Junior doctors' perceptions of their self-efficacy in prescribing,their prescribing errors and the possible causes of errors

Aims

The aim of the study was to explore and compare junior doctors'' perceptions of their self-efficacy in prescribing, their prescribing errors and the possible causes of those errors.

Methods

A cross-sectional questionnaire study was distributed to foundation doctors throughout Scotland, based on Bandura''s Social Cognitive Theory and Human Error Theory (HET).

Results

Five hundred and forty-eight questionnaires were completed (35.0% of the national cohort). F1s estimated a higher daytime error rate [median 6.7 (IQR 2–12.4)] than F2s [4.0 IQR (0–10) (P = 0.002)], calculated based on the total number of medicines prescribed. The majority of self-reported errors (250, 49.2%) resulted from unintentional actions. Interruptions and pressure from other staff were commonly cited causes of errors. F1s were more likely to report insufficient prescribing skills as a potential cause of error than F2s (P = 0.002). The prescribers did not believe that the outcomes of their errors were serious. F2s reported higher self-efficacy scores than F1s in most aspects of prescribing (P < 0.001).

Conclusion

Foundation doctors were aware of their prescribing errors, yet were confident in their prescribing skills and apparently complacent about the potential consequences of prescribing errors. Error causation is multi-factorial often due to environmental factors, but with lack of knowledge also contributing. Therefore interventions are needed at all levels, including environmental changes, improving knowledge, providing feedback and changing attitudes towards the role of prescribing as a major influence on patient outcome.     

A Computer-based Module for Prescribing Error Instruction

Objective

To evaluate an instructional module''s effectiveness at changing third-year doctor of pharmacy (PharmD) students'' ability to identify and correct prescribing errors.

Design

Students were randomized into 2 groups. Using a computer-based module, group 1 completed worksheet A, watched a presentation on medication errors, and then completed worksheets B and C. Group 2 completed worksheets A and B, watched the presentation, and then completed worksheet C.

Assessment

Both groups scored a median 50% on worksheet A and 66.7% on worksheet C (p < 0.001). Median scores on worksheet B differed between groups (p = 0.0014). Group 1 viewed the presentation before completing worksheet B and scored 62.5%, while group 2 viewed the presentation after scoring 50% on worksheet B.

Conclusion

The module effectively taught pharmacy students to identify and correct prescribing errors.     

Development of learning outcomes for an undergraduate prescribing curriculum (British Pharmacological Society prescribing initiative)

AIMS

The question of whether new medical graduates are adequately prepared for the challenge of prescribing has been raised. Although broad outcomes for prescribing competency have been agreed, clarity is needed on the detailed outcomes expected of new graduates. This study aimed to create a consensus on the required competencies for new graduates in the area of prescribing.

METHODS

We used a modified Delphi approach based on the findings of a systematic review of educational interventions for improved prescribing. Panellists were asked to rank the importance of a list of 53 possible learning outcomes and to add any additional outcomes felt to be missing.

RESULTS

Of the 48 experts who were invited to participate, 28 agreed (58%). Forty-five learning outcomes were included from the original list of 53. A further nine outcomes were suggested by panellists, of which five were included. The wording of three outcomes was changed in line with suggestions from the panellists. Many of the agreed outcomes relate to improving patient safety through medication review, checking appropriateness of the drug for the patient, recognizing the prescriber''s limitations and seeking advice when needed. Enhanced communication with the patient and healthcare team, better documentation in the notes and discharge letters were key areas featured in this Delphi exercise.

DISCUSSION

This study has identified 50 learning outcomes for teaching prescribing. These build on the existing British Pharmacological Society document by focusing specifically on prescribing, with greater emphasis on avoiding medication errors and better communication.     

Implementation of a Standardized Discharge Time-out Process to Reduce Prescribing Errors at Discharge

Background:

To reduce prescribing errors occurring on discharge from the hospital, a standardized discharge time-out process was implemented on a general medicine service at Wake Forest Baptist Medical Center. In the time-out process, the multidisciplinary care team reviewed the patient’s medical records together to determine the optimal discharge medication regimen. This regimen was recorded on a time-out form and then was used to develop the patient’s discharge documents.

Objective:

To evaluate the impact of a standardized discharge time-out process on prescribing errors that occur as patients are discharged from a general medicine service.

