Design and implementation of the Western Pennsylvania regional Stop the Bleed initiative.

BACKGROUND: Hemorrhage is the leading cause of preventable death in trauma, and nearly 40% of prehospital deaths can be attributed to blood loss. The Stop the Bleed program provides a structured curriculum for teaching hemorrhage control and the use of bleeding control kits. To overcome implementation barriers and to achieve the goal of making education on bleeding control as common as cardiopulmonary resuscitation, widespread implementation with outreach to the public and law enforcement is necessary. METHODS: We provide a description and analysis of the implementation of a regional Stop the Bleed program, which includes a step-by-step guide to the design of this program provided as a template to guide attempts at large-scale Stop the Bleed program development. RESULTS: Combining the efforts of regional trauma and nontrauma centers as a hub-and-spoke design, a region covering four states, 72 counties, and 30,000 square miles was targeted. A total of 27,291 individuals were trained in a 21-month period including 3,172 trainers, 19,310 lay public, and 4,809 law enforcement officers. A total of 436 bleeding control kits were distributed to 102 public schools, and tourniquets were provided to 4,809 law enforcement officers. Program development and community outreach resulted in official recognition of the program by the Pennsylvania State Senate. CONCLUSIONS: With the use of a multicenter outreach program design with emphasis on law enforcement and public education while developing a train-the-trainer program, widespread and rapid dissemination of Stop the Bleed teaching is feasible. The general steps described in this manuscript may serve as a template for new or developing programs in other areas to increase the national exposure to Stop the Bleed. LEVEL OF EVIDENCE: Economic/Decision study, level IV.

The involvement of occupational health services prior to ill-health retirement in NHS staff in Scotland and predictors of re-employment.

OBJECTIVE: To assess the process, causes and outcomes of retirement because of ill-health in NHS staff in Scotland. Particular areas to be investigated include the involvement of occupational health services, access to rehabilitation and redeployment, current health, whether working again and to identify predictors of re-employment. METHOD: An ill-health retirement (IHR) questionnaire was mailed to 863 NHS staff awarded IHR benefits by the Scottish Public Pensions Agency between April 1998 and March 2000. RESULTS: In all, 49% of the 863 postal questionnaires were returned. The most common reasons for retiring were diseases of the musculoskeletal system (38%) and mental disorders (21%). Seventy-one percent of the participants reported their ill-health was partly or completely work related and 29% not work related. Ninety-two percent of NHS staff had attended an occupational health department prior to IHR. Twenty-three percent of participants had no contact with their line manager during their illness prior to retiral. Eighteen percent of individuals were offered the opportunity of working part-time and 15% offered alternative work. Seventeen percent of participants have obtained other work. Predictors of re-employment after IHR were: medical condition, managerial responsibility, improvement of health, wanting to work again, occupation and age at retirement. CONCLUSION: This is the first comprehensive study investigating NHS staff experiences of IHR in Scotland. This study illustrates the need for improved support and rehabilitation for ill-health care workers and that there is the potential to reduce levels of ill-health retirement.

Contribution of Kv4 channels toward the A-type potassium current in murine colonic myocytes.

A rapidly inactivating K(+) current (A-type current; I(A)) present in murine colonic myocytes is important in maintaining physiological patterns of slow wave electrical activity. The kinetic profile of colonic I(A) resembles that of Kv4-derived currents. We examined the contribution of Kv4 alpha-subunits to I(A) in the murine colon using pharmacological, molecular and immunohistochemical approaches. The divalent cation Cd(2+) decreased peak I(A) and shifted the voltage dependence of activation and inactivation to more depolarized potentials. Similar results were observed with La(3+). Colonic I(A) was sensitive to low micromolar concentrations of flecainide (IC(50) = 11 microM). Quantitative PCR indicated that in colonic and jejunal tissue, Kv4.3 transcripts demonstrate greater relative abundance than transcripts encoding Kv4.1 or Kv4.2. Antibodies revealed greater Kv4.3-like immunoreactivity than Kv4.2-like immunoreactivity in colonic myocytes. Kv4-like immunoreactivity was less evident in jejunal myocytes. To address this finding, we examined the expression of K(+) channel-interacting proteins (KChIPs), which act as positive modulators of Kv4-mediated currents. Qualitative PCR identified transcripts encoding the four known members of the KChIP family in isolated colonic and jejunal myocytes. However, the relative abundance of KChIP transcript was 2.6-fold greater in colon tissue than in jejunum, as assessed by quantitative PCR, with KChIP1 showing predominance. This observation is in accordance with the amplitude of the A-type current present in these two tissues, where colonic myocytes possess densities twice that of jejunal myocytes. From this we conclude that Kv4.3, in association with KChIP1, is the major molecular determinant of I(A) in murine colonic myocytes.

Characterization of the A-type potassium current in murine gastric antrum.

A-type currents are rapidly inactivating potassium currents that operate at subthreshold potentials. A-type currents have not been reported to occur in the phasic muscles of the stomach. We used conventional voltage-clamp techniques to identify and characterize A-type currents in myocytes isolated from the murine antrum. A-type currents were robust in these cells, with peak current densities averaging 30 pA pF(-1) at 0 mV. These currents underwent rapid inactivation with a time constant of 83 ms at 0 mV. Recovery from inactivation at -80 mV was rapid, with a time constant of 252 ms. The A-type current was blocked by 4-aminopyridine (4-AP) and was inhibited by flecainide, with an IC(50) of 35 microM. The voltage for half-activation was -26 mV, while the voltage of half-inactivation was -65 mV. There was significant activation and incomplete inactivation at potentials positive to -60 mV, which is suggestive of sustained current availability in this voltage range. Under current-clamp conditions, exposure to 4-AP or flecainide depolarized the membrane potential by 7-10 mV. In intact antral tissue preparations, flecainide depolarized the membrane potential between slow waves by 5 mV; changes in slow waves were not evident. The effect of flecainide was not abolished by inhibiting enteric neurotransmission or by blocking delayed rectifier and ATP-sensitive K(+) currents. Transcripts encoding Kv4 channels were detected in isolated antral myocytes by RT-PCR. Immunocytochemistry revealed intense Kv4.2- and Kv4.3-like immunoreactivity in antral myocytes. These data suggest that the A-type current in murine antral smooth muscle cells is likely to be due to Kv4 channels. This current contributes to the maintenance of negative resting membrane potentials.