Peritoneoscopy in chronic peritoneal dialysis: use in evaluation and management of complications.
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Biomedical subjects
Publications and source records attributed to J T Cunningham.
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Six cases of multiple gastric telangiectasias are reported in association with patients on chronic hemodialysis who were investigated for acute gastrointestinal bleeding. The pathogenesis of this lesion is unknown and it is potentially an important source of intestinal hemorrhage.
A retrospective review and analysis of patients referred to the Division of Gastroenterology and the Section of Gastrointestinal Surgery with common bile duct complications after laparoscopic cholecystectomy was undertaken in order to identify injury patterns, management, and outcome. Sixteen patients were identified over a 20-month period. Twelve patients had major common bile duct injuries and four had minor injuries (cystic duct leaks). Seventy-one percent of injuries occurred with surgeons who had done more than 13 laparoscopic cholecystectomies. Eighty-three percent of patients who had major ductal injury did not have a cholangiogram prior to the injury. Sixteen percent of patients with major common bile duct injuries had findings of acute cholecystitis and 58% of these major injuries were "easy" gallbladders. One-third of major injuries were recognized at operation. Two-thirds of immediate repairs failed. All cystic duct leaks were managed nonoperatively. It appears that bile duct complications after laparoscopic cholecystectomy are more common in the community than is reported. Bile duct complications occur with surgeons who are experienced and inexperienced with laparoscopic cholecystectomy. Common bile duct injuries, unrecognized at laparoscopic cholecystectomy in the majority of cases, usually occur with "easy" gallbladders. Operative cholangiography is not utilized in the majority of common bile duct injuries. When immediate repair of common bile duct injuries is undertaken, the majority are unsuccessful. Endoscopic retrograde cholangiopancreatography (ERCP) is invaluable in the diagnosis and management of bile duct complications. Cystic duct leaks may be managed successfully with endoscopic stents.
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Stent occlusion may occur as the result of bacterial adherence and biofilm formation. This occlusion may be prompted by the material or design of the stents. In this study, a bile perfusion model was used to compare the biofilm formation on various stent materials. The copolymer and the wire mesh stents demonstrated less biofilm formation than the traditional stent. The development of new polymers may prolong stent patency.
Lateral pancreaticojejunostomy has demonstrated variable success in the management of chronic pancreatitis associated with ductal dilation, but its role in patients with nondilated ducts is poorly defined. The aim of this study was to assess the outcome of lateral pancreaticojejunostomy in chronic pancreatitis with nondilated pancreatic ducts. The records of all patients who underwent lateral pancreaticojejunostomy with a pancreatic duct measuring less than 7 mm in diameter were reviewed. Seventeen patients underwent lateral pancreaticojejunostomy for chronic pancreatitis and intractable pain between 1995 and 1996. Endoscopic retrograde cholangiopancreatography demonstrated features of chronic pancreatitis that were mild in seven patients, moderate in five, and severe in four. Postoperative complications occurred in two patients (11.7%). There were no deaths. Mean length of follow-up was 10.3 months (range 3 to 16 months). Rehospitalization for recurrent pancreatitis or pain was necessary in 59% of patients. Emergency room visits were reported by 76%. Narcotic use continued in 88%, with 76% of the patients reporting their pain as the same or worse than before the operation, and 65% continuing to view their health status as poor. In chronic pancreatitis patients with a nondilated pancreatic duct, lateral pancreaticojejunostomy appears to be of little benefit with respect to pain relief, subsequent hospitalization, continued narcotic use, or overall health status.
1. Precise control over the cardiovascular system requires the integration of both neural and humoral signals related to blood volume and blood pressure. Humoral signals interact with neural systems, modulating their control over the efferent mechanisms that ultimately determine the level of pressure and volume. 2. Peptide hormones such as angiotensin (Ang)II and arginine vasopressin (AVP) act through circumventricular organs (CVO) to influence cardiovascular regulation. 3. The area postrema (AP), a CVO in the brainstem, mediates at least some of the central actions of these peptides. Vasopressin appears to act in the AP to cause sympathoinhibition and a shift in baroreflex control of the sympathetic nervous system (SNS) to lower pressures. These effects of AVP and the AP appear to be mediated by alpha2-adrenoceptor and glutamatergic mechanisms in the nucleus tractus solitarius. 4. In contrast to AVP AngII has effects in the AP to blunt baroreflex control of heart rate and cause sympathoexcitation. The effects of chronic AngII to increase activity of the SNS may be due to AP-dependent activation of neurons in the rostral ventrolateral medulla.
The determinants of the nerve activity generated at the baroreceptor endings have been examined. 1) In the isolated carotid sinus, the placement of activated bovine aortic endothelial cells decreased baroreceptor activity (BRA) in a reversible manner. Both endothelin and nitric oxide (NO) suppress BRA, whereas prostacyclin (PGI2) increases activity. 2) The BRA in single units declines and often ceases during non-pulsatile increases in carotid sinus pressure sustained over several minutes. This "adaptation" is attenuated by the transient potassium channel (IA) blocker 4-aminopyridine (4-AP) and not by inhibition of the Na+/K+ pump. 3) In preliminary studies, mechano-electrical transduction was examined in isolated and cultured nodose ganglion neurons. Opening of stretch-activated (SA) channels by suction on the cell-attached patch was seen infrequently; however, probing the neurons consistently increased their intracellular calcium [Ca++]i measured with fura-2. This increase in [Ca++]i is blocked by gadolinium (Gd3+), a trivalent lanthanide reported to block SA channels. Gd3+ also blocks the BRA in the carotid sinus. We conclude that paracrine factors significantly modulate BR sensitivity, that selective ionic mechanisms (the 4-AP sensitive K+ channels) determine the degree of "adaptation" of BR to elevated pressure, and that SA channels sensitive to Gd3+ may be the mechano-electrical transducers in BR neurons.
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