Quality improvement of doctors' shift-change handover in neuro-critical care.

BACKGROUND: Clinical handover is a necessary process for the continuation of safe patient care; however, deficiencies in the handover process can introduce error. While the number of handover studies increases, few have validated implemented improvements with repeated audit. OBJECTIVE: To improve the morning handover round on a busy critical care unit and assess sustainability of improvement through repeated audit. DESIGN/METHODS: A quality improvement process based on prospective observational assessment of the doctor's shift-change handover was carried out, assessing the content of clinical information and effects of distractions, location and timing. The effect of a training session for the junior doctors with the introduction of a standardised handover protocol was assessed. RESULTS: The content of clinical information improved after the training session with introduction of a standardised protocol, but returned to baseline with a new cohort of untrained doctors. Distractions were associated with increased handover times for individual patients and for total handover time. Overall, handover time was shortest in the coffee room compared with ward and lecture theatre handovers. Individual patient handover time was positively correlated with clinical content scores. Four indices of critical illness all positively correlated with increased handover time. CONCLUSIONS: Early specific training is vital for quality clinical handover. Distractions during handover cause inefficiency and can adversely affect information transfer. Changing handover location according to local environment can yield improved efficiency, structure and ease of management. Adequate time must be allocated for clinical handover especially when dealing with very sick and complex patients.

The effect of additional teaching on medical students' drug administration skills in a simulated emergency scenario.

Medical students have difficulty calculating drug doses correctly, but better teaching improves their performance in written tests. We conducted a blinded, randomised, controlled trial to assess the benefit of online teaching on students' ability to administer drugs in a simulated critical incident scenario, during which they were scored on their ability to administer drugs in solution presented as a ratio (adrenaline) or percentage (lidocaine). Forty-eight final year medical students were invited to participate; 44 (92%) attended but only nine of the 20 students (45%) directed to the extra teaching viewed it. Nevertheless, the teaching module significantly improved the students' ability to calculate the correct volume of lidocaine (p = 0.005) and adrenaline (p = 0.0002), and benefited each student's overall performance (p = 0.0007). Drug administration error is a very major problem and few interventions are known to be effective. We show that focusing on better teaching at medical school may benefit patient safety.

Emergency tracheal catheterization for jet ventilation: a role for the ENT surgeon?

Stridor causing respiratory failure is an ENT and anaesthetic emergency requiring prompt management to secure a clear airway. We describe a case of subacute partial upper airway obstruction due to a large laryngeal carcinoma in an 81-year-old male resulting in respiratory failure. The patient became apnoeic after gaseous induction of general anaesthesia, and after two failed intubation attempts an emergency transtracheal airway catheter was placed by the surgeon under direct vision below the cricothyroid membrane, as this had tumour involvement. The patient was subsequently manually jet-ventilated with ease until a formal tracheostomy was made. Where difficulties with tracheal anatomy are encountered due to the presence of pathology, the insertion of a temporary airway catheter for jet ventilation by the surgeon can buy valuable time and be life-saving.

Role of tyrosine kinase activity of epidermal growth factor receptor in the lysophosphatidic acid-stimulated mitogen-activated protein kinase pathway.

Recent evidence indicates that the epidermal growth factor (EGF) receptor mediates a branch of lysophosphatidic acid (LPA)-induced signal transduction pathways that activate mitogen-activated protein (MAP) kinase. However, it is unclear whether the intrinsic tyrosine kinase activity of EGF receptor is involved. We previously showed that reactive oxygen species (ROS) were involved in the LPA-stimulated MAP kinase pathway. Here, we identify tyrosine phosphorylation of EGF receptor as an LPA signaling step that requires ROS. To evaluate the role of the tyrosine kinase activity of EGF receptor in the LPA-stimulated MAP kinase pathway, we examined the effects of an EGF receptor-specific tyrosine kinase inhibitor, PD158780. PD158780 potently inhibited the LPA-stimulated MAP kinase kinase 1/2 (MKK1/2) activation and EGF receptor tyrosine phosphorylation in HeLa cells, while it had no detectable effect on c-Src kinase activity. PD158780 also inhibited LPA-induced MKK1/2 activation and DNA synthesis in NIH 3T3 cells. Furthermore, we compared LPA-stimulated MKK1/2 and MAP kinase activation, transcriptional activity of the c-fos promoter, and DNA synthesis in B82L cells, which lack endogenous EGF receptor, and B82L cells expressing kinase-defective or wild-type human EGF receptor. Results obtained from analysis of these cell lines suggest that the EGF receptor tyrosine kinase contributes to the LPA-stimulated MAP kinase activation, c-fos transcription, and mitogenesis.