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FIG. 1. In vitro aCtiVity of Cefazolin against KIeb.
Studies have shown that following intravenous administration of cefazolin to normal volunteers, mean serum concentrations peaked at approximately 185 mcg ml and were approximately 4 mcg ml at eight hours for a 1 gram dose Results on AEs three of these studies were included for AEs only ; . All studies, apart from one Spanish trial, 13 were reported in English. Three studies1416 were published as an abstract only. The 16 studies included for effectiveness were all randomised controlled trials RCTs ; . Five trials were in cardiac surgery; 13, 1720 one trial included both cardiac and vascular procedures; 21 three trials were in vascular surgery; 16, 22, 23 five trials were in orthopaedic surgery; 14, 2427 one trial was in neurosurgery; 28 and one trial was in thoracic surgery.29 Most trials compared vancomycin or teicoplanin with a cephalosporin. The trial of cardiac and vascular surgery by Maki and colleagues21 included two cephalosporin arms, cefazolin and cefamandole. As the trial reported comparisons of vancomycin versus the combined cephalosporin arms for the primary outcome of SSI, the results of the two cephalosporin arms have been combined in this review. Three trials compared a glycopeptide to an alternative glycopeptide regimen: one cardiac trial compared vancomycin with teicoplanin; 13 one orthopaedic trial compared 400 mg of teicoplanin given regionally with 800 mg given systemically; 27 and a An increase in creatinine may be caused by a number of processes, but common causes are: Rejection Infection, e.g. urine, CMV Tacrolimus Ciclosporin toxicity Altered fluid balance Less common causes are: Vascular catastrophe Mechanical problem - urinary obstruction less likely if ureteric stent present ; , lymphocele. And at the same time allow only a very small number of , -lactam molecules to trickle into the periplasm. To our knowledge, quantitative estimation of neither of these parameters has been reported previously. In this study we determined these parameters by using one such constitutive mutant, E. cloacae 55M. By identifying the P-lactamase band on SDS-polyacrylamide slab gel and quantitating this band on gels of whole cell proteins, we could determine that the strain produced a very large amount of this enzyme, corresponding to 3.7% of the total cellular protein, or about 2 x 105 molecules per cell. This number is similar to the number of another very abundant periplasmic protein of E. coli, maltose-binding protein, which is reported to be present in 4 x 105 copies per cell 4 ; . If the cells are growing with a generation time of 20 min, a cell should be synthesizing, on an average, 2 x 105 ; 20 x 60 ; 167 molecules of new P-lactamase every second. The outer membrane permeability to cefazolin was low, estimated to be about 7% of the permeability coefficient previously determined in E. coli K-12 5 x 10-5 cm s [13] ; . Since most of the third-generation , -lactams, with the notable exception of imipenem, have permeability coefficients lower than 20% of that of cefazolin 21 ; , and since the major porin of E. cloacae appears to have a pore size slightly narrower than the E. coli porins 6, 12 ; , it is reasonable to assume that the permeability coefficients of the E. cloacae for them would be lower than 5 x 10-5 0.07 x 0.2 7 x 10-7 cm s-1 see also reference 13 ; . The maximal rate of influx of such agents across the outer membrane is v P C0, following Fick's first law of diffusion, where P, A, and C0 denote the permeability coefficient, area of the membrane per unit weight of cells, and the external concentration of the P-lactam, respectively. Using the value of 132 cm2 mg-1 for A 13 ; , and assuming C0 0.4 x 10-8 mol cm-3 or about 2 , ug ml-' with a 1-lactam molecular weight of 500, v 7 x 10-7 cm s-1 ; x 132 cm2 mg-1 ; x 0.4 x 10-8 mol cm-3 ; x 6.023 x 1023 molecules mol-' ; [2 x 109 cells mg-' ; ] 111 molecules per cell per s. Since, as we have seen, the cells are making new , -lactamases at a slightly higher rate, practically all the P-lactams slowly flowing into the periplasm can be trapped by this binding process, and thus in theory the mechanism should be able to produce a low level of resistance. In practice, however, we have some serious problems.

The purpose of this investigation was to compare the efficacy and costs of prophylaxis with cefazolin alone with cefazolin plus metronidazole.
1 21.4 le 155.8 20e 13 le 73 345 a Cefazolin was given as described in Table 1, footnote a. After equilibrium was reached and after two control periods of 30 min each, piretanide 0.1 mg kg ; was injected i.v., and four experimental periods of 30 min each followed. Control and experimental values were described in Table 1, footnote a. b Milliliters per minute per 1.73 m2 of body surface. c Percentage of infused cefazolin that was excreted. d Micrograms per minute per 1.73 m2 of body surface. e Significantly different from control value P 0.05 and cellcept.

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