BACKGROUND: Cholangiocarcinoma (CCA) is a lethal cancer of the biliary epithelium, originating from the liver (intrahepatic), at the confluence of the right and left hepatic ducts (hilar) or in the extrahepatic bile ducts. It is a rare malignancy associated with poor prognosis.
DATA SOURCES: We searched the PubMed/MEDLINE database for relevant articles published from 1989 to 2008. The search terms used were related to "cholangiocarcinoma" and its "treatment". Although no language restrictions were imposed initially, for the full-text review and final analysis, our resources only permitted the review of articles published in English. This review deals with the treatment of cholangiocarcinoma, the principles and the current trends.
RESULTS: The risks and prognostic factors, symptoms and differential diagnosis are thoroughly discussed. In addition, the tools of preoperative diagnosis such as endoscopic retrograde cholangiopancreatography, digital image analysis, fluorescence in situ hybridization and magnetic resonance cholangiopancreatography are reviewed. Moreover, the treatment of CCA is discussed.
CONCLUSIONS: The only curative treatment available is surgical management. Unfortunately, many patients present with unresectable tumors, the majority of whom die within a year of diagnosis. Surgical treatment involves major resections of the liver, pancreas and bile duct, with considerable mortality and morbidity. However, in selected cases and where indicated, appropriate management with aggressive surgery may achieve a good outcome with a prolonged survival expectancy.

BACKGROUND: Adenocarcinoma of the pancreas exhibits aggressive behavior in growth, inducing an extremely poor prognosis with an overall median 5-year survival rate of only 1%-4%. Curative resection is the only potential therapeutic opportunity.
DATA SOURCES: A PubMed search of relevant articles published up to 2009 was performed to identify information about the value of lymphadenectomy and its extent in curative resection of pancreatic adenocarcinoma.
RESULTS: Despite recent advances in chemotherapy, radiotherapy or even immunotherapy, surgery still remains the major factor that affects the outcome. The initial promising performance in Japan gave conflicting results in Western countries for the extended and more radical pancreatectomy; it has failed to prove beneficial. Four prospective, randomized trials on extended versus standard lymphadenectomy during pancreatic cancer surgery have shown no improvement in long-term survival by the extended resection. The exact lymph node status, including malignant spread and the total number retrieved as well as the lymph node ratio, is the most important prognostic factor. Positive lymph nodes after pancreatectomy are present in 70%. Paraaortic lymph node spread indicates poor prognosis.
CONCLUSIONS: Undoubtedly, a standard lymphadenectomy including >15 lymph nodes must be no longer preferred in patients with the usual head location. The extended lymphadenectomy does not have any place, unless in randomized trials. In cases with body or tail location, the radical antegrade modular pancreatosplenectomy gives promising results. Nevertheless, accurate localization and detailed examination of the resected specimen are required for better staging.

BACKGROUND: There is a constant and global shortage of deceased-donor organs for transplantation. Ways to identify areas for securing potential deceased-donor organs may improve the supply and hence benefit more patients in need of transplantation.
METHODS: We looked into the disparity of the number of deceased-donor liver transplantation (DDLT) performed at our hospital on different days of the weeks from January 2000 to the end of December 2009 (237 DDLTs). The number of DDLT performed on each day was compared with the other days of the week.
RESULTS: It was apparent that there were fewer DDLTs on Mondays, as shown by the numbers of DDLT performed on different days of the week in an ascending order: Monday 18 (7.6%), Sunday 30 (12.7%), Thursday 34 (14.3%), Friday 36 (15.2%), Wednesday 38 (16.0%), Tuesday 40 (16.9%), and Saturday 41 (17.3%). The difference reached statistical significance when Monday was compared with Tuesday (P=0.019), Wednesday (P=0.010), Friday (P=0.021), and Saturday (P=0.007). It was twice as unlikely a DDLT would be performed on Monday as compared with other days. Such a trend did not change even with an increase in the number of deceased-donor liver grafts in the last year. As consent to donation was obtained from the donor family the day before DDLT, fewer consents were thus obtained on Sundays.
CONCLUSION: These findings suggested that deceased-donor organ donation activities were less active on Sundays and could be improved. This further raises the concern of possible wastage of potential cases of organ donation.

