Search

Recently prophylactic placement of a trans-sphincteric pancreatic stent has successfully been applied to prevent post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis. Rescue ERCP and emergency application of small-caliber pancreatic stents during the early course of post-ERCP pancreatitis as a possible endoscopic therapy has not been reported yet.All patients who underwent ERCP were hospitalized for at least 24 h, with routine laboratory testing of amylase levels. Out of 1,225 ERCPs, evolution of severe post-ERCP pancreatitis was anticipated in six consecutive patients, based on severe pancreatic pain attack, more than tenfold elevation of serum amylase levels at 8 and 24 h, and moderate rise of white blood cell (WBC) and C-reactive protein (CRP) levels. Rescue ERCP and emergency application of small-caliber (4-5F, 4-cm, Geenen stent) pancreatic stents were successfully performed in all patients within 8-20 h after the initial ERCP.Moderate to severe papillary oedema was observed in all patients during the rescue ERCP. Pancreatic pain was promptly reduced after the rescue pancreatic drainage procedure and completely diminished within 24 h after pancreatic stenting. Serum amylase levels were exponentially reduced and normalized within 72 h in all patients; no pancreatic necrosis or any other late complications were observed. Pancreatic stents could be safely removed a few days later.Rescue pancreatic stenting with small-caliber prophylactic pancreatic stents seems to be a safe and effective procedure that might be feasible to stop the evolution of severe post-ERCP pancreatitis, but prospective controlled studies are clearly demanded to support this innovative approach.

Udgivelsesdato: 2008-Nov BACKGROUND AND AIMS: Somatosensory hyperalgesia in the referred pain area (RPA) in patients with acute or chronic abdominal pain syndromes may result from the convergence of nerve fibers from visceral and somatic tissues at the spinal and supraspinal levels. Chronic biliary pain in patients with the postcholecystectomy syndrome (i.e., biliary hypersensitivity) may be explained by persistent hyperexcitability of neurons in the central nervous system (CNS). The aim of this study was to evaluate the cutaneous neural sensory perception in the RPA in patients with chronic postcholecystectomy biliary pain and a sphincter of Oddi (SO) dysfunction (SOD). METHODS: Forty-two patients with persistent biliary pain and suspected SOD, 27 age-matched healthy volunteers, and 18 age-matched asymptomatic cholecystectomized controls were prospectively investigated by quantitative sensory testing (Neurometer CPT). The biliary symptoms and the severity of pain were classified on a visual analog pain severity scale system via a previously validated and standardized questionnaire. The patients helped the doctors locate the RPA in the right upper quadrant. The sensory detection threshold was determined noninvasively (Neurometer CPT) with transcutaneous electrical stimulation at 5, 250, and 2,000 Hz, and different current intensities (range from 0.01 to 9.99 mA) applied in a single (patient) blinded method. These three frequencies selectively excite small unmyelinated (C fibers), small myelinated (A-delta), and large myelinated (A-beta) fibers, which transmit dull pain, sharp pain, and touch, respectively. The contralateral region of the abdomen left upper quadrant served as the control area. The sensory current perception threshold ratio (SCPTR) of the data measured in the contralateral area and the RPA was calculated. RESULTS: The SCPTRs in the definite SOD patients with biliary pain, healthy volunteers, the asymptomatic cholecystectomized controls, and the symptomatic cholecystectomized patients but without SOD were 2.32 +/- 1.4 versus 1.06 +/- 0.24 versus 0.97 +/- 0.16 versus 0.83 +/- 0.35 at 2,000 Hz; 2.19 +/- 1.0 versus 1.01 +/- 0.26 versus 1.02 +/- 0.25 versus 0.88 +/- 0.35 at 250 Hz; and 2.19 +/- 1.1 versus 1.12 +/- 0.26 versus 0.99 +/- 0.37 versus 0.84 +/- 0.32 at 5 Hz, respectively. Significant hypersensitivity was detected in the RPA at different stimulation frequencies in the SOD patients with biliary pain versus the cholecystectomized controls: at 5 Hz: P = 0.00001; at 250 Hz: P = 0.00001; and at 2,000 Hz: P = 0.0001, respectively. CONCLUSION: Continuous visceral pain (biliary pain) caused by local inflammatory/sensitizing processes or a CNS malfunction could lead to significant hypersensitivity of the peripheral nociceptive nerve fibers in SOD patients. Postcholecystectomy pain may be explained by persistent hyperexcitability of the nociceptive neurons in the CNS with or without objective motility disorders of the SO.

AIM: To characterize functional biliary pain and other gastrointestinal (GI) symptoms in postcholecystectomy syndrome (PCS) patients with and without sphincter of Oddi dysfunction (SOD) proved by endoscopic sphincter of Oddi manometry (ESOM), and to assess the post-endoscopic sphincterotomy (EST) outcome. METHODS: We prospectively investigated 85 cholecystectomized patients referred for ERCP because of PCS and suspected SOD. On admission, all patients completed our questionnaire. Physical examination, laboratory tests, abdominal ultrasound, quantitative hepatobiliary scintigraphy (QHBS), and ERCP were performed in all patients. Based on clinical and ERCP findings 15 patients had unexpected bile duct stone disease and 15 patients had SOD biliary typeI. ESOM demonstrated an elevated basal pressure in 25 patients with SOD biliary-type III. In the remaining 30 cholecystectomized patients without SOD, the liver function tests, ERCP, QHBS and ESOM were all normal. As a control group, 30 ‘asymptomatic’ cholecystectomized volunteers (attended to our hospital for general cardiovascular screening) completed our questionnaire, which is consisted of 50 separate questions on GI symptoms and abdominal pain characteristics. Severity of the abdominal pain (frequency and intensity) was assessed with a visual analogue scale (VAS). In 40 of 80 patients having definite SOD (i.e. patients with SOD biliary typeIand those with elevated SO basal pressure on ESOM), an EST was performed just after ERCP. In these patients repeated questionnaires were filled at each follow-up visit (at 3 and 6 mo) and a second look QHBS was performed 3 mo after the EST to assess the functional response to EST. RESULTS: The analysis of characteristics of the abdominal pain demonstrated that patients with common bile duct stone and definite SOD had a significantly higher score of symptomatic agreement with previously determined biliary-like pain features than patient groups of PCS without SOD and controls. In contrary, no significant differences were found when the pain severity scores were compared in different groups of PCS patients. In patients with definite SOD, EST induced a significant acceleration of the transpapillary bile flow; and based on the comparison of VASs obtained from the pre- and post-EST questionnaires, the severity scores of abdominal pain were significantly improved, however, only 15 of 35 (43%) patients became completely pain free. Post-EST severity of abdominal pain by VASs was significantly higher in patients with predominant dyspepsia at initial presentation as compared to those without dyspeptic symptoms. CONCLUSION: Persistent GI symptoms and general patient dissatisfaction is a rather common finding after EST in patients with SOD, and correlated with the presence of predominant dyspeptic symptoms at the initial presentation, but does not depend on the technical and functional success of EST.