Factors leading to long-term hospitalization after laparoscopic appendectomy.

BACKGROUND: Randomized studies demonstrate that laparoscopic appendectomy yields better results compared with open techniques. We sought to identify factors that determine an extended hospital stay among patients undergoing laparoscopic appendectomy. METHODS: This was a prospective study including 669 patients undergoing laparoscopic appendectomy. We analyzed variables that can predict the length of hospital stay. RESULTS: Of 669 patients undergoing laparoscopic appendectomy, 141 stayed in the hospital for > or = 5 days (Group 1), and 97 stayed in the hospital for < or = 1 day after surgery (Group 2). The univariate analysis demonstrated that fever (P<0.0001), nausea and vomiting (P=0.060), leukocytosis (P<0.0001), gangrened or perforated intraoperative appearance of the appendix (P<0.0001), and appendix position behind the ileocecal junction (P<0.001) were related to a longer hospital stay. The multivariate analysis through logistical regression showed that the factors independently and significantly associated with an extended hospital stay were presurgical fever, appendix position behind the ileocecal junction, and intraoperative gangrened or perforated appearance of the appendix. CONCLUSION: Fever, appearance, and position of the appendix are factors related to an extended hospital stay.     

Acute pericarditis as the initial manifestation in Still's disease in an adult

Almost 90% of primary acute pericarditis are idiopathic. Between specifics forms, a very low percentage of cases are due to chronic rheumatic diseases. A case of adult Still's disease (juvenile chronic rheumatoid arthritis) with acute pericarditis being the first clinical manifestation (besides fever and general syndrome) is presented. Therapy with oral prednisone was rapidly effective, and pericardial effusion resolved after 3 weeks of treatment, as echocardiography showed.     

3D Reconstruction of Tomographic Images Applied to Largely Spaced Slices

This paper presents a full reconstruction process of magnetic resonance images. The first step is to bring the acquired data from the frequency domain, using a Fast Fourier Transform algorithm. A Tomographic Image Interpolation is then used to transform a sequence of tomographic slices in an isotropic volume data set, a process also called 3D Reconstruction. This work describes an automatic method whose interpolation stage is based on a previous matching stage using Delaunay Triangulation. The reconstruction approach uses an extrapolation procedure that permits appropriate treatment of the boundaries of the object under analysis.     

Central and peripheral control of postprandial pyloric motility by endogenous opiates and cholecystokinin in dogs

The role of endogenous opiates and cholecystokinin (CCK) in the control of postprandial pyloric myoelectric activity was investigated in conscious dogs with chronically implanted intraparietal electrodes at the gastroduodenal junction. Meals consisted of either 20 g/kg of canned food (standard meal) or the same food supplemented with 0.5 mL/kg of arachis oil (fat meal). During the 6 hours after standard and fat meals, the number of pyloric spike bursts, 2-4 seconds in duration, was 61.8 +/- 15.8 and 49.9 +/- 12.7/15 minutes, respectively. Administered 15 minutes before a fat meal, naloxone (50 micrograms/kg IV) decreased the number of spike bursts by 31.4%, whereas methyl-levallorphan, a peripheral opiate antagonist, increased postprandial spike activity by 22.2% when administered IV (0.5 mg/kg) and decreased it when administered intracerobroventricularly at a dose of 10 micrograms/kg. These two antagonists administered in the same conditions before a standard meal had no effect on the postprandial spike activity. A 1-hour infusion of cholecystokinin octapeptide (CCK-8), 500 ng.kg-1.h-1 IV and 50 ng.kg-1.h-1 intracerebroventricularly, performed 1 hour after a standard meal induced a 19.6% and 15.8% decrease in the number of pyloric spike bursts, respectively. Both naloxone IV (50 micrograms/kg) and methyl-levallorphan intracerebroventricularly (10 micrograms/kg) administered before the infusion of CCK-8 reinforced this pyloric inhibition, which was antagonized by methyl-levallorphan IV (0.5 mg/kg). The CCK antagonist asperlicin, 200 micrograms/kg IV and 20 micrograms/kg intracerebroventricularly, administered before a fat meal increased pyloric spike bursts by 22.0% and 31.5%, respectively. These results indicate that after a fat meal, endogenous opiates exert a peripheral inhibitory and central stimulatory control of pyloric motility; they suggest the involvement of both peripheral and central release of CCK.     

Involvement of central dopamine and D1 receptors in stress-induced colonic motor alterations in rats.

The role of central versus peripheral influence of dopamine (DA) in the genesis of emotional stress (ES) induced by fear to receive electric footshocks on colonic motility was evaluated in rats equipped with implanted electrodes on the proximal colon. In control rats, the frequency of colonic spike bursts increased from 7.5 +/- 1.9 to 16.0 +/- 2.1 per 10 min when the rats were placed in a test box where they had previously received electric footshocks. This increase induced by ES was significantly p less than 0.05, reduced by previous ICV or IP administration of (+)SCH 23390 (a D1 receptor antagonist) at doses of 10 and 100 micrograms/Kg, respectively. Although sulpiride (a D2 antagonist) injected ICV or IP at similar doses had no effect on the ES-induced increase in the frequency of colonic spike bursts. DA (100 micrograms/kg), and the selective D1 (SKF 38383) or D2 (quinpirole) receptor agonist injected ICV at a dose of 5 micrograms/kg also increased significantly by 48.7, 54.8, and 68.7%, respectively, the colonic spike burst frequency whereas they are inactive when injected IP at similar and higher doses. These results suggest that, in rats, (a) emotional stress stimulates colonic motility through the stimulation of dopaminergic neurons involving D1 receptors and (b) exogenous activation of central D1 and D2 receptors similarly stimulate colonic motility by increasing the occurrence of colonic spike bursts.