Methods:

The medical records of all patients discharged from a general medicine service during 60-day periods before (“pre-group”) and after (“post-group”) implementation of a standardized discharge time-out process were retrospectively reviewed by an internal medicine physician to determine the presence of discharge prescribing errors.

Results:

There were 142 and 124 evaluable patients in the pre- and post-groups, respectively. Compliance with the time-out process was 93% in the post-group. At least 1 prescribing error was detected in 49 (34.5%) of the discharges in the pre-group and 17 (13%) of the discharges in the post-group (P < .0001). All of the errors noted in the post-group occurred in discharges in which a clinical pharmacist was not involved.

Conclusions:

A multidisciplinary, standardized discharge time-out process was associated with a dramatic reduction in prescribing errors when patients were discharged from a general medicine service. The time-out process is one strategy to improve patient safety at hospital discharge.     

Insulin induced translocation of Na^＋/K^＋-ATPase is decreased in the heart of streptozotocin diabetic rats

Aim:

To investigate the effect of acute insulin administration on the subcellular localization of Na⁺/K⁺-ATPase isoforms in cardiac muscle of healthy and streptozotocin-induced diabetic rats.

Methods:

Membrane fractions were isolated with subcellular fractionation and with cell surface biotinylation technique. Na⁺/K⁺-ATPase subunit isoforms were analysed with ouabain binding assay and Western blotting. Enzyme activity was measured using 3-O-methylfluorescein-phosphatase activity.

Results:

In control rat heart muscle α1 isoform of Na⁺/K⁺ ATPase resides mainly in the plasma membrane fraction, while α2 isoform in the intracellular membrane pool. Diabetes decreased the abundance of α1 isoform (25 %, P<0.05) in plasma membrane and α2 isoform (50%, P<0.01) in the intracellular membrane fraction. When plasma membrane fractions were isolated by discontinuous sucrose gradients, insulin-stimulated translocation of α2- but not α1-subunits was detected. α1-Subunit translocation was only detectable by cell surface biotinylation technique. After insulin administration protein level of α2 increased by 3.3-fold, α1 by 1.37-fold and β1 by 1.51-fold (P<0.02) in the plasma membrane of control, and less than 1.92-fold (P<0.02), 1.19-fold (not significant) and 1.34-fold (P<0.02) in diabetes. The insulin-induced translocation was wortmannin sensitive.

Conclusion:

This study demonstrate that insulin influences the plasma membrane localization of Na⁺/K⁺-ATPase isoforms in the heart. α2 isoform translocation is the most vulnerable to the reduced insulin response in diabetes. α1 isoform also translocates in response to insulin treatment in healthy rat. Insulin mediates Na⁺/K⁺-ATPase α1- and α2-subunit translocation to the cardiac muscle plasma membrane via a PI3-kinase-dependent mechanism.     

eDrugCalc: an online self-assessment package to enhance medical students' drug dose calculation skills

AIMS

Dose calculation errors can cause serious life-threatening clinical incidents. We designed eDrugCalc as an online self-assessment tool to develop and evaluate calculation skills among medical students.

METHODS

We undertook a prospective uncontrolled study involving 1727 medical students in years 1–5 at the University of Edinburgh. Students had continuous access to eDrugCalc and were encouraged to practise. Voluntary self-assessment was undertaken by answering the 20 questions on six occasions over 30 months. Questions remained fixed but numerical variables changed so each visit required a fresh calculation. Feedback was provided following each answer.

RESULTS

Final-year students had a significantly higher mean score in test 6 compared with test 1 [16.6, 95% confidence interval (CI) 16.2, 17.0 vs. 12.6, 95% CI 11.9, 13.4; n = 173, P < 0.0001 Wilcoxon matched pairs test] and made a median of three vs. seven errors. Performance was highly variable in all tests with 2.7% of final-year students scoring < 10/20 in test 6. Graduating students in 2009 (30 months'' exposure) achieved significantly better scores than those in 2007 (only 6 months): mean 16.5, 95% CI 16.0, 17.0, n = 184 vs. 15.1, 95% CI 14.5, 15.6, n = 187; P < 0.0001, Mann–Whitney test. Calculations based on percentage concentrations and infusion rates were poorly performed. Feedback showed that eDrugCalc increased confidence in calculating doses and was highly rated as a learning tool.

