|Year : 2013 | Volume
| Issue : 3 | Page : 218-221
Giant pelvic hydatid cyst
Hari Charan Perigela, M Koti Reddy, B Vara Prasad, J Narahari
Department of General Surgery, Kurnool Medical College and Government General Hospital, Kurnool, Andhra Pradesh, India
|Date of Web Publication||29-Aug-2013|
Hari Charan Perigela
Department of General Surgery, Kurnool Medical College and Government General Hospital, Kurnool, Andhra Pradesh
Source of Support: None, Conflict of Interest: None
Hydatid disease, most commonly caused by the larval stage of Echinococcus granulosus, affects mainly human liver and lungs, and rarely other parts of the body. It is prevalent in most sheep-raising Mediterranean countries, Central Asia, the Middle East, Eastern Africa, and parts of South America. Peritoneal hydatid cyst, either primary or secondary, represents an uncommon but significant manifestation of the disease. The present case report describes a case of a giant secondary hydatid disease of the pelvic cavity with primary in the liver.
Keywords: Abdominal distension, CT scan abdomen, Pelvic hydatid cyst
|How to cite this article:|
Perigela HC, Reddy M K, Prasad B V, Narahari J. Giant pelvic hydatid cyst. J NTR Univ Health Sci 2013;2:218-21
| Introduction|| |
Hydatid disease is a zoonotic parasitic disease most frequently caused by Echinococcus granulosus or Echinococcus multilocularis. Echinococcus granulosus can reach any organ or tissue of the body where it develops into a small hydatid cyst. [1 ]
The characteristic imaging findings have been described as calcification of the cyst wall, the presence of daughter cysts, or membrane detachment.  However, the radiological signs are often nonspecific. Serological tests may be helpful in the diagnosis, But not reliable. [3 ] Unusual sites of this disease can frequently cause diagnostic problems and lead to diagnostic delays and many potentially serious complications.
Peritoneal hydatidosis could be either primary or more frequently secondary to hydatid cysts in liver or rarely in spleen. Primary peritoneal hydatidosis is rare and has been reported to occur in only 2% of all abdominal hydatid disease cases. We report a case of secondary hydatid disease of the intraperitoneal pelvic space with primary lesion in the liver.
| Case Report|| |
A 20-year-old male patient presented with a history of abdominal distension since 6 months and pain since 5 days. On examination, he was not anemic, pulse 90/minute, and BP:120/70 mmHg. The respiratory and cardiovascular systems were normal. Abdominal examination revealed generalized distension. Digital rectal examination revealed a large, smooth, symmetrical mass lying anterior to the rectum. Routine investigations were within normal limits. Liver function tests and coagulation profile revealed no abnormalities. X-ray abdomen was normal without calcification. Abdominal ultrasonography revealed a large hypoechoic mass with echogenic septations. Serological evaluation for hydatid cyst was carried out with a negative result. Computed tomography scan of the whole abdomen showed giant cyst of 25 cm × 20 cm with multiple well-defined cysts in it extending from left hypochondrium to pelvic cavity and a cyst in the right lobe of liver [Figure 1] and [Figure 2]. The diagnosis of hydatid cyst of liver and giant hydatid cyst of peritoneal cavity was made. At laparotomy, huge cyst was occupying most of the peritoneal cavity including rectovesical pouch [Figure 3], [Figure 4], [Figure 5]. Cyst wall was opened, the daughter cysts and hydatid sand were removed [Figure 6]. Pericystic cavity was washed with Betadine solution. Most of the pericyst was removed except for some portion which was adherent to the urinary bladder. Hepatic hydatid cyst was also removed. There were no similar cystic masses in any other abdominal viscera. Postoperative recovery was uneventful and the patient was discharged on 10th postoperative day. Final diagnosis was confirmed by pathological examination. He was advised to take per oral albendazole 400 mg twice daily for 6 months.
|Figure 2: CT scan of abdomen showing hydatid cyst with multiple daughter cysts|
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|Figure 5: Cyst wall grasped with two curved artery forceps before opening|
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|Figure 6: Image showing multiple cysts which were removed during surgery|
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| Discussion|| |
Hydatid disease or echinococcosis is a parasitic disease caused by infection with larva (metacestode) of the cestode Echinococcus. Four species of the genus echinococcus are known to cause infection in humans; Echinococcus granulosus (cystic hydatid disease), Echinococcus multilocularis (alveolar hydatid disease), Echinococcus vogeli, and Echinococcus oligarthus (both causing polycystic hydatid disease). [ 4] Echinococcus granulosus requires two hosts. Humans become accidental intermediate hosts. The most common site involved is the liver (59-75%), followed in frequency by lung (27%), kidney (3%), bone (1-4%), and brain (1-2%). Other sites such as the heart, spleen, pancreas, omentum, ovaries, parametrium, pelvis, thyroid, orbit or retroperitoneum, and muscles are very rarely affected. 