BACKGROUND: The specificity in discriminating pancreatitis is limited in the positron emission tomography (PET) using Fluorine-18-fluorodeoxyglucose. Furthermore, PET is not widely available compared to the single photon emission computed tomography (SPECT). Since amino acids play a minor role in metabolism of inflammatory cells, the potential of the SPECT tracer, 3-[123I]iodo-L-α-methyltyrosine (123I-IMT), for detecting pancreatic cancer was examined in xenotransplantation models of human pancreatic carcinoma in mice.
METHODS: 123I-IMT was injected to eight mice inoculated with subcutaneous or orthotopic pancreatic tumors. Fused high-resolution-micro-SPECT (Hi-SPECT) and magnetic resonance imaging were performed. The gene expression level of L amino acid transport-system 1 (LAT1) was analyzed and correlated with tumor uptake of 123I-IMT.
RESULTS: A high uptake of 123I-IMT was detected in all tumor-bearing mice. The median tumor-to-background ratio (T/B) was 12.1 (2.0-13.2) for orthotopic and 8.4 (1.8-11.1) for subcutaneous xenotransplantation, respectively. Accordingly, the LAT1 expression in transplanted Colo357 cells was increased compared to non-malignant controls.
CONCLUSIONS: Our mouse model could show a high 123I-IMT uptake in pancreatic cancer. Fused MRI scans facilitate precise evaluation of uptake in the specific regions of interest. Further studies are required to confirm these findings in tumors derived from other human pancreatic cancer cells. Since amino acids play a minor role in the metabolism of inflammatory cells, the potential for application of 123I-IMT to distinguish pancreatic tumor from inflammatory pancreatitis warrants further investigation.

BACKGROUND: Laparoscopic liver resection is one of the most complex procedures in hepatobiliary surgery. In the last two decades, laparoscopic liver surgery has emerged as an option at major academic institutions. The purpose of this study is to describe the initial experience of minimally invasive liver resections at a non-academic institution.
METHODS: We retrospectively reviewed medical records of patients undergoing laparoscopic liver resections between June 2006 and December 2009 at our center. Indications, technical aspects, and outcomes of these patients are described.
RESULTS: Laparoscopic liver resection was attempted in 28 patients. Of these, 27 patients underwent laparoscopic liver resection (22 total laparoscopic and 5 hand assisted) and one needed conversion to open surgery. Twenty patients had a benign lesion and 8 had malignant lesions. Three patients had multiple lesions in different segments requiring separate resections. The lesions were located in segments II-III (n=18), IV (n=3), V-VI (n=9), and VII (n=1). Tumor size ranged from 1.5 cm to 8.5 cm. The surgical procedures included left lateral sectionectomy (n=17), left hepatectomy (n=2), sectionectomy (n=8), and local resections (n=4). Median operative time was 110 minutes (range 55-210 minutes), and the median length of hospital stay was 2.5 days (range 1-7 days). There was no perioperative mortality. One patient developed hernia at the site of tumor extraction requiring repair at 3 months.
CONCLUSIONS: Laparoscopic liver resections can be safely performed in selected patients with benign and malignant liver tumors. With increasing experience, laparoscopic liver resections are likely to become a favorable alternative to open resection.

