Ceftazidime indications

Gram-negative cocci Non-tuberculous mycobacteria Nocardia Ceftriaxone 50 mg/mL or Ceftazidime 50 mg/mL or Fluoroquinolones 3 mg/mL Amikacin 20-40 mg/mL or Oral clarithromycin 500 mg every 12 hours Amikacin 20-40 mg/mL or Trimethoprim 16 mg/mL and sulfamethoxazole 80 mg/mL wearers as indicated... 

Answer The patient s high serum creatinine indicates compromised renal function. The aminoglycosides can be nephrotoxic and thus the drug was not employed. However, tobramycin might have been used together with ceftazidime if the dose were adjusted for renal function. 

In the second study [16], 62 subjects were treated with intravenous ceftazidime and amikacin. The treatment group also received aerosolized amikacin 100 mg twice daily. Treatments were given for an average of 15 days, and subjects were reevaluated four to six weeks after hospital discharge. During treatment, transient improvements in several outcome measures were noted (e.g., x-ray score, inflammation indices, and percentage underweight) however, there were no differences in any measure at the final evaluation point. As in the earlier study, eradication of bacteria from sputum was also transient. 

Bone infections in patients with a history of intravenous drug abuse require coverage for gram-negative organisms therefore, empirical treatment with ceftazidime 2 g intravenously every 8 hours plus an aminoglycoside is indicated. If compliance can be ensured, these patients are excellent candidates to receive oral ciprofloxacin 750 mg twice daily. Antibiotic therapy in these patients should be continued for at least 4 to 6 weeks. 

Beta-lactams such as cephaloridine, cephalothin, ce-fotiam and imipenem have been associated with nephrotoxicity in humans and experimental animals [9]. An understanding of their nephrotoxicity mechanisms may provide valuable information for elucidation of the biochemical mechanisms of newer P-Iactam nephrotoxicity. Similarly to cephaloridine, third- generation cephalosporins such as ceftazidime and cefsulodin and fourth-generation cephalosporins such as cefpirome and cefepime possess a quaternary nitrogen attached to the dihydrothiazine ring which may impart nephrotoxic potential [10]. Clinical and animal studies carried out with P-Iactams, such as cephaloglycin, cephaloridine, cephalothin or imipenem, indicated that they show a differential accumulation at the site of their toxicity, the renal cortex [11]. Elucidation of the mechanism of toxic action of these model (i-lactams has become the focus of several research efforts [12-16]. 

Ceftazidime, a third-generation cephalosporin antibiotic (1 g IV or IM q. 8 to 12 honrs), is indicated in the treatment of bacteremia, septicemia, and serions respiratory, nrinary, gynecologic, intra-abdominal, CNS, and skin infections from susceptible organisms. 

The fourth-generation cephalosporins are indicated for the empirical treatment of nosocomial infections where antibiotic resistance owing to extended-spectrum /J-lactamases or chromosomaUy induced /1-lactamases is anticipated. For example, cefepime is superior to ceftazidime and piperacillin for nosocomial isolates of Enterobacter, Citrobacter, and Serratia spp. 

Two kidney transplant patients had two- to fourfold rises in ciclosporin blood levels within 2 to 3 days of starting ceftriaxone 1 g twice daily. Levels fell when the antibacterial was stopped. The reason is uncertain but it was suggested that ceftriaxone possibly inhibits the metabolism of ciclosporin by the liver. However, a report of 51 kidney transplant patients stated that ceftriaxone and cefuroxime had no effect on ciclosporin blood levels and also that they were not nephrotoxic. This report also stated that ceftazidime did not affect serum ciclosporin levels, but it increased blood urea nitrogen and creatinine levels, indicating that it was nephrotoxic. A report briefly mentions that ceftazidime and latamoxef have also... 

Ceftazidime is reported to have low serum binding serum binding (determined by a filtration technique at a concentration of 25 p.g/ml) in the mice, rat, rabbit, dog, monkey, and human was 13, 19, 11, 20, 8, and 17%, respectively (O Callaghan et al., 1980). There was a wide species variation in peak serum concentration achieved after parenteral administration of ceftazidime (Acred et al., 1980). Experiments in rodents indicated that <5% of the administered dose was excreted in the bile. 

Ceftazidime was dosed intramuscularly and intravenously to human volunteers (Table XII). Peak serum concentrations of 10, 23, and 27 p,g/ ml were obtained after intramuscular doses of 0.25, 0.5, and 0.75 g. The plasma half-life varied from 1.4 hr for the low dose to 1.8 hr for the high dose. Serum concentrations of 8 p,g/ml were still present 1.5 (0.25 g dose), 4.2 (0.5 g dose), and 6.1 hr (0.75 g dose) after intramuscular administration. Urinary recovery of ceftazidime varied from 48 to 88% in 88% in humans. Serum levels of 61 fig/ml were measured immediately after intravenous administration of 0.5 g of ceftazidime to human volunteers. Preliminary experiments indicated that concomitant administration of probenecid had no effect on the rate of excretion of ceftazidime. This indicates that ceftazidime is excreted by glomerular filtration and not by tubular secretion. 

Based on safety concerns with cefepime compared to other antimicrobials, a retrospechve study was conducted to evaluate the clinical outcomes of 532 paediatric patients with cancer who received either ceftazidime or cefepime for suspecfed or proved infections. No statistically significant difference was seen in patienfs who received cefepime compared to those who received ceftazidime. While these data are encouraging, it should be interpreted cautiously due to the retrospective design and limited power of the study, though it does agree with the most recent FDA reporting of a meffl-analysis that reported no mortality disadvantage to cefepime use for its approved indications [61 , 62 ]. 

The ability to detect ESBLs has clinical relevance because it will have an impact on antibiotic therapy. Producers of ESBLs are suspected when susceptibility testing indicates resistance to ceftazidime (but may be paradoxically susceptible to ceftriaxone and cefotaxime by the minimal inhibitory concentration [MIC] or disc diffusion) and susceptible to the cephamycins (11). More recently, a breakpoint of 2 ig/mL to cefpodoxime has been suggested as a standard. Another method of detection is the use of the E-test strip with a gradient of ceftazidime on one side and ceftazidime in combination with clavu-lanate on the other. The ESBLs are thought to be present when enhancement of inhibition is demonstrated. Table 2 highlights some of the more common resistance mechanisms for antimicrobial agents used commonly in the treatment of nosocomial pneumonia. 

Typically, ESBL-producing isolates of E. coli and K. pneumoniae are resistant to ceftazidime and aztreonam however, susceptibility testing may indicate that the organism is susceptible to other extended-spectrum P-lactams (cefo-... 

---