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Volume 63 - 2000 - Fasc.3 - Symposium

Chylous ascites : diagnosis, causes and treatment

Chylous ascites is a rare form of ascites and generally associated with a poor outcome since it is often secondary to neoplasms. Its true incidence is not well established in the general medico-surgical population. Any source of lymph vessels obstruction or leakage can potentially cause chylous effusions in the peritoneal or retroperitoneal cavities. Any type of cancer and lymph node involvement may be associated with this uncommon type of ascites. Traumatic, and mainly surgical, vessels leakage is the second most common source of chylous effusions. Other even more rare underlying conditions have been described as leading to chyloperitoneum. Large fluid volume losses together with proteins, and lymphocytes can induce additional morbidity in a previously debilitated population or severely ill patients. This includes organ dysfunction related to volume and electrolytes losses, but mainly secondary infections due to impaired immunity by antibodies and lymphocytes depletion. Even if a vast majority of chylous effusions shall heat spontaneously, early and full treatment has to be initiated in order to reduce morbidity and mortality associated with this condition. Adapted oral diet is to be introduced to reduce lymph flow. Low lipid, high medium-chain triglycerides alimentation is the first measure to implement. Total parenteral nutrition is to be reserved to failures of oral diet. In addition, I*aracentesis is indicated to improve patient comfort, reduce intra-adbominal pressure and secondary renal dysfunction. Somatostatin analogues have been demonstrated to be effective in reducing lymphorragia and may be proposed prior to consider the surgical approach. Direct lymph vessels ligation can be indicated for large lymph vessets leakage demonstrated by radiologic techniques and when medical treatment has failed. Peritoneo-venous shunt becomes a less common technique in refractory chylous, effusion because of its high morbidity. Herein, the other causes of chylous effusions are reviewed as the diagnostic procedures. A treatment algorythm is proposed.

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Ascites fluid in severe acute pancreatitis : from pathophysiology to therapy

Several pathophysiological mechanisms are involved in the development of the inflammatory necrotizing process that takes place in the retroperitoneal area during the early phase of acute pancreatitis. They include premature intragiandular activation of pancreatic proenzymes (zymogens) and in particular trypsin, early niicrocirculatory impairment with subsequent ischaemia/ reperfusion and overstimulation of immune effector cells. Although intra-acinar or interstitial activation of trypsinogen is most probably the trigger of acute pancreatitis, in recent years much emphasis has been put on the role of leukocytes. Based on numerous experimental and human data several pro-inflammatory mediators including cytokines, arachidonic acid derivatives, activated oxygen species and proteases are released locally by overactivated neutrophils and monocytes/macrophages among other cells. They are now believed to play a central role in the development of pancreatic necrosis and, once they gain access to the systemic circulation, in the emergence of early multisystem organ failure. However the sequential and relative contribution of each of these 3 pathophysiological mechanisms remain controversial and the precise identification of the mediators incriminated in local and remote tissue injury is still awaited. Severe acute pancreatitis still carries a mortality of 20% to 30%. With advances in intensive care management 80% of the deaths occur somewhat late in the attack due to infected pancreatic necrosis. Nevertheless early remote organ failures still remain a lifethreatening condition for most of these patients. A peritoneal exudate rich in activated lipolytic and proteolytic enzymes, vasoactive substances and several other pro-inflammatory mediators collect in over 60% of the patients with severe acute pancreatitis. On the basis of favourable animal experiments early percutaneous or surgical peritoneal lavage with or without the addition of antiproteases has been carried out in human acute pancreatitis. The rationale behind this procedure was the washout of potential toxic mediators from the peritoneal cavity before they gain access to the systemic circulation. Contrary to animal and uncontrolled human data no prospective randomized study could ever demonstrated a significant effect of peritoneal lavage neither in the prevention and control of remote organ failures or in early mortality and ultimate survival after severe acute pancreatitis in humans. Differences between experimentally-induced pancreatitis, difference in the timing of the initiation of lavage and a type 11 error in controlled human studies may account for the discrepancy in the outcome between these studies. Anyway, this disparity should raise the question as whether the peritoneal cavity acts simply as a reservoir or as a route of transfer of toxic mediators to the systemic circulation. Although data are scarce, conflicting and limited to animal experiments and to a few molecules, peripancreatic veins and lymphatics seem to be the major routes of transfer whereas transperitoneal absorption is trivial. Nevertheless early peritoneal aspiration of ascitic fluid in acute pancreatitis and measurement of trypsinogen activation peptides may be used as a means of severity assessment and identification of pancreatic necrosis. This implies that even if not taking part actively in the emergence of remote organ failures ascitic fluid may reflect the peripancreatic necrotizing process. So careful comparative analysis of peritoneal exudate, plasma and lymph with regards to putative mediators of local and remote injury may provide essential pathophysiological clues. At the time of trials of antimediator therapy early in the attack this kind of insight is essential.

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The management of pancreatic ascites and pancreaticopleural effusion

Pancreatic ascites and pancreaticopleural effusion result from a complete or partial main pancreatic duct disruption or from a pseudocyst rupture with releasing of pancreatic juice into the surrounding tissues. The treatment requires to minimize pancreatic secretion, to favor pancreatic juice drainage into the digestive tract and to restore main pancreatic duct disruption. This can be achieved by endoscopic approach in more than 90% of the patients.