BACKGROUND: Hepatocellular carcinoma (HCC) is a common malignant tumor in China, and early diagnosis is critical for patient outcome. In patients with HCC, it is mostly based on liver cirrhosis, developing from benign regenerative nodules and dysplastic nodules to HCC lesions, and a better understanding of its vascular supply and the hemodynamic changes may lead to early tumor detection. Angiogenesis is essential for the growth of primary and metastatic tumors due to changes in vascular perfusion, blood volume and permeability. These hemodynamic and physiological properties can be measured serially using functional computed tomography perfusion (CTP) imaging and can be used to assess the growth of HCC. This study aimed to clarify the physiological characteristics of tumor angiogenesis in cirrhotic liver disease by this fast imaging method.
METHODS: CTP was performed in 30 volunteers without liver disease (control subjects) and 49 patients with liver disease (experimental subjects: 27 with HCC and 22 with cirrhosis). All subjects were also evaluated by physical examination, laboratory screening and Doppler ultrasonography of the liver. The diagnosis of HCC was made according to the EASL criteria. All patients underwent contrast-enhanced ultrasonography, pre- and post-contrast triple-phase CT and CTP study. A mathematical deconvolution model was applied to provide hepatic blood flow (HBF), hepatic blood volume (HBV), mean transit time (MTT), permeability of capillary vessel surface (PS), hepatic arterial index (HAI), hepatic arterial perfusion (HAP) and hepatic portal perfusion (HPP) data. The Mann-Whitney U test was used to determine differences in perfusion parameters between the background cirrhotic liver parenchyma and HCC and between the cirrhotic liver parenchyma with HCC and that without HCC.
RESULTS: In normal liver, the HAP/HVP ratio was about 1/4. HCC had significantly higher HAP and HAI and lower HPP than background liver parenchyma adjacent to the HCC. The value of HBF at the tumor rim was significantly higher than that in the controls. HBF, HBV, HAI, HAP and HPP, but not MTT and PS, were significantly higher in the cirrhotic liver parenchyma involved with HCC than those of the controls. Perfusion parameters were not significantly different between the controls and the cirrhotic liver parenchyma not involved with HCC.
CONCLUSIONS: CTP can clearly distinguish tumor from cirrhotic liver parenchyma and controls and can provide quantitative information about tumor-related angiogenesis, which can be used to assess tumor vascularization in cirrhotic liver disease.

BACKGROUND: Decreased cardiac contractility has been observed in cirrhosis, suggesting a latent cardiomyopathy in these patients. This study was designed to evaluate left ventricular structure and function in patients with end-stage liver disease by the model for end-stage liver disease (MELD) scoring system.
METHODS: We recruited 82 patients (72 male, 10 female; mean age 50.3±8.9 years) with end-stage liver disease who underwent orthotopic liver transplantation between January 2002 and May 2008. Seventy-eight patients had cirrhosis and 4 had primary liver cancer. Patients were categorized into three groups on the basis of MELD score: ≤9 (27 patients, 33%); 10-19 (40, 49%); and ≥20 (15, 18%). The relationship between MELD score and cardiac structure and function was determined. Preoperative assessments of blood biochemistry, blood coagulation, serum virology, echocardiography and electrocardiography were performed.
RESULTS: MELD score was positively correlated with enlarged left atrial diameter, increased interventricular septum thickness (IVST), increased aortic flow, corrected QT interval (QTc) extension and cardiac output (P=0.033, 0.002, 0.000, 0.000 and 0.009, respectively). International normalized ratio also had a correlation with the above parameters and enlarged left ventricular end-diastolic diameter (P=0.043, 0.010, 0.000, 0.001, 0.016 and 0.008, respectively). Serum creatinine was positively correlated with IVST (r=0.257, P=0.020), but negatively correlated with early maximal ventricular filling velocity/late diastolic or atrial velocity ratio (r=-0.300, P=0.006). A difference of QTc >440 ms among the three groups was statistically significant (χ2=9.791, P=0.007).
CONCLUSIONS: Abnormalities in cardiac structure and function are common in patients with end-stage liver disease. MELD score is a practically useful approach for the assessment of cardiac function in such patients.

