Surgical and endoscopic management of remnant cystic duct lithiasis after cholecystectomy--a case series.

INTRODUCTION: Postcholecystectomy syndrome (PCS) as a result of remnant cystic duct lithiasis (RCDL), or gallstones within the cystic duct after cholecystectomy, can cause persistent or recurrent symptoms after cholecystectomy. STUDY DESIGN: A retrospective descriptive analysis was performed for all patients with RDCL at a single institution between 2001 and 2012. Details of presentation, diagnosis, and surgical and endoscopic treatments, and outcomes were collected and analyzed. RESULTS: Twelve patients with RCDL were identified. The interval between cholecystectomy to RCDL discovery was 34.2 months (range 0.5-168 months). On a standard liver enzyme panel, 75% of patients had derangements in ≥1 indices, with the most common single laboratory test abnormality occurring in gamma-glutamyl transferase (GGT) (80%). Eight operative reports noted that the cystic duct was noticeably dilated at the time of cholecystectomy. Two patients developed a cystic duct leak (Strasberg type A bile duct injury) postoperatively, which was managed nonoperatively. Six cases of RCDL required surgery, and six were managed endoscopically. CONCLUSION: RCDL is a potential cause of postcholecystectomy syndrome, but the true incidence is unknown. Laboratory analysis and imaging are helpful in establishing the diagnosis of RCDL. Endoscopic therapy has a role in the treatment of RCDL, but surgical excision of the remnant cystic duct lithiasis may be required.

Computational analysis of the flow of bile in human cystic duct.

Computational fluid dynamic (CFD) simulations of the three-dimensional flow structures in realistic cystic ducts have been performed to obtain quantitative readings of the flow parameters to compare with clinical measurements. Resin casts of real patients' cystic ducts lumen that possess representative anatomical features were scanned to obtain three-dimensional flow domains that were used in the numerical analysis. The convoluting nature of the studied cystic ducts resulted in strong secondary flow that contributed towards a dimensionless pressure drop that is four times higher than those of a straight circular tube of an equivalent length and average diameter. The numerical pressure drop results across the cystic duct compared very well with those obtained from clinical observations which indicate that CFD is an appropriate tool to investigate the flow and functions of the biliary system. From the hydrodynamic point of view, the cystic duct lumen seems to serve as a passive resistor that strives to provide a constant amount of resistance to control the flow of bile out of the gallbladder. This is mainly achieved by the coupling of the secondary flow effects and bile rheology to provide flow resistance.

Non-Newtonian bile flow in elastic cystic duct: one- and three-dimensional modeling.

Bile flow is thought to play an essential role in the pathophysiological genesis of cholelithiasis (gallstone formation) and in gallbladder pain. In this paper, we extend our previous study of the human biliary system (Li et al., 2007, J. Biomech. Eng., 129:164-173) to include two important factors: the non-Newtonian properties of bile, and elastic deformation of the cystic duct. A one-dimensional (1D) model is analyzed and compared with three-dimensional (3D) fluid-structure interaction simulations. It is found that non-Newtonian bile raises resistance to the flow of bile, which can be augmented significantly by the elastic deformation (collapse) of the cystic duct. We also show that the 1D model predicts the pressure drop of the cystic duct flow well for all cases considered (Newtonian or non-Newtonian flow, rigid or elastic ducts), when compared with the full 3D simulations.

Estudo das células leucocitárias no ducto cístico do homem / Study of leukocyte cells in the human cystic duct

As alterações morfológicas detectadas no ducto cístico são similares às encontradas na vesícula biliar. Entretanto, não se encontra na literatura a descrição de células leucocitárias envolvidas nos processos patológicos deste ducto. Com o objetivo de analisar a população de células leucocitárias, ductos císticos de 61 pacientes foram seccionados em quatro segmentos e separadamente estudados. A célula leucocitária mais prevalente nos cortes A, B, C e D foi o linfócito, independentemente do processo inflamatório ser agudo ou crônico. O neutrófilo esteve presente nos processos agudos e crônicos, sem significância estatística entre os cortes. O eosinófilo esteve presente em todos os cortes. Plasmócito, histiócito e folículo linfóide estiveram presentes em um baixo percentual, sem significado estatístico e, especialmente, nos processos crônicos.

