A double-blind, randomized trial with placebo control was planned to evaluate the effects of corticosteroids (betamethasone, dexamethasone, methylprednisolone) in approximately equivalent doses (8 mg dexamethasone/day), and to compare their effects with that of tenoxicam, an antiinflammatory drug, on both the edema and ecchymosis in open rhinoplasty with osteotomies. For this study, 40 patients were divided randomly into five groups of 8 patients each, which received, respectively, betamethasone (group 1), dexamethasone (group 2), methylprednisolone (group 3), tenoxicam (group 4), and placebo (group 5). Open rhinoplasty with osteotomies was performed by the same surgeon with the patient under general anesthesia. Drugs were administered just before the induction of anesthesia and continued for 3 days. Only acetaminophen was used to control postoperative analgesia. Digital photographs of each patient were taken on postoperative days 1, 3, and 7. Scoring was performed separately for eyelid swelling and ecchymosis by three observers independently using a graded scale from 0 to 4. No statistically significant differences existed among the five groups in terms of age, sex, duration of surgery, amount of bleeding, and intravenous fluid administration during the surgery. On postoperative days 1, 3, and 7, no differences in the levels of ecchymosis or edema among the steroid groups, the tenoxicam group, and the control groups were observed. In conclusion, the authors observed no significant differences among the different kinds of steroids administered in equivalent doses (8 mg dexamethasone/day). Steroids used in these doses were not effective in preventing or reducing edema and ecchymosis after open rhinoplasty with osteotomies. Tenoxicam also was not effective. No complications caused by the use of steroids were observed during the 6-month follow-up period.

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Acinetobacter species other than Acinetobacter baumannii have rarely been reported to be associated with nosocomial outbreaks of bloodstream infections. Within a period of 1 week, seven Acinetobacter-like isolates were recovered from peripheral blood and catheter specimens of five patients at a neonatal intensive care unit (NICU) in a tertiary hospital in Turkey. All five patients had placement of central venous catheters and had received total parenteral nutrition before the onset of bacteremia. Two of the five patients died. Medical devices, tap water, aerators, water samples, various surfaces, intravenous fluids, and the hands of health care workers in the NICU were sampled and were culture negative for the bacterium. All seven of the isolates had identical biochemical reactions, antimicrobial susceptibility results, and pulsed-field gel electrophoresis patterns, indicating a clonal nosocomial outbreak. A panel of standard biochemical reaction profiles and three phenotypic commercial identification systems failed to identify these isolates. Phenotypically, the isolate differed from Acinetobacter ursingii by its hemolysis on sheep blood agar and its negative citrate utilization. Sequences of the full 16S rRNA gene, which contained at least three different gene copies with polymorphic sequences between nucleotide positions 70 and 206, were determined from the first recovered isolate. The complete 1,529-to 1,531-bp 16S rRNA gene sequences and partial 801-bp rpoB gene sequences had similarities of 99.5% and 97.2%, respectively, to an A. ursingii isolate. The DNA-DNA similarities of the strain against the type strain of A. ursingii were 64.7 and 68.7%, which were lower than the recommended threshold value of 70% for the definition of bacterial species. These data indicate that a novel Acinetobacter organism caused the nosocomial outbreak of bacteremia in the NICU unit. We propose the designation of Acinetobacter septicus sp. nov. for these isolates, with isolate AK001 as the type strain.