|Year : 1983 | Volume
| Issue : 4 | Page : 262-6
Hydatid cyst as a cause of common bile duct obstruction (a case report).
SK Mathur, RR Shah, AB Samsi, MD Kelkar
S K Mathur
|How to cite this article:|
Mathur S K, Shah R R, Samsi A B, Kelkar M D. Hydatid cyst as a cause of common bile duct obstruction (a case report). J Postgrad Med 1983;29:262-6
|How to cite this URL:|
Mathur S K, Shah R R, Samsi A B, Kelkar M D. Hydatid cyst as a cause of common bile duct obstruction (a case report). J Postgrad Med [serial online] 1983 [cited 2023 Oct 4 ];29:262-6
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Association of hepatic hydatid cyst with bile duct obstruction is not a common occurrence. For the first time it was described by Dew. It follows the rupture of hydatid cyst of the liver into the biliary tree and gives rise to a clinical picture simulating choledocholithiasis.,  In the countries where the hydatid disease is common, the reported incidence of intrabiliary rupture varies from 5-17% of the cases with hepatic involvement., , , 
Not even a single case report of bile duct obstruction by hydatid cyst was found in the Indian reported literature on hepatic hydatid disease., , 
This paper describes a case of common bile duct obstruction by hydatid daughter cysts, where the diagnosis could be established at operation only.
A 40 year old female resident of Madhya Pradesh was referred to us on 7th December 1982 for the management of obstruction of the lower end of the common bile duct by a retained calculus.
The history dated back to 13th October 1982 when the patient had the first attack of sudden pain in the right hypochondrium, associated with fever and nausea and was admitted to a local hospital. She was found to have mild fever, icterus and marked tenderness and guarding in the right hypochondrium. There was no palpable lump in the abdomen. A clinical diagnosis of acute cholecystitis was made; the patient improved with conservative treatment. Investigations done at that time did not show any abnormality in the haemogram. Liver functions showed that serum bilirubin was 3.0 mg%, SCOT 55 U/L, SGPT 79 U/L, and alkaline phosphatase was 475 U/L. Oral cholecystogram done a few days later showed non-opacification of the gall bladder. She was discharged with an advice to undergo cholecystectomy after 6 weeks. On 30-10-82 she was readmitted due to recurrence of pain in the abdomen, which became severe on 3-11-1982. At that stage a markedly tender, enlarged gall bladder lump was palpable. The surgeon incharge suspected it to be an empyema of the gall bladder with impending rupture and performed an emergency exploratory laporotomy on the same day. At operation, the gall bladder was found to be distended and congested. The common bile duct was also dilated. Cholecystectomy was done and the common bile duct was explored, but no calculi were found. Bake's dilater could be passed into the duodenum through the papilla of Vater without obstruction. A post-exploratory 'T' tube cholangiogram showed only a trickle of the dye entering the duodenum, but the same done on the 10th post-operative day showed a complete obstruction at the lower end of the common bile duct. The obstruction was thought to be due to a missed stone and the case was referred to us for further management.
Histopathological examination of the gall bladder showed evidence of acute inflammation.
The patient was admitted to the K.E.M. Hospital on 7-12-1982. General physical examination and abdominal examination were unremarkable. The repeat haemogram and liver function tests were found to be within normal limits. A 'T' tube cholangiogram was repeated which showed a persistent filling defect with concavity downwards at the lower end of the common bile duct (? stone) [Fig.1]. No dye entered the duodenum. Ultrasound showed hepatomegaly with dilated C.B.D. but no echogenic area and no acoustic shadow.
During the hospital stay the 'T' tube used to drain about 500-1000 ml of bile per day.
The patient was re-explored on 11-12-1982 with a tentative diagnosis of (1) retained stone in the C.B.D., (2) stricture at the lower end of the C.B.D. or (3) carcinoma of the head of the pancreas. The lower end of the common bile duct was explored through a transduodenal approach. The papilla of Vater appeared normal and no stone was palpable. At that stage the `T' tube was flushed with normal saline, but the fluid did not enter the duodenum, indicating on obstruction. Hence sphincteroplasty was performed to explore the lower part of the common bile duct under vision. At completion of sphincteroplasty, whitish material was found to be pouting from the bile duct which when pulled out with an artery forceps was found to be a daughter hydatid cyst. Still the bile did not start flowing into the duodenum, so the "T" tube was again flushed with saline and another daughter cyst came out. After that bile started flowing freely into the duodenum. A cholangiogram done at that stage did not reveal any more filling defects. The diagnosis was obvious that the obstruction of the bile duct was caused by these hydatid cysts coming from the liver. The liver was palpated thoroughly for the presence of a hydatid cyst on the surface but none could be found. The duodenum was closed in two layers. Each hydatid daughter cyst measured about 2.5 cm in diameter [Fig.2]. The histopathological examination confirmed the diagnosis.
