Conflict management in public university hospitals in Turkey: a pilot study

By nature, hospitals are extremely complex organizations, combining many different professional groups within an intricate administrative structure. Conflicts therefore expectedly arise between individuals, groups, and departments. It is in the interest of health care administrators to periodically assess the major factors giving rise to these conflicts. In this study, a questionnaire designed to measure sources of conflict in the workplace was completed by 204 staff members at Gazi University Hospital. Of the participants, 30.9% were physicians, and 12.5% were administrators at various levels; 61.5% were female, and 38.5% were male. In terms of work experience, 52.6% of participants had worked less than 5 years at the hospital. The results of the study show that educational differences among the hospital staff were a major barrier to good communication and information flow between groups. Professionals in the same specialties experienced fewer conflicts. Another source of conflict was that resource allocation was considered unfair across departments. Although the hospital management provided an ombudsman for staff concerns, staff rarely resorted to the ombudsman because of the stigma associated with complaining. A lack of opportunity for career advancement was mentioned by 52% of the participants as a source of conflict. At present, job performance and rewards are not closely related in public university hospitals in Turkey because promotions and pay raises are strictly limited by law. Bureaucracy was also perceived to be a source of conflict, with 48.4% of participants saying that their performance was less than optimal because of the presence of multiple supervisors. This pilot study suggests that in Turkey, legislative reform is needed to give public university hospitals more flexibility regarding work incentives, open-door policies at the administrative level, and social interactions to improve teamwork among hospital staff.     

Histopathologic changes in the lacrimal sac of dacryocystorhinostomy patients with and without silicone intubation

PURPOSE: To evaluate the histopathologic impact of dacryocystorhinostomy (DCR) and silicone intubation on the lacrimal sac. METHODS: Biopsy materials were taken from the sac wall and fixed (primary biopsy) in 224 patients undergoing DCR between 1995 and 2003 in our institution. A total of 23 patients underwent a second operation as the result of restenosis, and a secondary biopsy specimen was taken from the sac wall. During the initial operation, DCR and silicone intubation were combined in 13 patients (group 1), and only DCR without silicone intubation was performed in 10% patients (group 2). The histopathologic findings of the primary and secondary biopsy specimens were compared in these 23 recurrent cases. In addition, the secondary biopsy findings in the intubation and nonintubation groups were compared to determine the possible effects of the silicone intubation on the sac mucosa. RESULTS: Endonasal examination of restenosis cases revealed macroscopic cicatrization. One of the cases with silicone intubation had pyogenic granuloma and two had polypoid granulation tissue at the site of anastomosis. Inflammatory polypoid development at the site of anastomosis was also observed in one case without intubation. The primary biopsy specimens of those 23 patients undergoing a second operation revealed the following findings: chronic inflammatory changes, mild fibrosis, focal ulceration in the epithelium, and a decrease in the number of goblet cells. In the secondary biopsy specimens, 2 patients in group 1 had polypoid granulation tissue, 1 patient had pyogenic granuloma, and 3 patients had exudate reflecting acute inflammation. In group 2, granulation tissue was observed in 1 case, and 2 patients had acute inflammation. There were no differences in the primary and secondary biopsy specimens of the two groups with respect to chronic inflammatory changes, focal ulceration, and the number of goblet cells (p = 0.31; 0.31, 0.65). A marked increase in fibrosis was observed in the secondary biopsy specimens of all cases (p < 0.0001). There were no significant differences between the intubation and the nonintubation groups in terms of secondary biopsy specimens (p > 0.05). CONCLUSIONS: The marked increase in the intensity of fibrosis observed in the secondary biopsy specimens of all cases was the result of the tissue repair reaction against surgical manipulation rather than the effect of the silicone tube.     

Relation between inflammatory cytokine levels in serum and bronchoalveolar lavage fluid and gene polymorphism in young adult patients with bronchiectasis

Aim

Bronchiectasis develops as a result of genetic and environmental factors and its etiopathogenesis is not still clear. Recent studies have revealed that inflammatory cytokines, which are formed as a result of chronic infection and inflammation, play a role in the pathogenesis of bronchiectasis. For this purpose, the level of inflammatory cytokines in bronchiectasis and the presence or absence of a genetic predisposition with the gene polymorphism of these cytokines was investigated.

Material and methods

A total of 60 patients, 40 study cases and 20 controls, which were monitored with the diagnosis of bronchiectasis were included in the study. In these individuals, cytokine levels [interleukin (IL)-6, IL-8, IL-10, and tumor necrosis factor (TNF)-α] in serum and bronchoalveolar lavage (BAL) fluid, along with the routine blood tests, were determined. Furthermore, the polymorphism in IL-6, IL-8, IL-10, and TNF-α cytokine genes and its frequency were studied in the obtained DNA by the automatic sequence analysis method and the results were compared.

Findings

It was found that in serum and BAL fluid of the patient group, the IL-8 level was high, whereas the IL-10 level was low (P<0.05). No significant difference was detected in the other cytokines (P>0.05). It was found that in cytokine gene polymorphisms IL-8 -251 A/T, IL-10 -592 A/C, and IL-10 -819 T/C genotypes are associated with increased risk of bronchiectasis. It was detected that the IL-8 -251 A/T genotype increased the risk of having the disease by 4.19 fold. (OR =4.19, 95% CI =1.24-14.17, P=0.021). The IL-10 -592 C/A genotype increased the risk of having the disease by 5.71 fold (OR = 5.71, 95% CI =1.35-24.06, P=0.017) and the IL-10 -819 T/C genotype increased the risk of having the disease by 5.06 fold (OR =5.06, 95% CI =1.20-21.27, P=0.048). No significant correlation was found between the other polymorphisms and bronchiectasis.

Conclusions

The IL-8, IL-10 levels and the gene polymorphism of these cytokines differ. In addition to detecting higher levels of pro-inflammatory IL-8 and lower levels of anti-inflammatory IL-10, detection of gene polymorphism related to these two cytokines in bronchiectasis gives rise to the thought that cytokines may have role in a predisposition to bronchiectasis. However, as the number of patients is small, precise remarks could not be made on this subject. There is need for further studies include a larger number of patients.