US is a noninvasive, widely used, and rapid method for the investigation of the abdominal cavity and is the initial investigation of choice for hepatic hydatid cysts. In communicating rupture, US findings include a small cyst with undulating membranes. Extrahepatic biliary dilatation is a common finding. Sludge and daughter cysts appear as echogenic or nonechogenic areas without posterior shadowing inside the biliary tree. Only 20% of cases demonstrate direct communication.[32]
| Endoscopic Ultrasound | | |
Endoscopic ultrasound (EUS) is rapidly replacing diagnostic endoscopic retrograde cholangiography for the identification of biliary tract disorders. It should be the initial investigation for diagnosis of IBR of a hepatic hydatid cyst when the US is inconclusive. EUS has higher sensitivity for visualization of the biliary tree than other imaging modalities and is helpful for securing a diagnosis of IBR. The existence of a cysto-biliary communication or hydatid debris in the biliary tract in a patient with hepatic hydatid cyst on EUS is indicative of IBR.[31]
| Computed Tomography | | |
CT is the modality of choice for the diagnosis of complications such as IBR because it is readily accessible and can be performed rapidly. CT has an important diagnostic role in hepatic hydatid disease because it describes various images in detail. Findings suggestive of changes in cyst structure, existence of air or an air–fluid level inside the cyst, and enlargement or dilation of the biliary tree are all non-specific or indirect signs of biliary rupture. However, although enlargement of the biliary tree may indicate the rupture of a cyst, it could be the result of cholelithiasis or a mass effect exerted by a hydatid cyst on the biliary tree. The presence of an air–fluid level or inner air may indicate a breach into the biliary tree, a hollow viscus, superinfection, or bronchopleural fistula. A fat–fluid level is seen if there is a leak of fatty material into the cyst and is an indirect sign of biliary communication. Direct signs of biliary rupture include a break in the wall of the hepatic hydatid cyst and communication between the cyst and the biliary tree. Although an important imaging modality, CT has some limitations considering that most communicating ruptures are minute fissures that may be below the spatial resolution of CT, which limits its ability to find the exact location, although a slice thickness of 3 mm may increase the precision of evaluation. Discontinuity of the hydatid cyst wall and a linear attenuation filling defect inside the biliary tree are seen in 77% of ruptures on CT. Moreover, compared with US, CT is better able to depict hydatid material in the distal portion of the common bile duct.[9]
| Endoscopic Retrograde Cholangiopancreatography | | |
ERCP is considered to be the reference standard for the identification of biliary tract abnormalities and is possibly the best method for preoperative visualization of a biliary breach.[33] ERCP has both diagnostic and management value in cases of IBR. Swelling of the ampulla of Vater with spillage of hydatid material may be seen on ERCP. Enlargement of ducts with debris and daughter cysts may be seen as radiolucent filling defects. This condition can be differentiated from other causes of obstructive jaundice by the presence of irregular leaf-like material that changes in shape with changes in pressure.[32] Galati et al. reported that preoperative ERCP decreased the postoperative complication rate from 11.1% to 7.6% and was preferable in patients with cysto-biliary fistula because it helped to visualize the fistula and drainage of the biliary tree.[34] In all cases, the therapeutic intervention was sphincterotomy with the evacuation of all membranes and daughter cysts from the biliary tree with or without the use of an extraction balloon. However, MRCP is rapidly replacing ERCP because it is non-invasive and preferred when the diagnosis is the main concern.[35]
| Magnetic Resonance Cholangiopancreatography | | |
MRCP is an effective, noninvasive, and useful tool when the diagnosis is in question and does not have the risks associated with ERCP.[36] MRCP also shows the exact details of a hepatic hydatid cyst and its communication with the biliary tree.[37] MRCP also has an advantage over ERCP in that it can access ducts proximal to the obstruction. A cysto-biliary communication facing the surface of the liver may not be opacified on ERCP. MRCP provides all necessary information about the entire area involved in hydatid disease, shows the whole biliary tract despite obstruction, and assists with topographic assessment of hydatid cysts and the obstruction level. Findings on MRCP can be direct or indirect in a case of a ruptured hydatid cyst and be helpful for assessing IBR. A break in the cyst wall at its low-intensity rim with the expulsion of cyst material is a direct sign, while fluid levels, the presence of air, or changes in signal intensity with increased echogenicity are direct signs on MRCP. Obvious cysto-biliary communication is considered a direct sign of rupture. However, MRCP has low sensitivity, so the lack of a visible communication cannot exclude cyst rupture. MRCP is considered to have a sensitivity of about 91.7% and a specificity of approximately 82.8% in a patient with any of the four signs of IBR, namely, cysto-biliary communication, hydatid cyst deformation, a defect in the cyst wall, and beak-like extensions from the cyst wall.[36] Overall, MRCP is more sensitive for the diagnosis of IBR because of hepatic hydatid disease.