Post-operatively, the patient made an uneventful recovery. `T' tube cholangiogram done on the 10th post-operative day showed free flow of the dye into the duodenum. The `T' tube was removed on the 12th post-operative day.
Retrospectively, we reviewed her X-rays and found one of the plain skiagrams showing patchy rim of calcification in the right lobe of the liver. A repeat ultrasound revealed a cyst in the right lobe of the liver, 6 x 6 x 6 cm in size, showing multiple plaque-like calcification. Liver scan showed definite cold area in the right lobe of the liver on the posterosuperior aspect.
As the mother cyst from the liver was not removed, the patient was discharged on mebendazole therapy.
Rupture of hydatid cyst of the liver into the biliary tree allows the entry of the daughter cysts, hydatid sand and pieces of hydatid membrane into the bile duct, thereby causing partial or complete obstruction to the outflow of the bile and cholangitis. Most of the patients present with features of recurrent attacks of right hypochondriac pain, fever and intermittent or persistent obstructive jaundice and a palpable liver mass.,  Initially, the obstruction of the bile duct is partial, so that some bile may still trickle by the side of the hydatid membrane, and may become complete later on, as was seen in the present case. Out of 15 reported cases by Kattan, 7 had complete bile duct obstruction. A palpable gall bladder is exceptional and if present is thought to be empyema of the gall bladder. In the present case also the first operation was performed in emergency with a tentative diagnosis of empyema of gall bladder because of presence of a palpable, tense, tender mass.
It is difficult to suspect the diagnosis pre-operatively. In most of the reported cases, the diagnosis has been made only at operation, the pre-operative diagnosis being calculus jaundice,,  amoebic liver abscess, cholangitis, empyema of gall bladder or carcinoma of the head of the pancreas. In the present case also at the time of second surgery we considered the possibilities of common bile duct obstruction either due to missed stone (`T' tube cholangiogram suggested that), or carcinoma of the head of the pancreas or a stricture of the lower end of the bile duct.
Investigations are not of much help in establishing the diagnosis. Plain skiagram of the abdomen may be of some help in suggesting the diagnosis if it shows calcification in the hepatic region. Kattan found calcification of the hepatic hydatid cyst in 3 out of his 15 cases with intrabiliary rupture. In the present case, the calcification was so faint and patchy that it was missed pre-operatively and was seen only when the X-rays were reviewed after the diagnosis had already been established at operation.
A cholangiogram obtained either by the technique of fine needle percutaneous transhepatic punctures,,  or through "endoscopic retrograde cannulation of the bile duct", has been reported to be of help in establishing the correct preoperative diagnosis. It may demonstrate a communication between the main cyst and bile duct and show irregular, ill defined, filling defects in the biliary tree. But in the present case a cholangiogram obtained through a `T' tube did not help as it showed a rounded filling defect with concavity downwards (typical of a calculus) at the lower end of the common bile duct. It also did not show any communication between the mother cyst and the bile duct.
Ultrasonography has also been exploited for the diagnosis of hepatic hydatid cysts. But so far only one case of intrabiliary rupture has been tentatively diagnosed by it. In the present case also ultrasound failed to give the cause of common bile duct obstruction though it did show dilatation of the bile ducts.
Treatment is surgical exploration of the common bile duct and removal of the daughter cysts, membranes and hydatid stones with dilatation of ampulla of Vater. Mother cyst in the liver should be dealt with at the same time or subsequently and opening in the bile duct should be closed. However, in the present case the hepatic cyst was left alone as the location of the cyst in the liver was not known and could not be made out even by palpation. Moreover, pre-operative or per-operative cholangiogram did not show any communication between the biliary tree and the main liver cyst.
According to Kaitan, gall bladder should not be removed unless inflamed or full of daughter cysts or stones, as it might be required for bypass at a later date. In the present case the gall bladder was inflamed and hence was removed at the time of the first surgery.
We feel that sphincteroplasty must be done to prevent the future attacks of obstruction with daughter cysts, particularly if it has not been possible to remove the mother cyst. Barros has also favoured a sphincteroplasty in these cases.
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