BACKGROUND: Mesenchymal stem cells (MSCs) and fibroblasts have intimate relationships, and the phenotypic homology between fibroblasts and MSCs has been recently described. The aim of this study was to investigate the hepatic differentiating potential of human fibroblasts in cirrhotic liver.
METHODS: The phenotypes of fibroblasts in cirrhotic liver were labeled by biological methods. After that, the differentiation potential of these fibroblasts in vitro was characterized in terms of liver-specific gene and protein expression. Finally, an animal model of hepatocyte regeneration in severe combined immunodeficient (SCID) mice was created by retrorsine injection and partial hepatectomy, and the expression of human hepatocyte proteins in SCID mouse livers was checked by immunohistochemical analysis after fibroblast administration.
RESULTS: Surface immunophenotyping revealed that a minority of fibroblasts expressed markers of MSCs and hepatic epithelial cytokeratins as well as alpha-smooth muscle actin, but homogeneously expressed vimentin, desmin, prolyl 4-hydroxylase and fibronectin. These fibroblasts presented the characteristics of hepatocytes in vitro and differentiated directly into functional hepatocytes in the liver of hepatecto-mized SCID mice.
CONCLUSIONS: This study demonstrated that fibroblasts in cirrhotic liver have the potential to differentiate into hepatocyte-like cells in vitro and in vivo. Our findings infer that hepatic differentiation of fibroblasts may serve as a new target for reversion of liver fibrosis and a cell source for tissue engineering.

BACKGROUND: Hepatic fibrosis is a necessary step in the development of hepatic cirrhosis. In this study we used lentiviral vector-mediated transfection technology to evaluate the effect of peroxisome proliferator-activated receptor gamma (PPAR-γ) on rat hepatic fibrosis.
METHODS: Hepatic fibrosis in rats was induced by CCl4 for 2 weeks (early fibrosis) and 8 weeks (sustained fibrosis). The rats were randomly divided into four groups: normal control, fibrosis, blank vector, and PPAR-γ. They were infected with the recombinant lentiviral expression vector carrying the rat PPAR-γ gene by portal vein injection. The liver of the rats was examined histologically and hydroxyproline was assessed. In vitro primary hepatic stellate cells (HSCs) were infected with the recombinant lentiviral expression vector carrying the rat PPAR-γ gene. The status of HSC proliferation was measured by the MTT assay. The protein levels of PPAR-γ, α-smooth muscle actin (α-SMA) and type I collagen expression were evaluated by the Western blotting method.
RESULTS: In vitro studies revealed that expression of PPAR-γ inhibited expression of α-SMA and type I collagen in activated HSCs (P<0.01) as well as HSC proliferation (P<0.01). In vivo experiments indicated that in the early hepatic fibrosis group, the hydroxyproline content and the level of collagen I protein in the liver in the PPAR-γ transfected group were not significantly different compared to the hepatic fibrosis group and the blank vector group; whereas the expressions of PPAR-γ and α-SMA were different compared to the hepatic fibrosis group (P<0.01). In the sustained hepatic fibrosis group, there were significant differences in the hydroxyproline content and the expression of PPAR-γ, α-SMA, and type I collagen between each group.
CONCLUSION: PPAR-γ can inhibit HSC proliferation and hepatic fibrosis, and suppress α-SMA and type I collagen expression.

BACKGROUND: The glucose transporter-1 (Glut-1), a key rate-limiting factor in the transport and metabolism of glucose in cancer cells, is over-expressed in many human cancer cells and this over-expression is correlated with poor biological behavior. The increased levels of Glut-1 expression in hepatocellular carcinoma (HCC) cells functionally affect tumorigenicity. This study was undertaken to investigate effects of suppressing Glut-1 by an antisense oligodeoxynucleotide (AS-ODN) on the growth of human hepatocellular carcinoma (HepG-2) cells.
METHODS: We used AS-ODN targeting against the Glut-1 gene in a HepG-2 cell line. There were four experimental groups: empty pcDNA3.1 vector (mock transfection), pcDNA3.1-anti-Glut (+), pcDNA3.1-Glut (+), and non-transfected HepG-2 cells. The Glut-1 mRNA expression was detected by RT-PCR and the Glut-1 protein expression by Western blotting after cell culture, and the glucose uptake was detected after glucose stimulation in each group.
RESULTS: Compared with non-transfected HepG-2 or Glut-1 pcDNA3.1, a down-regulation of Glut-1 mRNA in HepG-2 cells transfected with anti-Glut-1 pcDNA3.1 was noted (P<0.05). Glut-1 protein in HepG-2 cells transfected with Glut-1 AS-ODN was decreased compared with non-transfected HepG-2, Glut-1 pcDNA3.1, or empty vectors. Glucose uptake by the HepG-2 cells transfected with AS-ODN was decreased at 1 hour after glucose stimulation.
CONCLUSIONS: The application of Glut-1 AS-ODN can down-regulate the expression of Glut-1 at mRNA and protein, and inhibit glucose uptake partially in HepG-2 cells. The Glut-1 gene maybe a potential therapeutic target for HCC.

