Effectiveness of the ultrasonic coagulating shears, LigaSure vessel sealer, and surgical clip application in biliary surgery: a comparative analysis.

Advancements in laparoscopic surgery are often dictated by the limitations of technical instrumentation. Energy sources other than electrosurgery have become popular with the promise of quick and effective vascular control. With their success surgeons have begun using these on structures other than blood vessels with little or no data establishing their efficacy or safety. This study evaluates alternative energy sources in sealing ductal structures for possible use in liver or gallbladder surgery. After elective cholecystectomy cystic ducts (n = 45) were resealed ex vivo with surgical clips (n = 14), ultrasonic coagulating shears (n = 16), or electrothermal bipolar vessel sealer (n = 15), and bursting pressures were measured. Nineteen additional human cystic ducts were randomized to seal by ultrasonic coagulating shears (n = 9) or electrothermal bipolar vessel sealer (n = 10) and fixed in 10 per cent buffered formalin for histologic evaluation of thermal spread (mm). After this nine adult pigs were randomized to laparoscopic ligation and transection of the common bile duct using surgical clips (n = 3), ultrasonic coagulating shears (n = 3), or electrothermal bipolar vessel sealer (n = 3). The animals underwent necropsy for assessment of seal integrity on the sixth postoperative day. In the ex vivo study the mean cystic duct bursting pressure was 621 mm Hg with surgical clips and 482 mm Hg with the electrothermal bipolar vessel sealer (P = 0.39). The mean cystic duct bursting pressure after ultrasonic coagulating shears was 278 mm Hg, which was statistically less than surgical clips (P = 0.007) and electrothermal bipolar vessel sealer (P = 0.02). The mean thermal spread was 3.5 mm for ultrasonic coagulating shears and 13.4 mm for electrothermal bipolar vessel sealer (P = 0.0002). All animals undergoing ligation and transection of the common bile duct with ultrasonic coagulating shears and electrothermal bipolar vessel sealer developed bile peritonitis by postoperative day 6 as a result of seal leak. All animals undergoing surgical clip ligation and transection of the common bile duct maintained seal integrity. The mean common bile duct pressure above the surgical clip was 12 mm Hg (range 10-14). In conclusion the acute ex vivo study demonstrated a significant difference in the cystic duct bursting pressure between surgical clips and ultrasonic coagulating shears and between electrothermal bipolar vessel sealer and ultrasonic coagulating shears. The ultrasonic coagulating shears and electrothermal bipolar vessel sealer failed to maintain seal integrity in the in vivo animal study. Given the failure of the ultrasonic coagulating shears and electrothermal bipolar vessel sealer in the animal model these energy sources should not be used for transection of the cystic duct or major hepatic ducts during hepatobiliary surgery.

Intravesical dimethyl sulfoxide for primary amyloidosis of the bladder.

Primary bladder amyloidosis is a rare disease. Treatment recommendations are necessarily anecdotal. We report a case of a 52-year-old woman treated successfully with intravesical dimethyl sulfoxide instillation.

Time-resolved changes in intracellular calcium following depolarization of rat brain synaptosomes.

1. Changes of cytoplasmic free calcium levels ([Ca2+]i) in isolated rat brain nerve terminals (synaptosomes), previously loaded with the fluorescent intracellular calcium indicator Fura-2, were measured 1-2 ms after depolarization with elevated K+ by stopped-flow fluorescence spectroscopy. 2. In physiological saline (PSS) containing 4 mM-K+, intraterminal Ca2+ was estimated to be in the range 150-250 nM. Depolarization of the nerve terminals with elevated external K+ in the presence of Ca2+ induced a prompt rise in [Ca2+]i, which occurred in two phases. No change in [Ca2+]i was seen when the terminals were depolarized in nominally Ca(2+)-free solutions, and only a small change was seen when the terminals were acutely exposed to Ca2+ in 4 mM-K+. 3. Predepolarization of the nerve terminals with K+ in nominally Ca(2+)-free solutions several seconds before the introduction of Ca2+ greatly decreased the magnitude of the fast phase, whilst leaving the slow phase largely intact. 4. In Na(+)-depleted nerve terminals, the fast phase of K(+)-stimulated Ca2+ uptake was essentially unaltered, but the slow phase of Ca2+ uptake was dramatically reduced. 5. The rapid phase of K(+)-stimulated uptake displayed voltage-dependent inactivation (tau approximately 50 ms at -10 mV), and the rate of inactivation was accelerated with increasing depolarization. In contrast, at constant [K+]o, increasing [Ca2+]o had little or no effect on the rate of inactivation, but did increase the initial rate of Ca2+ uptake. 6. The dihydropyridine calcium channel blockers nifedipine and nitrendipine had little effect on either component of Ca2+ uptake. However, the inorganic Ca2+ channel blockers La3+, Cd2+, and Co2+ were potent blockers of the fast phase of Ca2+ uptake, but blocked the slow phase only at higher concentrations. No consistent effect of the peptide neurotoxin omega-conotoxin was observed on either component of the Ca2+ rise. 7. These studies demonstrate that the dynamics of depolarization-activated intraterminal Ca2+ changes can be studied on a millisecond time scale in isolated nerve terminals. Moreover, our results indicate that two pathways contribute to depolarization-induced [Ca2+]i changes, namely a voltage-activated, inactivating Ca2+ channel, possibly of the N-type, and Na(+)-Ca2+ exchange operating in the 'reverse' mode.