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Table of Contents
CASE REPORT
Year : 2022  |  Volume : 11  |  Issue : 5  |  Page : 27-29

An infective cause of obstructive jaundice


Department of General Medicine, Nizam's Institute of Medical Sciences, Hyderabad, Telangana, India

Date of Submission18-Dec-2020
Date of Acceptance21-May-2025
Date of Web Publication30-Aug-2022

Correspondence Address:
Y Sathyanarayana Raju
Professor, Department of General Medicine, Nizam's Institute of Medical Sciences, Panjagutta, Hyderabad 500 082, Telangana
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/JCSR.JCSR_98_20

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  Abstract 


A 48-year-old mason, smoker and alcoholic came with complaints of yellowish discolouration of eyes with high coloured urine and pale stools for 15 days. The patient also had abdominal pain that increased on food intake and dyspnoea on exertion. The patient also had anorexia and significant weight loss. On examination, icterus was evident. The blood pressure was 70/50 mm Hg, features of shock were present. Leucocytosis with left shift was observed with conjugated hyperbilirubinaemia was present. Abdominal ultrasonography showed a cystic lesion with peripheral calcification. Contrast-enhanced computed tomography revealed stage 2 hydatid cyst with dilatation of common biliary duct (CBD), right hepatic duct (RHD) and left hepatic duct (LHD) and intrahepatic biliary radicles due to compression at the confluence of RHD and LHD. Endoscopic retrograde cholangio-pancreatography showed a dilated CBD with multiple filling defects and membranes on balloon sweepage. CBD Stenting was done. Patient's general condition improved and was taken up for surgery.

Keywords: Cholangitis, echinococcus, shock


How to cite this article:
Pappu SS, Kamani NB, Akula S, Raju Y S, Chandra N. An infective cause of obstructive jaundice. J Clin Sci Res 2022;11, Suppl S1:27-9

How to cite this URL:
Pappu SS, Kamani NB, Akula S, Raju Y S, Chandra N. An infective cause of obstructive jaundice. J Clin Sci Res [serial online] 2022 [cited 2022 Dec 7];11, Suppl S1:27-9. Available from: https://www.jcsr.co.in/text.asp?2022/11/5/27/355067




  Introduction Top


Echinococcosis is caused by the larval stage of Echinococcus granulosus sensu lato, E. multilocularis, or E. vogeli. E.granulosus produces cystic hydatid disease, with unilocular cystic lesions.[1] These infections are prevalent in areas where livestock is raised in association with Dogs and other canines. Humans are accidental and dead-end hosts. The disease is acquired by consuming contaminated food and water with canine feces. We present a case of sepsis secondary to cholangitis with underlying class 2 hydatid cyst.[1]


  Case Report Top


A 48-year-old male, mason with no prior comorbidities presented with complaints of yellowish discoloration of eyes for 15 days associated with pale stools and high colored urine. He complained of pain abdomen which was in the umbilical region and right upper quadrant and dyspnoea on exertion. He also complained of low-grade fever that subsided at presentation to the hospital. He had anorexia and a weight loss of 5 kg in 2 months. He denied any history of pruritus, vomitings or dyspeptic symptoms. He had no history of haematemesis or malena. He did not have any similar episodes in the past. He has a history of alcohol abuse and 10 pack-years of smoking.

On examination, the patient was in shock and had icterus. There were no stigmata on chronic liver disease. He had tender hepatomegaly 4 cm below the right costal margin. Laboratory investigations revealed leucocytosis of 29,900 with the left shift. Liver function tests showed conjugated hyperbilirubinaemia (4.5 mg/dL), serum alkaline phosphatase 148 IU/L, serum aspartate aminotransferase (AST) 123 IU/L, serum alanine aminotransferase (ALT) 81 IU/L, serum abumin 2.1 g/dL. The prothrombin time, activated partial thromboplastin time and international normalised ratio were within normal range. Serum procalcitonin was 3.52 ng/mL. Anti Echinococcus immunoglobulin G (IgG) antibody tested negative by enzyme linked immunosorbent assay (ELISA) method.