BACKGROUND: Hepatic ischemia-reperfusion injury is a common phenomenon in hepatic surgical procedures and can result in further severe damage. This study aimed to investigate the protective effects of glutamine preconditioning on hepatic ischemia-reperfusion injury in rats and its dose-dependency.
METHODS: Thirty-two healthy male Wistar rats were randomly divided into four groups (n=8 per group). One group received 0.9% NaCl (control) and the other three received glutamine (Gln groups) 4 hours before ischemia. The Gln groups were named GL, GM, and GH according to the glutamine dose. The liver was subjected to 1 hour of ischemia and 2 hours of reperfusion. Two hours later, the levels of alanine aminotransferase (ALT), intracellular free calcium (Ca2+), and activity of Na+/K+ adenosine triphosphatase (ATPase) and superoxide dismutase (SOD) were assessed, and liver tissue sections were examined under a microscope.
RESULTS: The Gln and control groups differed in the concentration of intracellular free calcium (P<0.05), and the activity of Na+/K+ ATPase and SOD in the Gln groups was higher than in the control group (P<0.05). The ALT level was lower in the GM and GH groups than in the control group (P<0.05). The levels of Na+/K+ ATPase and SOD rose gradually with increasing glutamine dose (P<0.05), and the concentration of Ca2+ declined gradually with increasing glutamine dose (P<0.05). The degree of hepatocyte injury was milder in the Gln groups than in the control group.
CONCLUSIONS: Glutamine preconditioning protected effectively against hepatic ischemia-reperfusion injury. These protective effects were related to the dose of glutamine and due to the reduction of intracellular calcium overload and the improvements in the activity of Na+/K+ ATPase and SOD.

BACKGROUND: Ischemic recurrent stricture after surgical repair for iatrogenic bile duct injury (BDI) remains a challenge in clinical practice. The present study was designed to investigate whether ischemia is universal and of varied severity at different levels of the proximal bile duct after BDI.
METHODS: A total of 30 beagle dogs were randomly divided into control, BDI, and BDI-repaired groups. The BDI animal model was established based on the classic pattern of laparoscopic cholecystectomy-related BDI. The animals were sacrificed on postoperative day 15, and bile duct tissue was harvested to assess microvessel density (MVD) at selected levels of the normal, post-BDI and BDI-repaired bile duct with the CD34 immunohistochemistry technique.
RESULTS: In the control group, MVD at level H (high level) was remarkably higher than that at level L (low level). No significant difference was found between MVDs at levels H and M (middle level), as well as at levels M and L. However, the tendency was noted that the closer the level to the hilus, the greater the MVD at that level. In both the BDI and BDI-repaired groups, MVDs at level H were generally greater than those at level L, despite the unremarkable differences between MVDs at neighboring levels. In these two groups, a similar tendency of MVD distribution to that in the control group was found; the closer the level to the injury site, the lower was the MVD at that level. Moreover, compared with the MDVs at the levels M and L in the control group, MVDs at the corresponding levels in the BDI and BDI-repaired groups were all remarkably reduced (P<0.05). In addition, MVDs at all three levels in the BDI group significantly declined further after BDI repair.
CONCLUSIONS: After BDI, universal ischemic damage in the injured proximal bile duct develops close to the injury site, while close to the hilus, ischemia is relatively slight. High hepaticojejunostomy, rather than low biloenterostomy or end-to-end duct anastomosis, should be recommended for BDI repair. Great care should be taken to protect the peribiliary plexus during repair.