A typical hydatid cyst is formed from its embryo. It consists of three layers.  The outer layer (pericyst or adventitia) consists of fibrous tissue, is grey in color, and blends immediately with the liver. It is formed from the host tissue as a result of chronic inflammatory reaction to the parasite. The pericyst usually increases in thickness as the cyst expands. Liver and spleen hydatid cysts have a thick pericyst as compared to peritoneal hydatid cysts, in which the pericyst is extremely thin. The hydatid cysts in the lung and brain have no pericyst at all. Complete calcification of the pericyst may interrupt the nutrient and oxygen supply to the parasites, and thus marks the death of the hydatid cyst. It is elastic, made up of gelatinous, chitinous material and when incised or ruptured, curls in on itself, exposing the inner layer. The innermost germinal layer is cellular and consists of a number of nuclei embedded in a protoplasmic mass. It is a very thin, vital layer of the cyst, and produces brood capsules with scolices, secretes hydatid fluid, and forms the outer layer. The cyst fluid is crystal clear and colorless with a specific gravity of 1005-1010, is slightly alkaline, and is highly antigenic and toxic. Contact with the fluid can give rise to anaphylactic shock. Hydatid cysts expand slowly and asymptomatically, and thus tend to be quite large at presentation. The high secretion pressure is responsible for the progressive enlargement of the cyst. Fluid pressure within a hydatid cyst can reach up to 70 cm of water. The clinical manifestations of hepatic hydatid disease depend upon the site, size and stage of development of the cyst; on whether the cyst is dead or alive and whether it is secondarily infected or not.th  As hydatid cysts grow, they can rupture into the surrounding tissues. Internal rupture occurs due to trauma or pressure necrosis from the growing cyst. Unusual complications of a hepatic hydatid cyst include rupture into the stomach, duodenum or small intestine. Rupture into the biliary tree can cause cholangitis, biliary colic and jaundice with excretion of germinative membranes in the stools  . Bile-stained cyst fluid is an indicator of communication of the cyst with the biliary tract. 
Rupture into the general peritoneal cavity may result in anaphylactic shock and formation of localized or generalized secondary echinococcosis. 
Peritoneal hydatid cyst, either primary or secondary, represents an uncommon but significant manifestation of the disease (approximately 13%). Intraperitoneal hydatid cysts are usually secondary to the rupture (spontaneous or accidental at surgery) of a primary hepatic, splenic, or mesentric cyst. [5 ] A solitary cyst in the pelvic cavity can be considered primary only when no other cysts are present. In such a case, the hydatid embryo gains access to the pelvis by hematogenous or lymphatic route. Pelvic hydatid cysts usually present as a nonspecific mass with pressure effects on adjacent organs such as the rectum and urinary bladder. Rarely, they can cause obstructed labor, obstructive uropathy, and renal failure. Sometimes, they can rupture spontaneously. [8 ]
Serology and imaging are the main tools for establishing diagnosis. Ultrasound is the preferred first-line imaging, but contrast enhanced computed tomography gives more precise information regarding the morphology (size, location, neighborhood, and number) of the cyst. Drug treatment with albendazole has been found to be successful in a proportion of cases, but drug therapy is generally not used as the primary treatment except in cases where the patient is not fit for surgery.
