Endoscopic treatment of postsurgical external pancreatic fistulas.

BACKGROUND AND STUDY AIMS: External pancreatic fistulas (EPFs) are managed primarily by conservative treatment with a success rate of 40-90%. Failures of conservative therapy have traditionally been dealt with using surgery; however, major morbidity and mortality are associated with operative treatment. The aim of this study was to evaluate the feasibility and effectiveness of endoscopic treatment in the closure of EPF. PATIENTS AND METHODS: A total of 16 consecutive patients with EPF (12 men, four women; median age 50, range 21-66) underwent an attempt at endoscopic management after failure of conservative therapy. Four patients had chronic pancreatitis. All patients had EPFs occurring after open abdominal surgery. The mean interval between the onset of the fistula and our intervention was 108 days (range 27-365 days). The mean output volume of the fistula was 205 ml/d (range 50-600 ml/ d). The aim of treatment was to lower the pancreatic duct pressure and to bypass the ductal disruption by placement of drains and/or stents to induce fistula healing. RESULTS: In all, 13 biliary and nine pancreatic sphincterotomies were performed in order to gain access to the pancreatic duct. Access through the minor papilla was required in one patient. Complete visualization of the main pancreatic duct as well as of the fistulous tract was obtained in 12 patients (75%). Treatment consisted of placement of a nasal pancreatic drain (NPD) across the pancreaticojejunal anastomosis in one patient after duodenopancreatectomy. In 11 of the remaining 15 patients (73%) a NPD could be placed in the pancreatic duct across the ductal leakage (n = 9) or nearby (n = 2). One patient died 24 hours after endoscopic treatment from severe sepsis and massive pulmonary embolism. Endoscopic drainage was effective in healing the EPF in all patients in whom NPDs had been successfully placed, except one. The fistula in this patient healed completely after insertion of an 8.5-Fr pancreatic stent. The mean interval between endoscopic treatment and fistula closure was 8.8 days (range 2-33 days). No complications related to the endoscopic treatment were recorded in this series. In the 12 successfully treated patients, fistulas did not recur in any of the 11 surviving patients after a mean follow-up of 24.7 months (range 3-63 months). CONCLUSIONS: Endoscopic pancreatic drainage, when feasible, is safe and effective for EPF and should be considered as a first-line therapy when EPFs do not respond to conservative therapy.

Endoscopic pancreatic stenting in pancreatic cancer.

Most pancreatic carcinomas are unresectable at the time of diagnosis; therefore, palliative treatment is very often the main concern of clinicians in this setting. The main symptoms resulting in the need for palliation in pancreatic cancer are obstructive jaundice, duodenal obstruction and pain. Therapeutic endoscopy plays a major role in the palliation of obstructive jaundice by stent placement into the biliary ducts. Initial experience has also been gained recently with endoscopic placement of expandable metallic stents to treat gastric outlet obstruction. Much less is known about the possible role of endoscopic pancreatic stenting in patients with unresectable pancreatic carcinoma. The main indication for pancreatic ductal stenting is 'obstructive' pain related to meals in patients with dilated main pancreatic duct beyond the stricture and intraluminal brachyradiotherapy. The technique of endoscopic pancreatic stenting does not substantially differ from that applied on the biliary tree. When technically possible, placement of 10 French plastic stents is preferred. According to the authors' indications, only about 15% of patients with advanced pancreatic cancer (55 of 355 in the present study) may potentially benefit from this technique. Pancreatic stenting may be obtained in more than 80% of these selected patients, with low morbidity (less than 10%) and no procedure-related mortality. According to the authors of the present and other studies reported in the literature, about 60% of patients treated because of 'obstructive' pain become symptom-free, and another 20% to 25% significantly reduce the amount of analgesic drugs required. Intraluminal brachyradiotherapy with 192iridium in the main pancreatic duct is a feasible and safe method to deliver high radiation doses to the tumour while sparing adjacent organs. Brachyradiotherapy may be performed alone or in conjunction with external beam radiotherapy. Because of the small number of patients suitable for this treatment, only a multicentre study will be able to detect whether intraluminal brachyradiotherapy in pancreatic cancer may have any positive impact on survival.

Radial scar of the breast.

Four cases of radial scar of the breast, primarily diagnosed as carcinoma are presented; the patients were found among 858 patients who were operated on at our Breast Unit over the last 4 years. The lesion was revealed on routine mammographic examination in 4 of our patients, while in the fourth it was found by palpation. In two of our patients mammographic examination revealed architectural distortion, in one patient micro-calcifications and in the fourth patient a stellate lesion was found. In the last two patients the lesion was localized before surgery with a hook wire. Diagnosis was established by histopathologic examination in all cases. The surgeon, the radiologist and the pathologist should be aware of this clinical entity which, in spite of its benign character, has the ability to simulate invasive carcinoma clinically, mammographically and histopathologically.

Low-dose heparin treatment does not inhibit SW480 human colon cancer growth and metastasis in vivo.

We investigated heparin effects on the biological behavior of SW480 human colon adenocarcinoma cells in vivo. Tumor growth, pathological features, metastatic potential and karyotype, were studied after the twelve week low-dose heparin treatment of nude mice subcutaneously injected with SW480 cells. A non statistically significant increase in tumor growth was observed (0.05 < p < 0.1, compared to the control group). No differences in tumor histology and karyotype were detected. Two of the six heparin-treated animals exhibited an increase in tumor vascularization. Metastasis to the lungs and liver was not inhibited. These results do not support the role of heparin in the prevention of the in vivo growth and metastasis of SW 480 colon cancer cells.