Since Fyke, Code and Schlegel (1956) first demonstrated the existence of a high pressure zone at the lower end of the oesophagus, there has been increasing interest shown in this structure by anaesthetists. This area is termed the lower oesophageal sphincter (LOS) and is the major barrier preventing regurgitation of acid gastric contents into the oesophagus. This is of considerable concern to anaesthetists, as any regurgitated material may be aspirated into the lungs and produce the acid aspiration (Mendelson's) syndrome. It is of vital importance, therefore, that anaesthetists are aware of the effect of the drugs which they use on the LOS. Regurgitation and subsequent aspiration of gastric contents remains a major cause of morbidity and mortality in clinical anaesthesia. The overall mortality from aspiration has changed little over the past 20 years in the U.K. (Edwards et al., 1956; Lunn and Mushin, 1982). In every published study on deaths attributable to anaesthesia, there have been reports of fatalities resulting from vomiting or regurgitation and subsequent aspiration (Harrison, 1978; Hovi-Viander, 1980). The occurrence of regurgitation has been estimated at 14-26% using older techniques of anaesthesia with ether, cyclopropane and uncuffed endotracheal tubes (Culver, Makel and Beecher, 1951; Berson and Adriani, 1954). Of these 7-16% had evidence of aspiration as judged by the appearance of tracer dye in the trachea at laryngoscopy and bronchoscopy. Using contemporary anaesthetic techniques and the same methodology it was shown in 1970 that the frequency of regurgitation had decreased to 7.8% and of this number, 8.6% of patients had aspirated (Blitt et al., 1970). The lower oesophageal sphincter Various mechanisms have been proposed in the prevention of gastro-oesophageal reflux. These in
Rectal diclofenac reduces morphine consumption, improves postoperative analgesia, and reduces the incidence of adverse effects such as sedation and nausea.
We have measured the effect of infiltration of the deep and superficial layers of the abdominal wound on morphine consumption and pain for 48 h after operation, in 40 patients undergoing total abdominal hysterectomy, in a double-blind randomized study. Patients received wound infiltration with 0.9% normal saline 40 ml or 40 ml of 0.25% bupivacaine with epinephrine 1:200,000. There were no significant differences between groups in morphine consumption, linear analogue scores for pain at rest or on movement, nausea or sedation during the first 48 h after operation. We conclude that infiltration of the deep and superficial layers of the wound of a Pfannenstiel incision with local anaesthetic solution did not confer additional analgesia in patients undergoing major gynaecological surgery.
We have compared pain scores at rest and on standardized movement, and morphine consumption using patient-controlled analgesia in 60 patients who had undergone total abdominal hysterectomy. Patients were allocated randomly to one of three groups: in the saline group, 0.9% sodium chloride 50 ml was administered into the pelvic cavity before closure of the peritoneum; in the second group, the solution administered was 20 ml of 0.5% bupivacaine solution with epinephrine 1:200,000 diluted with saline to a final volume of 50 ml; in the third group, the solution used was 20 ml [corrected] of 2% lidocaine with epinephrine 1:200,000 diluted with saline to a final volume of 50 ml. We found that there was no significant difference between the three groups in visual analogue pain scores at 8, 12, 36 or 48 h after operation at rest or on movement, and no significant difference in sedation or dose of antiemetic administered. Mean morphine consumption in the first 24 h was 54.6 (SEM 5.9) mg in the saline group, 55.5 (6.4) mg in the bupivacaine group and 52.5 (5.3) mg in the lidocaine group. In the second 24 h, morphine consumption was 34.9 (6.6) mg, 28.1 (3.5) mg and 28.0 (3.5) mg in the three groups, respectively. We conclude that i.p. administration of local anaesthetic solution into the pelvic cavity did not confer appreciable analgesia in patients undergoing abdominal hysterectomy.
In this preliminary randomized study, we have measured pain scores at rest and on movement, 24 and 48 h after operation in 19 control patients, who received 50 ml of saline i.p., and in 20 test patients, in whom 50 ml of saline solution containing lignocaine 200 mg and adrenaline 1:500,000 were instilled into the peritoneal cavity after total abdominal hysterectomy. We found that there was no difference in linear analogue scores for nausea, pain on movement or morphine consumption after operation between the two groups, but pain scores at rest were significantly lower in the lignocaine group at 24 and 48 h compared with the saline group. In the lignocaine group, blood sampling over a 3-h period revealed a mean maximum serum concentration of 0.4 microgram ml-1 at 3 h and a highest concentration in any patient of 0.87 microgram ml-1.
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