| Discussion | | |
Hydatid disease is common worldwide and is caused by the Echinococcus tapeworm (E. granulosus or E. multilocularis). Cystic echinococcosis is caused by E. granulosus, whereas alveolar echinococcosis is a disease caused by E. multilocularis.
The life cycle of E. granulosus includes two hosts. The first is the definitive host, which includes dogs or other carnivores. Once the host is infected, the adult worm lives in the proximal small intestine and its hooklets become attached to the mucosa. The worm then produces eggs, which are excreted in the feces. The intermediate hosts of the worm include sheep, which ingest the eggs while grazing, after which the eggs pass through the wall of the intestine into the portal circulation, settle inside the liver, and develop into cysts. The worm can also infect humans, such that they may become intermediate hosts either via contact with a definitive host, such as a domesticated dog, or by direct ingestion of eggs in contaminated water or on vegetables.
Spontaneous rupture into the biliary tree is the most common and feared complication of a hydatid cyst and can occur as a result of trauma, infection, or the pressure produced by an increase in the size of the cyst. The rupture can occur in the biliary tree, peritoneum, and thorax or can develop subcutaneously. There is communication with the biliary tree in about 90% of cases of hydatid cyst rupture.
A hydatid cyst exerts pressure on the surrounding liver parenchyma. As a result of its increasing size and pressure, the cyst ruptures and expels its contents into the small bile duct. IBR usually involves a centrally situated cyst with a pressure of about 80 cm H2O.[38] Cyst rupture is classified into contained, communicating, and direct. In a contained rupture, the cyst contents are sealed within the pericyst, whereas in a communicating rupture, the pericyst tears and expels cystic material into the biliary tree or within the bronchioles. In a direct rupture, the wall of the cyst tears completely and the cyst material leaks into the peritoneal or pleural cavity. About 55%–60% of ruptures involve the right hepatic duct and 25%–30% involve the left hepatic duct, with rare cases involving the confluence or gallbladder.[6] Formation of a gallbladder fistula is a rare entity that is usually not identified until surgery but may be found on imaging in some patients.
Obstruction is observed in about 5%–17% of cases of ruptured hepatic hydatid cyst.[39] If the cysto-biliary opening is greater than 5 mm, cystic material migrates into the biliary tree in about 65% of cases.[40] Obstructive jaundice occurs in 57%–100% of patients, particularly when the rupture occurs in a large bile duct.[38] Other complications include pain in the right upper quadrant (82%), fever (70%–90%), acute cholangitis (20%–37%), and abdominal mass (22%–39%), which can progress to acute pancreatitis, liver abscess, or septicaemia, and 5%–6% of cases may be asymptomatic. Acute cholecystitis following biliary rupture occurs infrequently.[41] Prompt diagnosis and management of IBR is important because delayed treatment has a high risk of morbidity and mortality.[8]
US is the most widely used initial investigation. Sludge and daughter cysts can be seen as echogenic or nonechogenic areas without posterior shadowing inside the biliary tree. Twenty percent of cases show direct communication. CT demonstrates detached undulating membranes and calcification of the cyst wall. An interrupted area on the cyst wall proximal to an enlarged duct may be recognized as a site of communication. This interrupted area is a direct sign of rupture and is seen in 75% of cases.[42] CT can show high-attenuation material passing through the defect in the wall of the cyst.[43] The precision of CT, along with the US is nearly 100% in uncomplicated cases of IBR.[38] ERCP is the best modality and shows swelling of the ampulla of Vater with hydatid material bulging outwards. Enlarged ducts with debris and daughter cysts appear as radiolucent filling defects. Irregular leaf-like structures that change in shape in response to a change in pressure distinguish IBR from other causes of obstructive jaundice.[38] MRCP is an extremely useful and non-invasive method for detecting IBR. A break in the low-intensity rim of the cyst wall with the expulsion of contents is a direct sign of IBR on MRCP, while increased echogenicity, a fluid level, the presence of air, and changes in signal intensity are considered to be indirect signs.