BACKGROUND: Sulfonylurea receptor 1 (SUR1) and multidrug resistance protein 1 (MRP1) are two prominent members of multidrug resistance proteins associated with insulin secretion. The aims of this study were to investigate their expression in insulinomas and their sole and synergistic effects in modulating abnormal insulin secretion.
METHODS: Fasting glucose, insulin and C-peptide were measured in 11 insulinoma patients and 11 healthy controls. Prolonged oral glucose tolerance tests were performed in 6 insulinoma patients. Insulin content, SUR1 and MRP1 were detected in 11 insulinoma patients by immunohistochemistry. SUR1 and MRP1 were also detected in 6 insulinoma patients by immunofluorescence.
RESULTS: Insulinoma patients presented the typical demons-trations of Whipple(s triad. Fasting glucose of each insulinoma patient was lower than 2.8 mmol/L, and simultaneous insulin and C-peptide were increased in insulinoma patients. Prolonged oral glucose tolerance tests showed that insulin secretion in insulinoma patients were also stimulated by high glucose. Immunohistochemistry and immunofluorescence staining showed that SUR1 increased, but MRP1 decreased in insulinoma compared with the adjacent islets.
CONCLUSIONS: The hypersecretion of insulin in insulinomas might be, at least partially, due to the enrichment of SUR1. In contrast, MRP1, which is down-regulated in insulinomas, might reflect a negative feedback in insulin secretion.

BACKGROUND: A growing body of evidence suggests that many tumors are initiated by both epigenetic abnormalities and gene mutations, which promote tumor progression. Epigenetic abnormalities include changes in DNA methylation and in the modification of histones. This study aimed to assess the status of methylation in the CpG island (CGI) of the tumor necrosis factor receptor superfamily member 10c (TNFRSF10C) with combined bisulfite restriction analysis (COBRA) and to evaluate its role in the progression of pancreatic cancer (PC).
METHODS: The methylation status of four PC cell lines was assessed using COBRA and/or bisulfite genomic sequencing (BGS). Changes in methylation and TNFRSF10C expression in PC cell lines before and after treatment with 5-aza-2-deoxycytidine (5-aza-dC) and/or trichostatin A (TSA) were assessed by BGS and real-time RT-PCR. Apoptosis in the four cell lines was tested by flow cytometry (FCM) and TUNEL assay.
RESULTS: The methylation status of the TNFRSF10C promoter was assessed in PC cells (BxPC-3: 68.84±8.71%; CFPAC-1: 0; PANC-1: 96.77±4.57%; SW1990: 54.97±7.33%) with the COBRA assay, which was confirmed by the results of BGS. After treatment with 5-aza-dC and/or TSA, apoptosis was induced in PC cells to different degrees, and the levels of TNFRSF10C transcriptional expression in the PC cell lines (except CFPAC-1) increased markedly after 5-aza-dC treatment.
CONCLUSIONS: A high frequency of CGI methylation in the TNFRSF10C promoter results in inactivation of the gene and enhancement of tumor growth in most PC cell lines (except CFPAC-1). Inactivation of TNFRSF10C by CGI hypermethylation can play an important role in PC progression and be potentially useful as a diagnostic marker and a new therapeutic approach for PC.

BACKGROUND: Primary hepatic carcinosarcoma is a rare malignant tumor containing an intimate mixture of carcinomatous and sarcomatous elements. Reports on risk factors, epidemiology, and pathogenesis of the tumor as well as the experience in its treatment are limited.
METHOD: We present a case of primary carcinosarcoma of the liver in a 69-year-old man who complained of right hypochondrial pain and weight loss for two months.
RESULTS: Magnetic resonance imaging revealed a 14×12 cm mass in segments 7-8 and 4 of the liver with vena hepatica invasion. An ultrasonography-guided biopsy showed osteoid tissue without osteoblastic rimming. Vascular structures accompanied the osteoid tissue. The patient underwent surgery after a diagnosis of hemangioma. Intraoperative frozen sections revealed a carcinosarcoma associated with an osteosarcoma and cholangiocellular carcinoma components.
CONCLUSIONS: Preoperative diagnosis of this rare primary hepatic malignant tumor may be difficult by biopsy owing to intratumoral heterogeneity. Highly mature areas of the osteosarcomatous component may lead to misdiagnosis of metaplastic bone tissue. Clinicopathologic features of this rare entity are discussed.