Abdominal ultrasonography showed a heterogeneously hyperechoic lesion with hypoechoic linear strands, lateral to the portal vein in the right lobe of the liver with no vascularity. The liver was normal Echotexture. Contrast-enhanced computed tomography (CECT) revealed a large 10.1 cm × 8.5 cm well defined non-enhancing cystic lesion with peripheral calcifications in the right lobe of the liver extending into the sub capsular region, compressing the confluence of the right and left hepatic ducts suggestive of a stage 2 hydatid cyst [Figure 1]. There was dilatation of common biliary duct, right and left hepatic ducts, and hepatic biliary radicule dilatation. The CT also showed cholangitic abscesses in the left lobe of the liver.
Figure 1: Contrast-enhanced computed tomography showing a well-defined, nonenhancing cystic lesion with peripheral rim calcification in the right lobe of the liver, extending up to the sub capsular region

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The patient was managed with inotropic support and intravenous (IV) piperacillin-tazobactum and IV metronidazole for cholangitic abscesses. The transamnitis resolved in due course but the serum alkaline phosphatase was persistently elevated, consistent with obstructive jaundice. He was also started on 10 mg/kg albendazole. The patient had improved, the leucocytosis resolved and was taken up for surgery as there was sub capsular extension of the cyst.


  Discussion Top


E. granulosus has a worldwide distribution. E. multilocularis, causes multilocular alveolar lesions that are locally invasive. E. vogeli causes polycystic hydatid disease.[1] The definitive hosts are canines that pass eggs in their faeces. After the ingestion of eggs, cysts develop in the intermediate hosts–sheep, cattle, humans, goats.

The adult E. granulosus has three proglottids and the gravid proglottid splits to release eggs. After humans ingest the eggs, embryos penetrate the intestinal mucosa and are carried most commonly to the liver and lungs. Larvae of E. granulosus develop into fluid-filled unilocular hydatid cysts that consist of an external membrane and an inner germinal layer. Daughter cysts develop from the inner aspect of the germinal layer, as do germinating cystic structures called brood capsules.

Hydatid cysts are usually asymptomatic. As the cysts grow within the liver, they begin to cause low-grade fever, pain, tender hepatomegaly (usually affecting the right lobe), and eosinophilia. Compression of a bile duct or leakage of cyst fluid into the biliary tree may mimic recurrent cholelithiasis, and biliary obstruction can result in jaundice. Rupture of hydatid cysts, which can occur spontaneously or at surgery, may lead to multifocal dissemination of protoscolices, which can form additional cysts. More extensive rupture into the peritoneum or lungs may lead to a life-threatening anaphylactic reaction to the cyst contents.[2]

Diagnosis of Echinococcosis is achieved by a combination of serologic tests and imaging. The liver enzyme tests are abnormal in only 40% of patients. Serum alkaline phosphatase is commonly elevated, while aspartate/alanine transaminase ratios and bilirubin levels typically remain within the normal limits. Calcification can be seen on radiographs in up to 30% of cystic echinococcosis (CE) cases.[3] The calcifications are usually curvilinear or ring-like and are deposited in the pericyst.

The sensitivity and specificity of both ultrasonography and computed tomography (CT) in confirming the diagnosis are high.[4] Both modalities can demonstrate intra cystic septations and daughter cyst formation in about half of the cysts. Diagnostic accuracies for ultrasound reach close to 90%.[5] On ultrasonography, the cyst wall has a hypoechoic layer, flanked by an echogenic line on either side.