Albendazole or mebendazole is often administered preoperatively to reduce the risk of recurrence and to decrease intracystic pressure during surgery.[39] Another treatment for IBR is endoscopic sphincterotomy with the evacuation of the retained ruptured membrane or daughter cyst in the common bile duct. Endoscopic procedures include sphincterotomy, nasobiliary drainage in patients with biliary fistula, balloon dilatation and stenting in patients with biliary stricture, and sphincterotomy with balloon removal in patients who have material remaining inside the bile duct. Surgical procedures for IBR include Roux-en-Y cysto-jejunostomy, sutured fistula plus tube drainage, sutured fistula plus omentoplasty, tube drainage plus omentoplasty, and drainage of the common bile duct using a T-tube. However, surgery is associated with many postoperative complications, including persistent postoperative biliary drainage, infection in the residual cavity, sinus formation, and recurrence.[43]
| Conclusion | | |
IBR of a hepatic hydatid cyst is a serious life-threatening complication of hydatid disease and should be kept in mind as a differential diagnosis in a patient admitted with symptoms of abdominal pain, fever, and jaundice. IBR can lead to complications such as cholecystitis, cholangitis, pancreatitis, and septicemia. Early detection and aggressive management are essential. Radiologists should keep in mind the imaging findings and complications of hydatid disease to ensure accurate diagnosis and appropriate management.
Abdominal US and CT are the initial diagnostic methods of choice for IBR. Although ERCP was previously considered to be the gold standard for the diagnosis for IBR, MRCP is emerging as a field of interest in the diagnosis and management of IBR and various other biliary diseases. Preoperative ERCP is still considered the primary diagnostic and therapeutic tool for frank IBR but not in cases where there is the involvement of large or multiple cysts, caudate or hilar lobe cysts, or minimal intrahepatic dilatation of the bile ducts proximal to the cyst. Furthermore, ERCP is unable to detect simple communications and can result in the formation of postoperative biliary fistula. However, MRCP can detect cysto-biliary communication and provide necessary information about the entire area affected by hydatid disease. An advantage of MRCP over ERCP is its ability to assess ducts proximal to an obstruction.
Ethic statement
Not appliable.
Acknowledgment
We thank Liwen Bianji (Edanz) (www. liwenbianji. cn) for editing the English text of a draft of this manuscript.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | Alvarez Rojas CA, Romig T, Lightowlers MW. Echinococcus granulosus sensu lato genotypes infecting humans-review of current knowledge. Int J Parasitol 2014;44:9-18.  |
| 2. | McManus DP. Current status of the genetics and molecular taxonomy of Echinococcus species. Parasitology 2013;140:1617-23. |
| 3. | McManus DP, Zhang W, Li J, Bartley PB. Echinococcosis. Lancet 2003;362:1295-304. |
| 4. | Eckert J, Deplazes P. Biological, epidemiological, and clinical aspects of echinococcosis, a zoonosis of increasing concern. Clin Microbiol Rev 2004;17:107-35. |
| 5. | Dolay K, Akbulut S. Role of endoscopic retrograde cholangiopancreatography in the management of hepatic hydatid disease. World J Gastroenterol 2014;20:15253-61. |
