Partnered pharmacist charting on admission in the General Medical and Emergency Short-stay Unit - a cluster-randomised controlled trial in patients with complex medication regimens.

WHAT IS KNOWN AND OBJECTIVE: Patients admitted to general medical units and emergency short-stay units are often complex with multiple comorbidities, polypharmacy and at risk for drug-related problems associated with increased morbidity and mortality. The aim of this study was to evaluate the effectiveness of a partnered pharmacist charting model completed at the time of admission to prevent medication errors. METHODS: We conducted an unblinded cluster randomized controlled trial comparing partnered pharmacist charting to standard medical charting among patients admitted to general medical units and emergency short-stay units with complex medication regimens or polypharmacy. This trial was conducted at an adult major referral hospital in metropolitan Melbourne, Australia, with an annual emergency department attendance of approximately 60 000 patients. The evaluation included patients' medication charts written in the period of 16 March 2015 to 27 July 2015. Patients randomized to the intervention were managed using the partnered pharmacist charting model. The primary outcome variable was a medication error identified by an independent assessor within 24 h of admission, who was not part of the patient's admission process. RESULTS: Of the 473 patients who received standard medical staff charting during the study period, 372 (78·7%) had at least one medication error identified compared to 15 patients (3·7%) on the partnered pharmacist charting arm (P < 0·001). The relative risk of an error with standard medical charting was 21·4 (95% CI: 13·0-35·0) with a number needed to treat (NNT) to prevent one error of 1·3 (95% CI: 1·3-1·4), and the relative risk of a high or extreme risk error with standard medical charting was 150·9 (95% CI: 21·2-1072·9) with a NNT to prevent one high or extreme error of 2·7 (95% CI 2·4-3·1). WHAT IS NEW AND CONCLUSION: Partnering between medical staff and pharmacists to jointly chart initial medications on admission significantly reduced inpatient medication errors (including errors of high and extreme risk) among general medical and emergency short-stay patients with complex medication regimens or polypharmacy.

Learning physiology through service.

A service-learning component has been successfully incorporated into an introductory physiology course at Wheaton College. In addition to regular course work, each of the 24 students spent 12 hours shadowing and assisting staff at Sturdy Memorial Hospital, Attleboro, MA, with 4 hours in the emergency room and 8 hours in two other departments. Every student kept a log of his or her observations, reactions, and learning in the field and wrote a paper on a pathophysiological condition encountered in the hospital. To compare and contrast the real hospital experience with a fictional one, the students also studied patients from the television show ER. Each week in lab, two students showed a short videotape of one particular patient and discussed the diagnosis, symptoms, treatments, and surgical procedures involved. Questionnaire evaluations indicated that this program is effective in helping students learn more physiology and exposing them to community service. Health workers and patients also agreed that providing social support to patients while shadowing and assisting hospital staff was a valuable service.

Release of norepinephrine by sympathetic nerve stimulation from rabbit lungs.

Rabbit lungs were perfused via the pulmonary artery and norepinephrine (NE) measured in the outflows. The basal NE level was approximately 3 ng/min. Electrical stimulation (50 V, 1 ms, 10 Hz) of the sympathetic nerves doubled the NE release. Hexamethonium (10(-4) and 10(-5) M) had no effect on the release of NE. Administration of a monoamine oxidase (MAO) inhibitor, pargyline (70 mg/kg) resulted in a 20-fold NE increase by nerve stimulation, implying that the bulk of the amine does not reach the systemic circulation due to an active MAO. Methacholine (1 and 10 micrograms/ml) inhibited NE release by nerve stimulation. This inhibition was abolished by atropine (5 micrograms/ml). It is suggested that a muscarinic inhibitory mechanism may regulate the NE release in the lung. PGE2 (100 ng/ml), but not PGS2alpha, (100 ng/ml), depressed NE release during nerve stimulation, whereas indomethacin (10 mg/kg) enhanced NE release before, during, and after nerve stimulation in seemingly normal animals. This indicates the existence of another presynaptic inhibitory mechanism for NE release in the lung: a PGE-mediated inhibition.

An investigation of sodium transport in barnacle muscle fibres by means of the microsyringe technique.

1. The cation composition of single barnacle muscle fibres following damage by axial insertion of a microsyringe has been measured. The Na and Ca contents of these fibres were raised.2. Electronmicroscopic studies of fibres following insertion of a microsyringe indicated that the damage done resulted in tubular obstruction of the T-system.3. Fibres loaded with radiosodium by micro-injection showed that the Na(*) efflux declined exponentially with time, but that in most fibres the slope ratio of d/dt ln [Na(*)](1) to d/dt (ln d[Na(*)](i)/dt) was less than unity. Injections of distilled water deep in the fibre failed to influence the course of the Na(*) efflux.4. K removal reduced the Na efflux by 47%. However, a few fibres displayed very little K-dependence.5. When measured in fibres already soaked in a K-free medium for long periods the sodium efflux consisted of a brief rapid phase, followed by a slow phase of Na loss.6. In the presence of 30 mM-K, there was little or no rise in the Na efflux. Raising the external K to 50 or 100 mM caused a marked rise in the Na efflux. Raising the external K to 30 mM in the absence of external Ca(2+) led to a rise in the Na efflux. A high K solution always caused shortening of these fibres.7. Internal application of 1 M or 1 mM-CaCl(2) often caused a significant rise in the Na efflux.8. Internal application of 2.5 or 5 M saline caused a prompt and large fall in the Na efflux. In the presence of high K saline-loaded fibres failed to contract.9. Internal application of 0.5 M-ATP stimulated the Na efflux. A larger effect was not observed in fibres pre-treated with 2 M-MgCl(2). Internal application of 0.5 M-ArP was without effect.10. The results indicate that the barnacle fibre is a suitable preparation for the study of Na fluxes by means of the micro-injection technique. They also indicate that the mechanism regulating the Na efflux is not quite the same as that found in squid axon or frog muscle.