Pain patterns after distension of the gallbladder in patients with acute cholecystitis.

BACKGROUND: Visceral pain is characterized by poor pain localization and a referred or radiating pain pattern. Its clinical importance in the abdomen is stressed by the finding that about one-third of patients still complain of abdominal pain after cholecystectomy. A better understanding of symptoms arising from the gallbladder and the underlying pathophysiology is therefore desirable. The aim of the present study was consequently primarily to characterize the symptom patterns after distension of the gallbladder. Secondary aims were to describe the pressure-volume relation in the gallbladder and the cystic duct opening pressure. METHODS: Twelve patients (nine women, three men) treated with cholecystostomy for acute cholecystitis were investigated. Simultaneous cholescintigraphy and measurement of changes in intraluminal gallbladder pressure after injections of saline through a gallbladder catheter were performed. After each injection of saline the localization of pain and the presence of nausea and vomiting were registered. The injections continued until the patient felt abdominal pain necessitating cessation of the investigation or until the cystic duct opened (visualized on cholescintigraphy). RESULTS: Distension of the gallbladder caused pain in 10 of the 12 patients. In 70% the pain was localized under the right costal margin or in the epigastrium. No mathematical formula could describe the pressure-volume relation in the gallbladder. The cystic duct opening pressure varied between 3 and 44 mmHg. CONCLUSIONS: Pain caused by increased gallbladder pressure is localized mostly, but not always, under the right curvature and in the epigastrium. A substantial variation in cystic duct opening pressure was found.

Biliary dyskinesia: role of the sphincter of Oddi, gallbladder and cholecystokinin.

The availability of objective and quantitative diagnostic tests in recent years has allowed more precise documentation of biliary dyskinesia. Biliary dyskinesia consists of two disease entities situated at two different anatomical locations: sphincter of Oddi spasm, at the distal end of the common duct, and cystic duct syndrome, in the gallbladder. Both conditions are characterized by a paradoxical response in which the sphincter of Oddi and the cystic duct contract (and impede bile flow) instead of undergoing the normal dilatation, when the physiological dose of cholecystokinin is infused. Quantitative cholescintigraphy can clearly differentiate one disease entity from the other. The therapies of choice are sphincterotomy, sphincteroplasty or antispasmodics for sphincter of Oddi spasm and cholecystectomy for cystic duct syndrome. After quantitative cholescintigraphy, the final impression should identify the disease entity by name to assist the referring physician in making an appropriate therapeutic decision; a mere statement that a test is consistent with biliary dyskinesia is no longer sufficient.

Cystic duct patency in malignant obstructive jaundice. An ERCP-based study relevant to the role of laparoscopic cholecystojejunostomy.

OBJECTIVE: This endoscopic retrograde cholangiopancreatography-(ERCP)based study estimates the potential role of laparoscopic cholecystojejunostomy for palliation of patients with malignant obstructive jaundice. SUMMARY BACKGROUND DATA: Traditional treatment of malignant obstructive jaundice has used a standard bilioenteric anastomosis. Laparoscopic biliary bypass via a gallbladder conduit currently is an established technique; it provides a low initial morbidity alternative to open procedures, similar to endoscopic stenting. No study has specifically addressed anatomic factors relevant to cholecystojejunostomy, such as prior cholecystectomy, stricture location in reference to the hepatocystic junction, and cystic duct patency in patients with malignant obstructive jaundice. METHODS: Retrograde cholangiograms were reviewed from consecutive patients with malignant obstructive jaundice and a control group without biliary disease who underwent ERCP during a 2-year period. Patients with either prior biliary surgery or hilar tumors were excluded. The presence of gallbladder or cystic duct filling was assessed. In patients with patent cystic ducts, the distance from obstruction to the cystic duct takeoff was classified as either greater or less than 1 cm. RESULTS: Nearly half the patients with malignant obstructive jaundice were ineligible for cholecystojejunostomies because of prior biliary surgery (29%) or hilar tumors (17%). Half (50 of 101) of the remaining potential candidates had patent hepatocystic junctions. Patients with ampullary carcinoma and patent hepatocystic junctions (5 of 9) were all ideal candidates for cholecystojejunostomies, having biliary obstruction more than 1 cm from the cystic duct takeoff. Two thirds of the remaining eligible patients (28 of 45) had obstructions less than 1 cm from patent hepatocystic junctions. CONCLUSIONS: Palliation of malignant obstructive jaundice by laparoscopic cholecystojejunostomy should only be attempted after direct cholangiography demonstrates a patent hepatocystic junction that is well separated from the malignant stricture. The majority of patients with malignant obstructive jaundice are ineligible for cholecystojejunostomies because of prior cholecystectomies, hilar obstructions, or tumor involvement of the hepatocystic junction. Nonoperative treatments will continue to be indicated for the majority of patients with malignant obstructive jaundice.

