Implementation of early warning system in the clinical teaching unit to reduce unexpected deaths.

BACKGROUND: Early detection of patients with clinical deterioration admitted to the hospital is critical. The early warning system (EWS) is developed to identify early clinical deterioration. Using individual patient's vital sign records, this bedside score can identify early clinical deterioration, triggering a communication algorithm between nurses and physicians, thereby facilitating early patient intervention. Although various models have been developed and implemented in emergency rooms and paediatric units, data remain sparse on the utility of the EWS in patients admitted to general internal medicine wards and the processes and challenges encountered during the implementation. LOCAL PROBLEM: There is a lack of standardised tools to recognise early deterioration of patient condition. METHODS: This was a quality improvement project piloted in the clinical teaching unit of a tertiary care hospital. Data were collected 24 weeks pre-EWS and 55 weeks post-EWS implementation. A series of Plan, Do, Study, Act cycles were conducted to identify the root cause, develop a driver diagram to understand the drivers of unexpected deaths, run a sham test trial run of the EWS, educate and obtained feedback of clinical care teams involved, assess adherence to the EWS during the pilot project (6 weeks pre-EWS and 6 weeks post-EWS implementation), evaluate outcomes by extending the duration to 24 weeks pre-EWS and 55 weeks post-EWS implementation, and retrospectively review the uptake of the EWS. INTERVENTIONS: Implementation of a standardised protocol to detect deterioration in patient condition. RESULTS: During the pre-EWS implementation phase (24 weeks), there were 4.4 events per week (1.2 septic workups, 1.9 observation unit transfers, 0.7 critical care transfers, 0.13 cardiac arrests and 0.46 per week unexpected deaths). In the post-EWS implementation phase (55 weeks), there were 4.2 events per week (1.0 septic workup, 1.9 observation unit transfers, 0.82 critical care transfers, 0.25 cardiac arrests and 0.25 unexpected deaths). CONCLUSION: The EWS can improve patient care; however, more engagement of stakeholders and electronic vital sign documentation may improve the uptake of the system.

Clinical Outcomes of Start-Low, Go-Slow Methadone Initiation for Cancer-Related Pain: What's the Hurry?

BACKGROUND: Methadone has been shown to be effective for cancer pain. Most published switching methods are complete in less than three days, requiring very close supervision, usually in an inpatient setting. This need for hospitalization is a barrier to access. We present a large retrospective study of slow outpatient methadone starts and describe our starting method. METHODS: Charts were reviewed of patients referred to the Pain and Symptom Management/Palliative Care clinics at the six BC Cancer Agency's regional centers that underwent initiation of methadone for analgesia over a 14-year period. Patient characteristics, method of start, and outcomes of methadone treatment were recorded. RESULTS: Of the 652 identified patients, we were able to determine outcomes of methadone initiation in 564 (86.5%). Among these, 422 (74.8%) were deemed successful initiations, as determined by whether or not the patient remained on methadone at follow-up with subjective improvement in pain control, on a stable dose of methadone. Of the unsuccessful trials, 97/142 were primarily due to adverse events, 16 of which were considered serious enough to require hospitalization, including two due to sudden cessation of opioid therapy leading to withdrawal. Some of the included adverse events were not necessarily causal from the initiation of methadone, for example, development of bowel obstruction or delirium. Only one death occurred from a deliberate overdose of multiple medications, including methadone. CONCLUSIONS: Initiation of methadone for analgesia in ambulatory cancer patients can be done safely in an outpatient setting using a start-low go-slow method, and can be expected to be helpful in ∼75% of patients. Discontinuation is more likely to be for side effects than for inadequate analgesia. Access to methadone therapy can safely be widened by slow initiation, avoiding more dangerous rapid switching protocols and reducing the need for hospitalization.

Inhibition of P-glycoprotein in the blood-brain barrier alters avermectin neurotoxicity and swimming performance in rainbow trout.

The importance of the blood brain barrier (BBB) and the contribution to its function by the efflux transporter P-glycoprotein (P-gp) in teleosts were examined using the P-gp substrates and central nervous system neurotoxins ivermectin (22,23-dihydroavermectin B1a+22,23-dihydroavermectin B1b) [IVM]) and emamectin benzoate (4″-deoxy-49″epimethylaminoavermectin B1 benzoate [EB]). Trout were injected intraperitoneally with 0.01-1.0 and 1-50mg/kg of IVM or EB, respectively either alone or in combination with cyclosporin A (CsA: a P-gp substrate) at 1mg/kg. IVM affected the swimming performance (critical swimming speed, burst swimming distance, and schooling) at significantly lower concentrations than EB. When fish were exposed to IVM or EB in the presence of CsA, alterations to swimming were increased, suggesting that competition for P-gp in the BBB by CsA increased IVM and EB penetration into the CNS and decreased swimming capabilities. The effect of co-administration of CsA on swimming-related toxicity was different between IVM and EB-treated fish; EB toxicity was increased to a greater extent than IVM toxicity. The greater chemosensitization effect of EB vs. IVM was examined using a P-gp competitive inhibition assay in isolated trout hepatocytes with rhodamine 123 as a substrate. At the cellular level, IVM was a more potent inhibitor of P-gp than EB, which allowed for a greater accumulation of R123 in hepatocytes. These results provide evidence for a role of P-gp in the BBB of fish, and suggest that this protein protects fish from environmental neurotoxins.