CONCLUSIONS

Medical student performance of dose calculations improved significantly after repeated exposure to an online formative dose-calculation package and encouragement to develop their numeracy. Further research is required to establish whether eDrugCalc reduces calculation errors made in clinical practice.     

High dose methotrexate chemotherapy: pharmacokinetics, folate and toxicity in osteosarcoma patients

AIMS

To investigate the relationships between pretreatment folate concentrations, MTX pharmacokinetics and acute toxicities following high dose methotrexate (HD MTX) therapy.

METHODS

MTX and its major extracellular metabolite 7-OH-MTX were measured in eight serum samples per HD MTX cycle in 65 consecutive osteosarcoma patients (288 cycles) and AUC (area under the blood concentration–time curve) was calculated. Pretreatment concentrations of folate in serum (S) and erythrocytes (ER) were determined. Hepatic, renal and haematological toxicities, assessed by routine laboratory parameters, as well as mucositis were graded according to National Cancer Institute Common Terminology Criteria for adverse events (CTCAE v.3.0). Dermatitis and pleuritis were reported as occurred or not.

RESULTS

S- and ER-folate pretreatment concentrations increased significantly with increasing number of HD MTX cycles (P < 0.001). ER-folate pretreatment concentrations were higher among males (median 610 nmol l⁻¹, 95% CI 550, 680) compared with females (median 465 nmol l⁻¹, 95% CI 430, 520, P < 0.001), but showed no correlation with MTX or 7-OH-MTX pharmacokinetics. We found correlations between alanine aminotransferase peak concentration (ALAT_max) and clearance of MTX (P < 0.001), gender (P < 0.001), age (P < 0.001) and 7-OH-MTX concentrations (P < 0.001), the latter being the main factor influencing ALAT_max.

CONCLUSION

Our results suggest that 7-OH-MTX is involved in the development of HD MTX hepatic toxicity and that young female patients are most affected.     

Effectiveness of a national approach to prescribing education for multiple disciplines

Aims

To evaluate the effectiveness of a national approach to prescribing education on health professional students’ prescribing and therapeutics knowledge, across multiple disciplines.

Methods

In a university examination setting, 83 medical, 40 pharmacy and 13 nurse practitioner students from three different universities completed a set of multiple choice questions (MCQs) before and after completing an online module from the National Prescribing Curriculum (NPC). To minimize overestimation of knowledge, students had to indicate the level of certainty for each answer on a three‐point scale. MCQs were scored using a validated certainty‐based marking scheme resulting in a composite score (maximum 30 and minimum −60). Students were asked to rate their perception of usefulness of the module.

Results

At the pre‐module phase, there were no significant differences in the composite MCQ scores between the medical (9.0 ± 10.3), pharmacy (10.2 ± 10.6) and nurse practitioner (8.0 ± 10.7) students. The scores improved significantly for all groups at the post‐module phase (P < 0.01 for all groups) by similar extents (post‐module results: medical, 14.5 ± 9.6; pharmacy, 14.4 ± 9.9; nurse practitioner, 12.1 ± 9.6). 39.4% of the MCQs answered incorrectly with high level of certainty at the pre‐module phase were still answered incorrectly with high level of certainty at the post‐module phase. Almost all students (with no significant difference between the groups) found the NPC modules, post‐module MCQs and feedback useful as a learning tool.

Conclusions

A national online approach to prescribing education can improve therapeutics knowledge of students from multiple disciplines of health care and contribute towards streamlining interdisciplinary learning in medication management.     

Different magnitude of resistance to nondepolarizing muscle relaxants in the denervated mouse skeletal muscle

Aim:

To test the hypothesis that different magnitude of resistance of denervated skeletal muscle to nondepolarizing muscle relaxants (NDMRs) is related to their varying potencies at ɛ-AChR and γ-AChR.

Methods:

Both innervated and denervated mouse muscle cells, and human embryonic kidney 293 (HEK293) cells expressing ɛ-AChR or γ-AChR were used. The effects of NDMRs on nAChR were explored using whole-cell patch clamp technique.