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Medical treatment for peritoneal carcinomatosis from colorectal cancer


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The medical management of severe acute and chronic ulcerative colitis. Current recommendations from the Belgian Working group


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Initial medical management of severe acute ulcerative colitis

Severe colitis is life-threatening complication of ulcerative colitis. Early recognition of the severity of the colitis, intensive medical therapy and prompt surgery when necessary have all contributed to improved outcome. Initial medical treatment should be instituted as soon as the diagnosis is made with an intravenous corticosteroid associated with supportive treatment. If the patient fails to response to this intensive treatment after 5-7 days, cyclosporin should be initiated. If cyclosporin is not used then colectomy should be performed immediately. Moreover, significant deterioration at any point during medical therapy is an indication for colectomy. The gravity of the patient's condition require close interaction between physician an surgeon.

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Ulcerative colitis and malignancy

Ulcerative colitis is associated with an increased risk for colorectal cancer. The increase is approximately six to ten times the expected in the general population. Disease duration and extension are the major risk factors. Concomitant primary sclerosing cholangitis is an additional independent risk factor. The relative risk is approximately 14.8 for patients with pancolitis while it is 1.7 for patients with disease restricted to the rectum. The risk increases rapidly after 20 years of disease evolution. Active treatment might decrease the risk. The increased cancer risk is a major problem for longterirn management of patients with ulcerative colitis. It is the rationale for, various surveillance programs and the search for dysplasia. Two major types of dysplasia must be distinguished in ulcerative colitis : sporadic adenomas and ulcerative colitisassociated dysplasia. Sporadic adenomas can be treated by simple potypectomy. The diagnosis of dypsplasia relies mainly on microscopic analysis of biopsy samples. Additional techniques, including flow cytometry and the search for DNA abnormalities and immunohistochemistry or molecular techniques looking for genetic defects can help to improve the diagnostic yield.

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Fulminant acute and diffuse chronic ulcerative colitis - the argument for surgery


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Approach of suspected common bile duct stones - Current recommendations from the Belgian Working group


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Clinical and biochemical suspicion of common bile duct stones


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Imaging prior to laparoscopic cholecystectomy transabdominal US, CT, and MRI


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Approach of suspected common bile duct stones : endoscopic ultrasonography

Recent studies have shown that endoscopic ultrasonography (EUS) is the most sensitive method for diagnosing choledocholithiasis. I-ligh sensitivities of more than 95% have been reported by several authors. Imaging the extrahepatic bile ducts and the gallbladder and searching for biliary stones are easy tasks for EUS. EUS has the advantages over ERCP to be less invasive (complication rate similar to diagnostic upper GI endoscopy) and to be able to detect small stones and sludge that can easily be masked by contrast medium during ERCP. In comparison with magnetic resonance imaging (MRI), EUS has the advantage to be close to the investigated areas and to allow the detection of very small stones or sludge, even in non dilated bile ducts. Technical limitations of biliary imaging by EUS are few : upper GI stenosis, previous gastrectomy or Billroth 11 resection. Imaging can be obscured by the presence of air (previous sphincterotomy or surgical bypass), surgical clips calcifying pancreatitis or a duodenal diverticulum. Main indications of EUS include the detection of choledocholithiasis in patients with a low and intermediate probability of presence of stones, in idiopathic acute pancreatitis, in mild and moderate pancreatitis after normal transabdominal ultrasonography, in pregnant women, in intensive care patients, in the diagnosis of gallbladder lithiasis or sludge, and also when MRI is contraindicated (claustrophobia and metallic implants) or fails to provide a diagnosis or is not available. Screening of choledocholithiasis with EUS has also been proposed in patients scheduled for laparoscopic cholecystectomy, but this is not common practice in Belgium. (Acta gastroentetol. belg., 2000, 63, 295-298).

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Endoscopic treatment of common bile duct lithiasis


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Treatment of choledocholithiasis : Therapeutic ERCP versus peroperative extraction during laparoscopic cholecystectomy

Limitation for preoperative ERCP / ES before laparoscopic cholecystectomy in patients scheduled for laparoscopic cholecystectomy are (1) Additional invasiveness of endoscopic procedures in patients supposed to be fitted for surgery, (2) A high rate of useless procedures due to the low predictive value of suspicion criteria for common bile duct stones (CBDS), (3) an inability to detect and treat all patients with CBDS, and (4) so far, an absence of demonstration of the superiority of this split therapeutic approach versus a one stage surgical treatment. Published series of CBDS extraction during laparoscopic cholecystectomy have included more than 2000 patients. Results and complications of this one stage laparoscopic approach compares favourably to the conventional open surgical treatment. In one randomized trial endoscopy plus laparoscopy was not demonstrated superior to laparoscopy alone. Intraoperative diagnosis and treatment of CBDS during laparoscopic cholecystectomy is the most cost efficient approach for patients with or without preoperative suspicion of CBDS, provide they are fitted for surgery.

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Curative management of adenocarcinoma of the oesophagus and oesogastric junction - Current recommendations of the Belgian Working Group


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Curative management of adenocarcinoma of the esophagus Endoscopic treatment


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