CT has a sensitivity rate approaching 94%.[6] It detects biliary and vascular involvement, cyst ruptures and underlying infection.[7],[8] CECT may display avascular cysts with ring enhancement. ELISA has a sensitivity of 84% to 90% in the diagnosis.[1] Assays for detecting circulating antigens are likely to provide additional diagnostic benefits in the future. Casoni's test is presently not used.[9],[10]

Treatment is based on the location and staging of the cyst ranging from non-invasive puncture, aspiration, injection (of a scolicidal agent), and re-aspiration (PAIR) to lobectomy of the liver. PAIR is recommended for CE1 and uncomplicated CE3 cysts. PAIR is contraindicated for superficially located cysts, cysts with multiple thick internal septal divisions, and for cysts communicating with the biliary tree. For prophylaxis of secondary peritoneal echinococcosis due to inadvertent spillage during PAIR, the administration of albendazole (10–15 mg/kg daily in two divided doses) should be initiated 2 days before the procedure and continued for at least 4 weeks afterwards.[11]

Surgery remains the treatment of choice for complicated cystic echinococcosis (e.g., cysts communicating with the biliary tract),[2] for most thoracic and intracranial cysts. For liver cysts, the preferred surgical approach is total cystectomy, in which the entire cyst and the surrounding fibrous tissue are removed. Response to treatment is best assessed by serial imaging studies.

Declaration of patient consent

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

Financial support and sponsorship

Nil.

Conflicts of interest

Y Sathyanarayana Raju is an Editor of Journal of Clinical and Scientific Research. The article was subject to the journal's standard procedures, with peer review handled independently of these faculty and their research groups.



 
  References Top

1.
McManus DP, Zhang W, Li J, Bartley PB. Echinococcosis. Lancet 2003;362:1295-304.  Back to cited text no. 1
    
2.
Murali MR, Uyeda JW, Tingpej B. Case records of the massachusetts general hospital. case 2-2015. A 25-year-old man with abdominal pain, syncope, and hypotension. N Engl J Med 2015;372:265-73.  Back to cited text no. 2
    
3.
Beggs I. The radiology of hydatid disease. Am J Roentgenol 1985;145:639-48.  Back to cited text no. 3
    
4.
Czermak BV, Akhan O, Hiemetzberger R, Zelger B, Vogel W, Jaschke W, et al. Echinococcosis of the liver. Abdom Imaging 2008;33:133-43.  Back to cited text no. 4
    
5.
WHO Informal Working Group. International classification of ultrasound images in cystic echinococcosis for application in clinical and field epidemiological settings. Acta Trop 2003;85:253-61.  Back to cited text no. 5
    
6.
Marrone G, Francesca Crino SC, Mamone G, Carollo V, Milazzo M, Gruttadauria S, Luca A, Gridelli B. Multidisciplinary imaging of liver hydatidosis. World journal of gastroenterology: WJG 2012;18:1438.  Back to cited text no. 6
    
7.
Langer JC, Rose DB, Keystone JS, Taylor BR, Langer BE. Diagnosis and management of hydatid disease of the liver. A 15-year North American experience. Annals of surgery 1984;199:412.  Back to cited text no. 7
    
8.
Stojkovic M, Rosenberger K, Kauczor HU, Junghanss T, Hosch W. Diagnosing and staging of cystic echinococcosis: how do CT and MRI perform in comparison to ultrasound?. PLoS Negl Trop Dis 2012;6:e1880.  Back to cited text no. 8
    
9.
Richter J, Hatz C, Häussinger D. Ultrasound in tropical and parasitic diseases. Lancet 2003;362:900-2.  Back to cited text no. 9
    
10.
Brunetti E, Kern P, Vuitton DA. Expert consensus for the diagnosis and treatment of cystic and alveolar echinococcosis in humans. Acta tropica. 2010;114:1-6.  Back to cited text no. 10
    
11.
Keshmiri M, Baharvahdat H, Fattahi SH, Davachi B, Dabiri RH, Baradaran H, et al. Albendazole versus placebo in treatment of echinococcosis. Transactions of the Royal Society of Tropical Medicine and Hygiene 2001;95:190-4.  Back to cited text no. 11
    


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