Results:

NDMRs vecuronium (VEC), atracurium (ATR) and rocuronium (ROC) produced reversible, dose-dependent inhibition on the currents induced by 30 μmol/L acetylcholine both in innervated and denervated skeletal muscle cells. Compared to those obtained in innervated skeletal muscle cells, denervation shifted the concentration-response curves rightward and significantly increased the 50% inhibitory concentration (IC₅₀) values (VEC: from 11.2 to 39.2 nmol/L, P<0.01; ATR: from 24.4 to 129.0 nmol/L, P<0.01; ROC: from 37.9 to 101.4 nmol/L, P<0.01). In HEK293 cell expression system, ATR was less potent at γ-AChR than ɛ-AChR (IC₅₀ values: 35.9 vs 22.3 nmol/L, P<0.01), VEC was equipotent at both receptor subtypes (IC₅₀ values: 9.9 vs 10.2 nmol/L, P>0.05), while ROC was more potent at γ-AChR than ɛ-AChR (IC₅₀ values: 22.3 vs 33.5 nmol/L, P<0.05).

Conclusion:

Magnitude differences of resistance to different NDMRs caused by denervation are associated with distinct potencies of NDMRs at nAChR subtypes.     

Comparison of nebivolol and atenolol on blood pressure, blood sugar, and lipid profile in patients of essential hypertension

Background:

Nebivolol is a third-generation β-blocker, with highest β₁ selectivity and nitric-oxide-derived vasodilatation. It also exhibits antiproliferative and antioxidant property that has beneficial metabolic profile compared to second-generation β blockers like atenolol. This study was planned to study the comparative effects of nebivolol and atenolol on metabolic parameters in patients with essential hypertension.

Materials and Methods:

A prospective, randomized, parallel, open-label clinical study was carried out on patients with essential hypertension. The patients were randomly assigned to receive tablet atenolol (Group A) and nebivolol (Group B) for a period of 24 weeks. Investigations were carried out at baseline and at the end of study period, that is, 24 weeks. Out of 69 patients, 60 completed the study and the data was analyzed using student''s t-test. P < 0.05 was considered statistically significant.

Results:

Atenolol and nebivolol both showed significant (P < 0.001) antihypertensive action after 24 weeks. Mean blood sugar and lipid profile were found to be significantly (P < 0.001) elevated after 24 weeks of treatment with atenolol but not with nebivolol. Heart rate was significantly (P < 0.001) decreased in both groups at 24 weeks.

Conclusion:

In view of metabolic adverse effects of atenolol, nebivolol is the better choice whenever β-blockers have to be used in essential hypertension.     

Sodium/hydrogen exchange inhibition with cariporide reduces leukocyte adhesion via P-selectin suppression during inflammation

Background and purpose:

The Na⁺/H⁺ exchange (NHE) inhibitor cariporide is known to ameliorate ischaemia/reperfusion (I/R) injury by reduction of cytosolic Ca²⁺ overload. Leukocyte activation and infiltration also mediates I/R injury but whether cariporide reduces I/R injury by affecting leukocyte activation is unknown. We studied the effect of cariporide on thrombin and I/R induced leukocyte activation and infiltration models and examined P-selectin expression as a potential mechanism for any identified effects.

Experimental approach:

An in vivo rat mesenteric microcirculation microscopy model was used with stimulation by thrombin (0.5 μ ml⁻¹) superfusion or ischaemia (by haemorrhagic shock for 60 min) and reperfusion (90 min).

Key results:

Treatment with cariporide (10 mg kg⁻¹ i.v.) significantly reduced leukocyte rolling, adhesion and extravasation after thrombin exposure. Similarly, cariporide reduced leukocyte rolling (54±6.2 to 2.4±1.0 cells min⁻¹, P<0.01), adherence (6.3±1.9 to 1.2±0.4 cells 100 μm⁻¹, P<0.01) and extravasation (9.1±2.1 to 2.4±1.1 cells per 20 × 100 μm perivascular space, P<0.05), following haemorrhagic shock induced systemic ischaemia and reperfusion. The cell adhesion molecule P-selectin showed a profound decrease in endothelial expression following cariporide administration in both thrombin and I/R stimulated groups (35.4±3.2 vs 14.2±4.1% P-selectin positive cells per tissue section, P<0.01).

Conclusions and implications:

The NHE inhibitor cariporide is known to limit reperfusion injury by controlling Ca²⁺ overload but these data are novel evidence for a vasculoprotective effect of NHE inhibition at all levels of leukocyte activation, an effect which is likely to be mediated at least in part by a reduction of P-selectin expression.