The quality of tracheal intubation contributes to laryngeal morbidity, and excellent conditions are less frequently associated with postoperative hoarseness and vocal cord sequelae. Adding atracurium to a propofol-fentanyl induction regimen significantly improved the quality of tracheal intubation and decreased postoperative hoarseness and vocal cord sequelae.

A total of 370 patients underwent colorectal resection: 320 had a primary single-layer seromucosal anastomosis without a protective colostomy, 22 had Hartmann's procedure and 28 abdominoperineal resection. There were 260 elective procedures and 110 patients had peritonitis and/or bowel obstruction at the time of surgery. Overall the mortality rate was 2.7 per cent, the morbidity rate was 18.3 per cent and clinical anastomotic leak rate 3.4 per cent. After elective operation, the leak rate for intraperitoneal anastomosis was 0.6 per cent and for low extraperitoneal anastomosis 7 per cent. The mortality rate was 1.2 per cent and morbidity rate 11.9 per cent. Patients with peritonitis had a significant increase in morbidity rate (46 per cent) in comparison with those having elective surgery (chi 2 = 31.5, 1 d.f., P < 0.0001). Patients who had bowel obstruction and no bowel preparation had a significantly higher morbidity rate of 26 per cent and mortality rate of 7 per cent, compared with those having an elective procedure (chi 2 = 11.2, 1 d.f., P < 0.001; chi 2 = 8.7, 1 d.f., P < 0.005 respectively). Patients having palliative surgery had the highest mortality rate (19 per cent), compared with those operated on with curative intent (1.5 per cent) (chi 2 = 28.7, 1 d.f., P < 0.0001). Cost-saving hand-sutured anastomosis is effective and, in experienced hands, technically feasible after all kinds of colorectal resection and should remain the standard in colorectal surgery.

Transfusion of blood may contribute to immunomodulation. Leuco‐depleted standard blood products are supposed to result in less immunomodulation compared with whole blood. To determine the influence of leuco‐depleted blood products on the cytokine response, red blood cell concentrates (RBC), fresh frozen plasma (FFP) and platelet concentrates (PC) were investigated in an in vitro model of blood transfusion. Leuco‐depleted standard blood bank RBC, FFP and PC were mixed in vitro with AB0 compatible venous blood from healthy volunteers in ratios of 3:1, 1:1 and 1:3. Specimens were incubated in presence or absence of lipopolysaccharide, 1 μg/ml. After 24 h of incubation cytokine release of tumour necrosis factor (TNF)‐α and interleukin‐10 (IL‐10) was measured in cell culture supernatants by means of enzyme‐linked immunsorbent assay. Addition of RBC, FFP and PC to venous blood from healthy volunteers led to a significant and dose‐dependent increase in spontaneous TNF‐α and IL‐10 release. After endotoxin stimulation, RBC, FFP and PC significantly suppressed the TNF‐α response, while the stimulated release of IL‐10 tended to increase, reaching significance only after high doses of FFP. Addition of leuco‐depleted blood products changed the spontaneous and stimulated cytokine response in an in vitro model of transfusion. These data may suggest a possible contribution of transfused FFP and PC to immunomodulation after transfusion similar to RBC.

In patients undergoing laparoscopic cholecystectomy, remifentanil-based anaesthetic regimens in conjunction with propofol or desflurane are suitable and allow for rapid recovery from anaesthesia. However, the use of propofol results in less postoperative analgesic consumption and nausea as compared to desflurane.

SummaryThis prospective, clinical trial evaluated the effects of short-term propofol administration on triglyceride levels and serum pancreatic enzymes in children undergoing sedation for magnetic resonance imaging. Laboratory parameters of 40 children, mean age (SD; range) 67 (66; 4-178) months undergoing short-term sedation were assessed before and 4 h after having received propofol. Mean (SD) propofol loading dose was 2.2 (1.1) mg.kg )1 followed by continuous propofol infusion of 6.9 (0.9) mg.kg )1 .h )1 . Serum lipase levels (p = 0.035) and serum triglyceride levels (p = 0.003) were raised significantly after propofol administration but remained within normal limits. No significant changes in serum pancreatic-amylase levels were seen (p = 0.127). In two (5%) children, pancreatic enzymes and in four (10%) children triglyceride levels were raised above normal limits; however, no child showed clinical symptoms of pancreatitis. We conclude that even short-term propofol administration with standard doses of propofol may have a significant effect on serum triglyceride and pancreatic enzyme levels in children. Little is known about drug-induced pancreatitis, although it is reported to have been caused by over 85 different drugs [1,2]. Drug-induced pancreatitis is a relatively rare disorder, with a prevalence of 1.4% among patients presenting with acute pancreatitis from all causes [1]. Propofol, a sedative-hypnotic agent, is used for sedation as well as for induction of general anaesthesia in children and adults. Propofol is a lipid-based, global central nervous depressant which has a rapid onset of sedation with a dose-related hypnotic effect and a quick and smooth recovery profile. Dose dependent hypotension is the most common complication [3]. Hypertriglyceridaemia is another possible adverse effect [4][5][6][7][8][9][10]. Since its approval in 1989, there have been reports indicating a possible link between the use of propofol and the development of acute pancreatitis [11][12][13][14][15][16][17][18][19]. This was mostly in an intra-or postoperative setting and most of these patients received propofol continuously for several days. Furthermore, in these cases, a number of different drugs were co-administered, thus preventing the establishment of a clear causal link between propofol and the occurrence of acute pancreatitis [12,13,[15][16][17][18][19][20]. Recently, we reported a definite association between short-term propofol administration in an 11-year-old girl and the occurrence of acute pancreatitis [11].The mechanism of propofol-induced pancreatitis remains unknown. Although induction of hypertriglyceridaemia has been described and is therefore a suspected mechanism, it seems unlikely that short-term administration of propofol could raise serum lipid levels as much as to induce pancreatitis. To our knowledge, only one clinical trial (n = 21), focusing on pancreatic function in adult patients under postoperative sedation with propofol, has been published so far and no elevated markers of altered pancreatic ...