Aphs circuit newsletter february 2014

February 2014

circuit

clinical initiatives, research and current updates in treatment New and Emerging Therapies for Metastatic Melanoma Jodie Lyons, APHS Pharmacy Holy Spirit Northside Melanoma is the third most common cancer in Australia, with over 12,000 new cases diagnosed and 1,500 deaths per year.1 Australia has the world’s highest incidence of melanoma, with the majority of cases diagnosed early and treated with surgical excision. Historically, metastatic melanoma has been considered one of the most difficult cancers to treat, and a true ‘cure’ remains elusive. However, a range of new drug therapies are altering treatment goals and promising patients long term survival.1 A better understanding of both the activation of the immune system and the role of activation of pathogenic pathways has led to the identification of several targets for drug therapy, such as BRAF, MEK, and Ras proteins.

Ras

P Proliferation Differentiation Migration Survival/Apoptosis

Raf

P P

MEK1/2

ERK1/2 Figure 1 Targeting melanoma - The Ras-Raf → MEK-ERK pathway.28 CTLA-4 Inhibitors Ipilimumab (Yervoy®) is a monoclonal antibody targeted at cytotoxic T-lymphocyte antigen 4 (CTLA-4), a negative regulator of T cell activation which serves as a ‘brake’ on the activated immune system. Ipilimumab prevents this, allowing a T-cell mediated immune response against the tumour.2

Given its mechanism of action, evaluation of the effectiveness of ipilimumab requires a unique perspective, as the patterns of response differ from those with molecularly targeted agents or cytotoxic chemotherapy. Rather than the traditional pattern of improvement after treatment, patients may have a transient worsening of the disease (up to and including the appearance of new lesions) before the disease stabilises or regresses. Response may also take considerably longer to become apparent, with continued disease regression frequently observed well after completion of initial induction therapy (as late as 5.5 months after initial ipilimumab infusion).2,3 The danger with this is that if those assessing the patients are unfamiliar with immune-related response criteria, the patient may be prematurely discontinued on treatment which may have otherwise eventually led to a response or prolonged disease stabilisation.3 Current guidelines suggest not conducting initial post therapy tumour assessment until week 12, after induction therapy is complete.2 Ipilimumab’s PBS listing is based on a 676 patient phase III trial in those with previously treated metastatic stage III or IV melanoma. Patients were randomised to receive ipilimumab (at 3mg/kg) with gp100 (an investigational vaccine), ipilimumab monotherapy, or gp100 vaccine monotherapy. The rate of overall survival for ipilimumab at 1 year was 45.6%, independent of age, sex, metastasis, stage of disease and baseline serum LDH levels.4,5 In addition, 60% of patients who had achieved a partial or complete response remained free of relapse at 2 years, with ongoing responses observed at up to 44 months.5 Of the patients who did progress or relapse, a further course of re-induction therapy led to a partial or complete response in 67%.5 The ongoing PBS listing for ipilimumab is dependent upon the drug being able to replicate the clinical trial results in a real world setting.

As a result of its mode of action, immune related adverse events (irAE) have been observed in 60% of patients treated with ipilimumab, with 10-15% of these classified as grade 3 or 4.5 The likelihood of these types of effects is greatest during the 10 week induction period, however they can occur weeks or months afterward. Liver function tests (LFTs) and thyroid function tests should be undertaken at baseline and before each dose of ipilimumab, as well as at completion of symptom checklists. The most frequently encountered irAE are: • Gastrointestinal – diarrhoea and colitis in 31% of patients (identified as having led to cases of bowel perforation, sepsis and death).5,6 • Hepatic – hepatitis in 2% - 9% of patients (at least one death recorded due to liver failure).5,7 • Dermatological – pruritis, vitiligo or alopecia seen in 40% of patients (StevenJohnson syndrome and toxic epidermal necrolysis also recorded in 2.5% of patients).5,8 • Endocrinopathies – wide ranging, potentially affecting the pituitary, thyroid or adrenal glands.