BACKGROUND: Focal nodular hyperplasia, a benign hepatic tumor, is usually asymptomatic. However, rarely the entity can cause symptoms, mandating intervention.
METHOD: We present a case of focal nodular hyperplasia of the liver, which caused a considerable diagnostic dilemma due to its atypical presentation.
RESULTS: A 29-year-old woman presented with a 15-year history of a progressively increasing mass in the right upper quadrant which was associated with pain and emesis. Examination showed a firm, mobile mass palpable below the right subcostal margin. A computed tomography scan of the abdomen showed an exophytic mass arising from hepatic segments III and IVb. Trucut biopsy of the hepatic mass was equivocal. Angiography showed a vascular tumor that was supplied by a tortuous branch of the proper hepatic artery. Surgical intervention for removal of the mass was undertaken. Intra-operatively, two large discrete tumors were found and completely resected. Histopathological examination showed features consistent with focal nodular hyperplasia.
CONCLUSION: This description of an unusual case of focal nodular hyperplasia of the liver highlights the point that the diagnosis of otherwise benign hepatic tumors may be difficult despite extensive work-up in some cases.

To the Editor:
We read with great interest the article by Chong and Jalihal[1] regarding endoscopic management of biliary disorders during pregnancy which reaffirms that endoscopic retrograde cholangiopancreatography (ERCP) is safe and effective in managing choledocholithiasis during pregnancy. The authors use ERCP under fluoroscopic guidance with lead apron shielding as well as non-fluoroscopic cannulation using bile flow and bile aspiration as indicators of successful bile duct cannulation. We discuss an emerging technology for direct cholangioscopy which aids in confirmation of duct clearance and eliminates the need for fluoroscopy.
A 26-year-old G3P2 female in her first trimester of pregnancy presented to hospital with post-prandial epigastric pain and vomiting. She had obstructive jaundice and pancreatitis by laboratory evaluation. Transabdominal ultrasound showed choledocholithiasis and common bile duct dilation.
Urgent ERCP was performed with sphincterotomy and stone extraction facilitated by the SpyGlass Direct Visualization System (Boston Scientific, Natick, MA, USA). A 4.4 Fr sphinctertome was angled in the biliary orientation and a hydrophilic 0.35" guidewire was gently advanced into the major papilla resulting in bile flow around the guidewire. The sphincterotome was advanced over the wire and aspiration of 10 ml of clear yellow bile confirmed the location within the bile duct. A biliary sphincterotomy was performed. Sweep with a 9-mm extraction balloon easily removed a single 8-mm stone from the bile duct. The SpyGlass SpyScope was exchanged over the guidewire and cholangioscopy directly visualized the common bile duct, common hepatic duct and left and right intrahepatic ducts. Saline lavage through the cholangioscope flushed debris and two 2-mm residual stones from the bile duct into the duodenum. No fluoroscope was used during the entire procedure. The patient tolerated the procedure well with clinical and laboratory resolution.
Multiple non-radiating techniques for ERCP in the pregnant patient have been described in the literature.[2-5] To date, 7 pregnant patients undergoing (including the current report) SpyGlass cholangioscopy–assisted ERCP have been reported.[5, 6] The technique allows for the limitation or elimination of ionizing radiation through direct intraductal visualization and stone clearance confirmation. The diagnostic and therapeutic capability of ERCP is increased in a manner that contributes to patient safety and hopefully better maternal and fetal outcomes. The availability of this equipment remains limited, but in institutions where the equipment and expertise is available, the use of direct intraductal visualization should play a role in the management for this common complication of pregnancy.