Communication in the operating theatre.

BACKGROUND: Communication is extremely important to ensure safe and effective clinical practice. A systematic literature review of observational studies addressing communication in the operating theatre was conducted. The focus was on observational studies alone in order to gain an understanding of actual communication practices, rather than what was reported through recollections and interviews. METHODS: A systematic review of the literature for accessible published and grey literature was performed in July 2012. The following information was extracted: year, country, objectives, methods, study design, sample size, healthcare professional focus and main findings. Quality appraisal was conducted using the Critical Appraisal Skills Programme. A meta-ethnographic approach was used to categorize further the main findings under key concepts. RESULTS: Some 1174 citations were retrieved through an electronic database search, reference lists and known literature. Of these, 26 were included for review after application of full-text inclusion and exclusion criteria. The overall quality of the studies was rated as average to good, with 77 per cent of the methodological quality assessment criteria being met. Six key concepts were identified: signs of effective communication, signs of communication problems, effects on teamwork, conditions for communication, effects on patient safety and understanding collaborative work. CONCLUSION: Communication was shown to affect operating theatre practices in all of the studies reviewed. Further detailed observational research is needed to gain a better understanding of how to improve the working environment and patient safety in theatre.

The efficacy of stretching for prevention of exercise-related injury: a systematic review of the literature.

The objective of this study was to conduct a systematic analysis of the literature to assess the efficacy of stretching for prevention of exercise-related injury. Randomized clinical trials (RCTs) and controlled clinical trials (CCTs) investigating stretching as an injury prevention measure were selected. A computer-aided search of the literature was conducted for relevant articles, followed by assessment of the methods of the studies. The main outcome measures were scores for methodological quality based on four main categories (study population, interventions, measurement of effect, and data presentation and analysis) and main conclusions of authors with regard to stretching. One RCT (25%) and three CCTs (100%) concluded that stretching reduced the incidence of exercise-related injury. Three RCTs (75%) concluded that stretching did not reduce the incidence of exercise-related injury. Only two studies scored more than 50 points (maximum score=100 points) indicating that most of the studies selected were of poor quality. Neither of the two highest scoring RCTs showed positive effects for stretching. Due to the paucity, heterogeneity and poor quality of the available studies no definitive conclusions can be drawn as to the value of stretching for reducing the risk of exercise-related injury.

Differential effects of L-NAME on blood pressure and heart rate responses to acetylcholine and bradykinin in cynomolgus primates.

NG-nitro-L-arginine methyl ester (L-NAME) has been reported to have variable effects on the vasodilator response to acetylcholine (ACh) and bradykinin (BK) in vivo. Whether administration of L-NAME affects mean arterial pressure (MAP) or heart rate (HR) responses to ACh or BK was examined in conscious cynomolgus primates. ACh (0.1-10 micrograms/kg i.v.) lowered MAP by 6% to 37%, responses which were inhibited (25-62%) in the presence of L-NAME (1-100 mg/kg i.v.). Although L-NAME increased MAP similarly at doses of 10 and 100 mg/kg, only the 100-mg/kg dose inhibited the hypotensive responses induced by the higher doses of ACh. By comparison, nitroprusside (5 micrograms/kg i.v.)-induced hypotensive responses were not inhibited by L-NAME. Phenylephrine (20 micrograms kg-1 min-1 i.v.) increased MAP and lowered HR to levels statistically similar to that of L-NAME but did not alter ACh-induced hypotensive responses. ACh dose-dependently decreased HR, both in the absence and presence of L-NAME or phenylephrine. In pentobarbital-anesthetized monkeys, ACh-induced hypotensive responses were inhibited by 75% to 94% in the presence of L-NAME; BK (0.3-1 microgram/kg i.v.) responses were only modestly affected (< or = 50%). Therefore, in conscious primates, L-NAME affects the basal release of nitric oxide (NO) at lower doses than those required to inhibit its release stimulated by ACh. Also, L-NAME does not appear to act as a cholinergic antagonist or affect the functional mechanisms that control baroreflex responses.(ABSTRACT TRUNCATED AT 250 WORDS)

Inhibition of human leukocyte elastase by N-substituted peptides containing alpha,alpha-difluorostatone residues at P1.

A series of tripeptides which contain alpha,alpha-difluorostatone residues at P1-P1' and span the S3-S1' subsites have been shown to be potent inhibitors of human leukocyte elastase (HLE). The tripeptides described contain the nonproteinogenic achiral residue N-(2,3-dihydro-1H-inden-2-yl)glycine at the P2-position. This redidue has previously been shown in the case of HLE to be a good bioisosteric replacement for L-proline. Of the peptides prepared, those which contain the alpha,alpha-difluoromethylene keton derivative of L-valine (difluorostatone) are the preferred residue at the P1-primary specificity position. Substitution at P1 by the corresponding alpha,alpha-difluoromethylene ketones of L-leucine and L-phenylalanine gives inactive compounds. Of the tripeptides described the most potent in vitro compound is ethyl N-[N-CBZ-L-valyl-N-(2,3-dihydro-1H-inden-2-yl)glycyl]- 4(S)-amino-2,2-difluoro-3-oxo-5-methylhexanoate (17B) (IC50 = 0.635 microM). It is presumed that the inhibitor 17b interacts with the S3-S1' binding regions of HLE. Additionally extended binding inhibitors were prepared which interact with the S3-S3' binding subsites of HLE. In order to effect interaction with the S1'-S3' subsites of HLE, the leaving group side of cleaved peptides, spacers based upon Gly-Gly, and those linked via the N epsilon of L-lysine were utilized. One of the most potent extended compounds (P3-P3') in vitro is methyl N6-[4(S)-[[N-[N-CBZ-L-valyl-N- (2,3-dihydro-1H-inden-2-yl)glycyl]amino]-2,2-difluoro-3-oxo-5- methylhexanoyl]-2(S)-(acetylamino)-6-aminohexanoate (24b) (IC50 = 0.057 microM). The described in vitro active inhibitors were also evaluated in hamsters in an elastase-induced pulmonary hemorrhage (EPH) model. In this model, intratracheal (it.) administration of 22c, 5 min prior to HLE challenge (10 micrograms, it.) effectively inhibited hemorrhage (94.6%) in a dose-dependent manner. The described alpha,alpha-difluoromethylene ketone inhibitors are assumed to act as transition-state analogs. The inhibition process presumably acts via hemiketal formation with the active site Ser195 of HLE, and is facilitated by the strongly electron withdrawing effect of the alpha,alpha-difluoromethylene functionality.