| 6. | Zaouche A, Haouet K, Jouini M, El Hachaichi A, Dziri C. Management of liver hydatid cysts with a large biliocystic fistula: Multicenter retrospective study. Tunisian Surgical Association. World J Surg 2001;25:28-39. |
| 7. | Manouras A, Genetzakis M, Antonakis PT, Lagoudianakis E, Pattas M, Papadima A, et al. Endoscopic management of a relapsing hepatic hydatid cyst with intrabiliary rupture: A case report and review of the literature. Can J Gastroenterol 2007;21:249-53. |
| 8. | Pedrosa I, Saíz A, Arrazola J, Ferreirós J, Pedrosa CS. Hydatid disease: Radiologic and pathologic features and complications. Radiographics 2000;20:795-817. |
| 9. | Alghofaily KA, Saeedan MB, Aljohani IM, Alrasheed M, McWilliams S, Aldosary A, et al. Hepatic hydatid disease complications: Review of imaging findings and clinical implications. Abdom Radiol (NY) 2017;42:199-210. |
| 10. | Lewall DB. Hydatid disease: Biology, pathology, imaging and classification. Clin Radiol 1998;53:863-74. |
| 11. | Marti-Bonmati L, Menor Serrano F. Complications of hepatic hydatid cysts: Ultrasound, computed tomography, and magnetic resonance diagnosis. Gastrointest Radiol 1990;15:119-25. |
| 12. | de Diego Choliz J, Lecumberri Olaverri FJ, Franquet Casas T, Ostiz Zubieta S. Computed tomography in hepatic echinococcosis. AJR Am J Roentgenol 1982;139:699-702. |
| 13. | Lewall DB, McCorkell SJ. Rupture of echinococcal cysts: Diagnosis, classification, and clinical implications. AJR Am J Roentgenol 1986;146:391-4. |
| 14. | von Sinner WN. New diagnostic signs in hydatid disease; radiography, ultrasound, CT and MRI correlated to pathology. Eur J Radiol 1991;12:150-9. |
| 15. | Wen H, Yang WG. Public health importance of cystic echinococcosis in China. Acta Trop 1997;67:133-45. |
| 16. | Wang Q, Qiu JM, Schantz P, He JG, Ito A, Liu FJ. Investigation of risk factors for development of human hydatidosis among households raising livestock in Tibetan areas of western Sichuan province. Zhongguo Ji Sheng Chong Xue Yu Ji Sheng Chong Bing Za Zhi 2001;19:93-6. |
| 17. | Chautems R, Bühler LH, Gold B, Giostra E, Poletti P, Chilcott M, et al. Surgical management and long-term outcome of complicated liver hydatid cysts caused by Echinococcus granulosus. Surgery 2005;137:312-6. |
| 18. | Symeonidis N, Pavlidis T, Baltatzis M, Ballas K, Psarras K, Marakis G, et al. Complicated liver echinococcosis: 30 years of experience from an endemic area. Scand J Surg 2013;102:171-7. |
| 19. | Agayev RM, Agayev BA. Hepatic hydatid disease: Surgical experience over 15 years. Hepatogastroenterology 2008;55:1373-9. |
| 20. | Polat P, Atamanalp SS. Hepatic hydatid disease: Radiographics findings. Eurasian J Med 2009;41:49-55. |
| 21. | Spârchez Z, Osian G, Onica A, Bărbântă C, Tanţău M, Pascu O. Ruptured hydatid cyst of the liver with biliary obstruction: Presentation of a case and review of the literature. Rom J Gastroenterol 2004;13:245-50. |
| 22. | Bektaş M, Dökmeci A, Cinar K, Halici I, Oztas E, Karayalcin S, et al. Endoscopic management of biliary parasitic diseases. Dig Dis Sci 2010;55:1472-8. |
| 23. | Mermi EU, Fidan N, Murat M. Focal biliary system obstruction and atypical liver mass: Intrabiliary ruptured cyst hydatid case report. Pol J Radiol 2017;82:110-3. |
| 24. | Gómez R, Moreno E, Loinaz C, De la Calle A, Castellon C, Manzanera M, et al. Diaphragmatic or transdiaphragmatic thoracic involvement in hepatic hydatid disease: Surgical trends and classification. World J Surg 1995;19:714-9. |