Oral cholecystography compared to cholescintigraphy for evaluation of cystic duct patency prior to ESWL treatment.

In a prospective, blinded study of 109 patients with cholecystolithiasis, oral cholecystography and 99Tcm-EHIDA cholescintigraphy were compared in terms of reliability for demonstrating cystic duct patency: one of the prerequisites for extracorporeal shock wave lithotripsy (ESWL) treatment of cholecystolithiasis. Patients with a positive result on one or both tests were regarded as having cystic duct patency. Patients with negative and uncertain result of both tests or one of each were regarded as having no cystic duct patency. Concordance between the two tests was obtained in 93 of 109 patients. The diagnostic reliability of cholescintigraphy and oral cholecystography were 95 and 86%, respectively (P < 0.05), suggesting a more precise determination of gallbladder filling with scintigraphy.

The value of sonography in determining cystic duct patency.

A prospective blinded comparison of ultrasonography (US) and oral cholecystography (OCG) was performed in 100 patients with symptomatic gall-stones to determine whether US would enable an accurate assessment of cystic duct patency to be made. Patency of the cystic duct was defined as gall-bladder opacification on OCG or a greater than 20% decrease in gall-bladder volume by US post-fatty meal. The ellipsoid method of volume measurement was used. Any patient who had a non-opacified gall-bladder on OCG but a greater than 20% volume decrease on US had cholescintigraphy performed (DISIDA). Oral cholecystography demonstrated cystic duct patency in 88 patients (88%), and fatty-meal gall-bladder US met the specified study criteria for patency in 86 patients (86%). False negative results were identified in four of the OCG and in six of the US examinations. The results of this study indicate that gall-bladder sonography with a post-fatty meal contraction of greater than 20% is a very accurate predictor of cystic duct patency. A contraction of less than 20%, however, cannot be considered a reliable predictor of cystic duct occlusion.

[Anti-reflux biliary-digestive anastomosis including the gallbladder in the light of long-term results]. / Arefliuksnye biliodigestivnye anastomozy s zhelchnym puzyrem v svete otdalennykh rezul'tatov.

The authors provide the long-term results of cholecysto-digestive + anastomoses in 59 patients operated on for nontumorous diseases. The gallbladder anastomosed with the upper parts of the alimentary tract preserved reservoir and concentration functions, ability for visualization during cholecystocholangiography. The discrete pulse mechanism of bile secretion via the bile diverting anastomoses and their antireflux function eliminated the risk of chronic pancreatitis and terminal cholangitis. The recovery of deranged liver functions and excretory functions of the pancreas were traced during the postoperative period within 2 to 21 years.

Alterations in biliary motility correlate with increased gallbladder prostaglandin synthesis in early cholelithiasis in prairie dog.

