Decision-making by medical officer in charge during major incidents: a qualitative study.

BACKGROUND: An incident command structure is commonly used to manage responses to major incidents. In the hospital incident command structure, the medical officer in charge (MOC) is in a key position. The decision-making process is essential to effective management, but little is known about which factors influence the process. Therefore, the current study aimed to describe factors influencing decision-making of MOCs. METHODS: A conventional content analysis was conducted based on 16 individual interviews with medical doctors who had been deployed as MOCs at Swedish hospitals during major incidents. RESULTS: The results showed that the decision-making and re-evaluation process was a comprehensive analysis influenced by three categories of factors: event factors, including consequences from the type of event, levels of uncertainty and the circumstances; organizational factors, including the doctor's role, information management and the response to the event; and personal factors, such as competence, personality and mental preparedness. CONCLUSIONS: Reliable and timely information management structure enabling the gathering and analysis of essential information, a clear command structure and appropriate personal qualities were essential and contributed to successful MOCs decision making in major incidents.

Bile acids and the intestinal kallikrein-kinin system.

We have measured concentrations of tissue kallikrein-like amidase (TKLA) in blood-free rat gastrointestinal tissue. TKLA was present in the gut wall from the stomach to the rectum with concentration peaks in the duodenum and caecum. When rats, fasted for 24 hr were compared with normally fed animals, the mean fasted TKLA levels rose significantly in the duodenum and proximal and distal colons and fell in the caecum. No other tissues showed concentration changes. Sodium chenodeoxycholate and other bile acids have biological actions on the rat intestinal wall which are similar to those produced by the kallikrein-kinin system. We have previously reported that bile acids released TKLA from the rat colon wall. This TKLA was totally inhibited by aprotinin. We now report that intraluminal sodium chenodeoxycholate (30 mM) increases both colonic motility and colonic mucosal leakage. These increases are largely blocked by aprotinin. The ability of intraluminal sodium taurochenodeoxycholate to increase vascular leakage in the rat stomach and colon was parallelled by its ability to release TKLA from these issues. Our results are compatible with the mediation of these biological actions of the tested bile acids via activation of a serine proteinase, possibly tissue kallikrein.