| 25. | Akcan A, Sozuer E, Akyildiz H, Ozturk A, Atalay A, Yilmaz Z. Predisposing factors and surgical outcome of complicated liver hydatid cysts. World J Gastroenterol 2010;16:3040-8. |
| 26. | Gunay K, Taviloglu K, Berber E, Ertekin C. Traumatic rupture of hydatid cysts: A 12-year experience from an endemic region. J Trauma 1999;46:164-7. |
| 27. | Karavias DD, Vagianos CE, Kakkos SK, Panagopoulos CM, Androulakis JA. Peritoneal echinococcosis. World J Surg 1996;20:337-40. |
| 28. | Varedi P, Saadat Mostafavi SR, Salouti R, Saedi D, Nabavizadeh SA, Samimi K, et al. Hydatidosis of the pelvic cavity: A big masquerade. Infect Dis Obstet Gynecol 2008;2008:782621. |
| 29. | Srinivasan S. Retrovesical hydatid cyst presenting with urinary retention and left kidney atrophy. Urol Ann 2014;6:70-1. [Full text] |
| 30. | Horchani A, Nouira Y, Chtourou M, Kacem M, Ben Safta Z. Retrovesical hydatid disease: A clinical study of 27 cases. Eur Urol 2001;40:655-60. |
| 31. | Avcu S, Ünal Ö, Arslan H. Intrabiliary rupture of liver hydatid cyst: A case report and review of the literature. Cases Journal 2009;2:6455. |
| 32. | Wani I, Bhat Y, Khan N, Mir F, Nanda S, Shah OJ. Concomitant rupture of hydatid cyst of liver in hepatic duct and gallbladder: Case report. Gastroenterology Res 2010;3:175-9. |
| 33. | Magistrelli P, Masetti R, Coppola R, Costamagna G, Durastante V, Nuzzo G, et al. Value of ERCP in the diagnosis and management of pre- and postoperative biliary complications in hydatid disease of the liver. Gastrointest Radiol 1989;14:315-20. |
| 34. | Galati G, Sterpetti AV, Caputo M, Adduci M, Lucandri G, Brozzetti S, et al. Endoscopic retrograde cholangiography for intrabiliary rupture of hydatid cyst. Am J Surg 2006;191:206-10. |
| 35. | Gupta P, Debi U, Sinha SK, Prasad KK. Role of endoscopic retrograde cholangiography in ruptured hepatic hydatid cyst. Trop Gastroenterol 2015;36:21-4. |
| 36. | Erden A, Ormeci N, Fitoz S, Erden I, Tanju S, Genç Y. Intrabiliary rupture of hepatic hydatid cysts: Diagnostic accuracy of MR cholangiopancreatography. AJR Am J Roentgenol 2007;189:W84-9. |
| 37. | Kumar R, Reddy SN, Thulkar S. Intrabiliary rupture of hydatid cyst: Diagnosis with MRI and hepatobiliary isotope study. Br J Radiol 2002;75:271-4. |
| 38. | Akkiz H, Akinoglu A, Colakoglu S, Demiryürek H, Yagmur O. Endoscopic management of biliary hydatid disease. Can J Surg 1996;39:287-92. |
| 39. | Ivanis N, Rubinić M, Gudović A, Zeidler F. Ultrasound image of an echinococcus daughter cyst in the gallbladder. Ultraschall Med 1994;15:269-71. |
| 40. | Erzurumlu K, Dervisoglu A, Polat C, Senyurek G, Yetim I, Hokelek M. Intrabiliary rupture: An algorithm in the treatment of controversial complication of hepatic hydatidosis. World J Gastroenterol 2005;11:2472-6. |
| 41. | Martí-Bonmatí L, Menor F, Ballesta A. Hydatid cyst of the liver: Rupture into the biliary tree. AJR Am J Roentgenol 1988;150:1051-3. |
| 42. | al Karawi MA, Yasawy MI, el Shiekh Mohamed AR. Endoscopic management of biliary hydatid disease: Report on six cases. Endoscopy 1991;23:278-81. |
| 43. | Agarwal S, Sikora SS, Kumar A, Saxena R, Kapoor VK. Bile leaks following surgery for hepatic hydatid disease. Indian J Gastroenterol 2005;24:55-8. [ PUBMED] [Full text] |
|
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