Abnormal biliary motility has been observed in humans with gallstones and in animal models; however, the mechanism by which these abnormalities occur remains unknown. In this study we investigated the relationship between cholesterol gallstone formation, changes in biliary motility, and rates of gallbladder prostaglandin synthesis in prairie dogs receiving a 0.34% cholesterol diet for two, four, or six weeks. Gallstones did not occur until four weeks, when the incidence was 14%; after six weeks the incidence was 64%. Gallbladder emptying increased slightly at two weeks before becoming significantly decreased at four and six weeks. In contrast, there was a near linear increase in basal cystic duct resistance which began by two weeks of cholesterol feeding, although sphincter of Oddi resistances remained normal throughout the period of study. The synthesis of prostaglandins E and F2 alpha by the gallbladder was also increased beginning at two weeks and rose to a plateau at four and six weeks. In view of the potent effects of prostaglandins on biliary smooth muscle, these findings suggest that prostaglandins may mediate early changes in gallbladder and cystic duct motility which ultimately result in impaired gallbladder emptying.

Choledochal cyst presenting as acute pancreatitis.

A case of a 2 year old boy who presented with pancreatitis in association with choledochal cyst is reported. The pathogenesis, clinical presentation and surgical management are discussed.

Effects of histamine receptor stimulation on diseased gallbladder and cystic duct.

The effects of histamine receptor stimulation on the motility of diseased human gallbladder and cystic duct were studied on tissue strips in vitro. Histamine produced concentration-dependent contractions in normal tissues and in tissues from each disease group, but the sensitivity of the strips to histamine as measured by the median effective dose was dependent upon the grade of disease: normal, 90.0 microM; mild chronic cholecystitis, 32.4 microM; advanced chronic cholecystitis, 12.5 microM; and acute cholecystitis, 3.0 microM. There were no differences in histamine sensitivity among different regions (body, neck, and cystic duct) of the biliary system. Studies with receptor-selective agonists and antagonists indicated that the contractile effects were mediated via histamine H1 receptors. Histamine H2 receptor agonists caused only small relaxant responses in about 30% of strips from gallbladder body, but were without effect in gallbladder neck and cystic duct. We conclude that the effects of histamine on the motility of diseased human gallbladder may depend upon the severity of the cholecystitis.

Impaired gallbladder emptying before gallstone formation in the prairie dog.

Several human and experimental observations suggest that gallbladder stasis is an important link between the hepatic secretion of cholesterol saturated bile and the formation of cholesterol gallstones. In the cholesterol-fed prairie dog model, gallbladder stasis occurs before gallstone formation. In this study we sought to determine the specific defects in extrahepatic biliary physiology responsible for gallbladder stasis in this model. Adult male prairie dogs were fed either a trace cholesterol or a 0.4% cholesterol-enriched diet. In acute terminal experiments, gallbladder contents were examined for cholesterol crystals and gallstones, and gallbladder function was determined at rest and in response to intravenous cholecystokinin-octapeptide. The following alterations in gallbladder function developed concurrently with biliary cholesterol crystallization, but before gallstone formation: (a) decreased gallbladder emptying, (b) increased intragallbladder pressure in response to cholecystokinin-octapeptide, (c) increased cystic duct closing pressure, and (d) increased resistance to outflow through the cystic duct.

Stasis before gallstone formation: altered gallbladder compliance or cystic duct resistance?

Gallbladder stasis occurs before gallstone formation and provides the link between the hepatic secretion of supersaturated bile and cholesterol cholelithiasis. We recently observed that cystic duct resistance increases while sphincter of Oddi resistance is unchanged in the presence of lithogenic bile without gallstones. Whether alterations in gallbladder function also lead to gallbladder stasis has been unclear. Therefore, we tested the hypothesis that before gallstone formation, stasis results from increased cystic duct resistance and altered gallbladder compliance. Adult, male prairie dogs were fed either a trace cholesterol (control) or a 0.4 percent cholesterol-enriched diet. Cystic duct resistance increased but gallbladder compliance was unchanged before gallstone formation. A significant correlation (p less than 0.001) was found between the lithogenic index and cystic duct resistance in pregallstone animals. We conclude that increased resistance to flow across the cystic duct, and not altered gallbladder compliance, is etiologically related to bile stasis, an important event in gallstone formation.