Abstracts Bile duct iqjuries after laparoscopic report oa management of 53 patients.
/Netherlands
cholecystectomy
Journal (Lc);
J.J.G.H.M. Bergman ‘, G.R. van den Brink i, E.A.J. Rauws ‘, L.T. de Wit 2, H. Obertop 2, K. Huibregtse ‘, G.N.J. Tytgat ‘, D.J. Gouma 2.
Departments of ’ Gastroenterology and Medical Centre, Amsterdam, Netherlands.
2 Surgery,
Academic
From January 1990 to June 1994,53 patients with bile duct injuries after LC were managed at our hospital. There were 16 males and 37 females with a mean age of 47 years. Follow-up was established in all patients for a median of 17 months (range l-38). Four types of ductal injury were identified. Type A (18 pts) had leakage from cystic ducts or peripheral hepatic radicles, type B (11 pts) had major bile duct leakage, type C (9 pts) had an isolated ductal stricture, and type D (15 pts) had complete transection of the bile duct. Diagnosis: ERCP established the diagnosis in all type A, B, and C lesions. In type D lesions percutaneous cholangiography was required to delineate the proximal extent of the injury. Initial management (until resolution of symptoms and discharge from hospital) comprised endoscopy in 36 patients and surgery in 26 patients: Endoscopic management: Endoscopic management was possible and successful in 16/18 of type A lesions, 5/7 of type B lesions, and 3/9 of type C lesions. The majority of failures were due to inability to pass strictures or leaks at the initial endoscopy. During initial management additional surgery was required in 7 patients. Fourteen patients underwent percutaneous and/or surgical drainage of bile collections. After endoscopic treatment early complications occurred in 3 patients, with a fatal outcome in 2. During follow-up 6 patients developed late complications. Surgical management: All 15 patients with complete transection and 4 patients with major bile duct leakage were initially managed surgically. Two patients required additional endoscopic stenting. Early complications occurred in 8 patients. During follow-up 7 patients developed stenosis of the anastomosis. Conclusions: The majority of type A and B bile duct injuries after LC can be managed endoscopically. In patients with more severe ductal injury (type C and D) surgery is often required. A multidisciplinary approach to these lesions is advocated.
of Medicine
47 (1995)
Al -A42
A29
Sprague-Dawley rats with the following controls: sham, ileal transection, unoperated, proximal and distal jejunectomy, ileo-colonic transposition and ileocaecectomy. In additional sets of experiments in both ileectomized and ileal transected animals, we prevented coprophagy by means of a 6-cm cervical collar and steel wire caging. Transient diarrhoea (2-3 days) occurred in 75% of ileectomies, 67% of ileocaecectomies, 33% of distal jejunectomies, 33% of ileal transections and 17% of ileo-colonic transpositions, and in none of the sham-operated animals. On 3, 5, 8 and 11 postoperative days, the bile duct was cannulated and bile collected for 5 h. B conjugates and unconjugated B (UCB) were measured by HPLC and BS were assayed by standard methods. During O-30 min of cannulation, which is most representative of “intact” EHC of bile salts CBS), total B secretion was significantly (p < 0.001) increased 3 days after ileectomy, distal jejunectomy, ileo-colonic transposition and ileocaecectomy compared with controls. Progressive adaptation of the residual small bowel occurred following ileectomy and restored BS absorption and abolished enterohepatic cycling of B by the 11th postoperative day. BS secretion was also increased significantly (p 5 0.005) 3 days following ileectomy compared with sham-operated rats; however, prevention of coprophagy decreased BS secretion dramatically, whereas B secretion was not affected appreciably. This suggests that in ileectomized animals oral ingestion of faeces contributed to enterohepatic cycling of BS, but not of B. Di-/monoconjugate ratios of B were significantly (p I 0.005) increased following ileectomy and distal jejunectomy compared with sham, unoperated and proximal jejunectomized animals and UCB secretion was invariably < 1% of total B secretion. In no animal did haemolysis occur as evident by the clinical haemogram and UCB in caecal extracts was invaribly elevated in ileectomized animals. Conclusions: Distal small bowel resection in rats results in increased biliaty secretion of B to 1.5-2-fold that of controls. Most likely this occurs because increased levels of BS in the proximal colon may solubilize deconjugated B, prevent its conversion to urobilinogen and promote its passive absorption. We conclude that these results are consistent with the hypothesis that enterohepatic cycling of UCB is induced by distal small bowel resection, providing a pathophysiological basis for pigment gallstone formation in patients with heal disease, resection or bypass.
Enterobepatic cycling (EHC) of bilirubin in the ileectomized rat: pathophysiological implications. M.A. Brink *, N. Mindez-Sanchez ‘, M.C. Carey 3. t Department of Gastroenterology, Academic Medical Centre, Amsterdam, Netherlands; 2 National Institute of Nutrition, Mexico City, Mexico; 3 Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA.
Soluble ICAMin primary biliiry citisis combined treatment with ursodeozychollc and azathioprlne. F.H.J. Wolfhagen I,
A.G. Lim 2, A. Verma *, H.R. van Buuren *, R.P. Jazrawi 2, T.C. Northfield ‘, S.W. Schalm ‘. ’ Department of Internal Medicine II, University
Recent studies have shown that patients with ileal disease, resection or bypass are at risk of developing pigment gallstones. Since total bilirubin (B) levels in gallbladder bile play an important role in pigment gallstone formation, we investigated whether ileal resection in rats results in increased biliary B secretion. We performed 100% ileectomy in
Intercellular adhesion molecule-l @CAM-l) is important for leucocyte migration into the liver and T-cell activation, which both play a role in the pathogenesis of PBC. ICAMand its soluble counterpart (sICAM-1) are shed by activated lymphocytes and inflammatory cytokine-stimulated liver cells. In PBC, sICAM-1 levels are elevated and reflect disease
Hospital, Rotterdam, St. George’s Hospital,
Netherlands; 2 Department London, UK.
(PBC) during acid, prednisone
of Medicine.