Surgery is the most effective treatment. Combination of preoperative albendazole therapy, surgery, and postoperative albendazole therapy (for 6-8 weeks) is a useful regimen. Albendazole suppresses the development of hydatid cysts following intraperitoneal inoculation of protoscolices.  In order to prevent the rupture and spillage, meticulous dissection has to be done and the area surrounding the cyst should be packed with mops soaked in scolicidal agent. En bloc resection without inducing rupture and spreading the daughter cyst is recommended treatment strategy and accepted to be curative for intramuscular hydatid disease. ,
It has been traditional to inject scolicidal agents into the unopened hydatid cyst because of the risk of spillage into the peritoneal cavity leading to recurrent disease. Cyst fluid contains thousands of protoscoleces and each one has the potential to grow into a new hydatid cyst. Among the various scolicidal agents advocated in the past, formalin was the first and most frequently used agent. Despite its effectiveness, it is no longer used because of the associated toxicity. Ethyl alcohol is the scolicidal agent that is usually preferred for ultrasonic-guided percutaneous aspiration, injection, and reaspiration (PAIR) of hydatid cysts. Unfortunately, it can cause caustic damage to the epithelium of communicating bile ducts leading to sclerosing cholangitis and it is strongly concentration dependent. Hydrogen peroxide has not gained wide acceptance because of low efficacy and complications. Betadine (R) is a disinfectant that is used as a scolicidal agent by many surgeons, but PVP (polyvinylpyrrolidone) storage disease, renal shutdown, sterile peritonitis, and sclerosing serositis are the associated complications and its use is restricted to preoperative local antisepsis of intact adult skin. 
Hypertonic saline and cetrimide have become the scolicidal agents of choice over the past years. Lowest concentration of saline should be 20% and it should not be used in patients who have cysts communicating with biliary tree because of the danger of causing caustic sclerosing cholangitis.
Cetrimide is a potent disinfectant and effective scolicidal agent. Low concentrations of cetrimide (0.1-0.5%) have been used by many surgeons. Cetrimide with chlorhexidine was also recommended as a scolicidal agent  because this combination is a widely available disinfectant solution named as Savlon® . The results of a study showed that Savlon is a very potent scolicidal agent even at very low concentrations that makes it the scolicidal agent of choice in the situations where it is hard to anticipate the volume of the cyst and adjust for dilution of the scolicidal agent.
| Conclusion|| |
Pelvic echinococcosis is rare, with an incidence of 0.2-2.25%. Pelvic hydatid cysts may have varied and nonspecific presentation. Hydatid cyst extending from pelvis to upper abdomen is a rarity. It has to be differentiated from mesenteric cyst. Ultrasonography and computed tomography are both excellent imaging modalities for the detection of hydatid cysts. The treatment of choice for pelvic hydatid cyst is principally a careful and complete surgical excision.
| References|| |
|1.||Lewall DB. Hydatid disease: Biology, pathology, imaging and classification. Clin Radiol 1998;53:863-74. |
|2.||Pedrosa I, Saiz A, Arrazola J, Ferreiros J, Pedrosa CS. Hydatid disease: Radiological and pathological features and complications. Radiographics 2000;20:795-817. |
|3.||Beggs I. The radiology of hydatid disease. AJR Am J Roentgenol 1985;145:639-48. |
|4.||Khuroo MS. Hydatid disease: Current status and recent advances. Ann Saudi Med 2002;22:56-64. |
|5.||Yuksel M, Demirpolat G, Sever A, Bakaris S, Bulbuloglu E, Elmas N. Hydatid disease involving some rare locations in the body: A pictorial essay. Korean J Radiol 2007;8:531-40. |
|6.||Milicevic M. Hydatid disease. In: Blumgart LH, editor. Surgery of the Liver and Biliary Tract. 2 nd ed. New York: Churchill Livingstone; 1994. p. 1121-50. |
|7.||Dew HR. Some complications of hydatid disease. Br J Surg 1930;18:275-93. |
|8.||Seenu V, Misra MC, Tiwari SC, Jain R, Chandrasekhar C. Primary pelvic hydatidcyst presenting with obstructive uropathy and renal failure. Postgrad Med J 1994;70:930. |
|9.||Parray FQ, Ahmad SZ, Sherwani AY, Chowdri NA, Wani KA. Primary paraspinal hydatid cyst: A rare presentation of echinococcosis. Int J Surg 2010;8:404-6. |
|10.||Arazi M, Erikoglu M, Odev K, Memik R, Ozdemir M. Primary echinococcus infestation of the bone and muscles. Clin Orthop Relat Res 2005;432:234-41. |
|11.||LeVeen HH, LeVeen RF, LeVeen EG. The mythology of povidone-iodine and the development of self-sterilizing plastics. Surg Gynecol Obstet 1993;176:183-90. |
|12.||Langer JC, Rose DB, Keystone JS, Taylor BR, Langer B. Diagnosis and management of hydatid disease of the liver. A 15-year North American experience. Ann Surg 1984;199:412-7. |
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6]