• Neurological – rarely Guillain Barre syndrome.5,10 Ipilimumab irAE management guidelines identify and provide management recommendations based on the severity of presenting symptoms, classifying patients by whether or not they are safe to proceed with scheduled treatment.2

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cont >

February 2014

The optimal dose of ipilimumab has not been definitively established, particularly in first line therapy. Ongoing phase III clinical trials will evaluate the efficacy of 10mg/kg doses and continuing maintenance therapy. Phase II trials have indicated overall survival may be increased with greater doses, however doselimiting adverse effects and economic considerations may define the influence of such results.11 BRAF Inhibitors Dabrafenib (Tafinlar®) is a potent inhibitor of BRAF, a mutation that is present in approximately 40 to 60% of advanced melanomas, and was listed on the PBS from 1 December 2013.12 A phase III trial demonstrated significantly increased progression-free survival versus dacarbazine (5.1 to 2.7 months). A statistically significant improvement in overall survival was not demonstrated due to 36 out of the 63 patients originally treated with dacarbazine receiving dabrafenib after progression.15 The most common adverse effect with dabrafenib in the phase III study were febrile reactions, experienced by 28% of patients, and required discontinuation or dose reduction in approximately 4% as a result.22 However, any overview of the adverse effects of BRAF inhibitors is dominated by their ability to cause cutaneous toxicity and secondary tumours.17 Squamous cell carcinomas develop in 19 to 26% of cases and are generally treated with excision.18 Of greater concern, 8 out of 337 patients in one phase III trial developed a second primary melanoma.15,19 This proliferation of malignancies has been traced to paradoxical activation of the mitogen activated protein kinase (MAPK) pathway that bypasses the inhibition of BRAF. It is also traced to the presence of pre-existing Ras mutations, which enhance the activation of downstream proteins in the MAPK pathway when subject to BRAF inhibition.20 Ras proteins are molecular ‘switches’ inside a cell which, when activated, turn on a signaling pathway that leads to cell growth and proliferation.

Mutations in these proteins which lead to a permanently ‘on’ state, are therefore associated with tumour development and progression.

MEK Inhibitors MEK is a protein that exists downstream from Ras in the MAPK pathway and is the target of a number of inhibitors currently in development.23 Trametinib is the only MEK inhibitor currently FDA approved in the USA. It is indicated for BRAF positive unresectable or metastatic melanoma in patients who have not previously received a BRAF inhibitor.23 This approval was based on an open-label randomised trial, comparing once daily oral trametinib to traditional chemotherapy (paclitaxel or dacarbazine intravenously every 3 weeks), which demonstrated improved progression free survival (4.8 months compared to 1.5 months).24 Combining a BRAF inhibitor (dabrafenib) with a MEK inhibitor (trametinib) has been hypothesised as a way to increase the efficacy and improve the adverse effect profile of BRAF inhibitors, and a phase Ib trial showed a statistically significant increase in progression-free survival (9.4 months for dabrafenib and trametinib compared with 5.8 for dabrafenib alone).

The study also showed a clinically meaningful reduction in the incidence of secondary tumors.25 This combination of two complementary inhibitors shows a great deal of promise and is the focus of much research.

PD-1 Inhibitors There is mounting speculation that the future of advanced melanoma treatment may lie with PD-1 (programmed cell death protein 1) immune checkpoint inhibitors, which have demonstrated impressive anti-tumour activity in early stage studies.27 Determining the appropriate sequencing for the plethora of new medications that may soon exist is certain to cause debate, with BRAF-targeted therapy currently considered first line, followed by treatment with ipilimumab.

Ultimately economic considerations for these increasingly expensive new options may provide the greatest barrier to their use, particularly as world economies seek to control health expenditure.

References available on request.

New Oral Anticoagulants for Stroke Prevention in Atrial Fibrillation Sarah Coleman, APHS Holy Spirit Northside Hospital Pharmacy Atrial fibrillation (AF) is a chronic condition, which results in increased inflammation and damage to the atrial endothelium, and this, combined with poor atrial emptying, promotes thrombus formation.1,2 The resulting thrombus may be embolised, causing ischaemic stroke.1,2 The overall risk of stroke is increased five-fold in AF, and is associated with particularly severe ischaemic strokes.1 Damage to the atrial endothelium may lead to activation of the coagulation cascade and subsequent thrombogenesis. AF prevalence increases from less than 1% in patients younger than 60 years, to almost 10% in patients over the age of 80 years.2 One of the primary aims in treating a patient with AF is to reduce the risk of stroke by administration of long-term oral anticoagulants to prevent thromboembolism.1 The newer oral anticoagulants (NOACs), rivaroxaban (Xarelto®), dabigatran (Pradaxa®) and apixaban (Eliquis®), have shown comparable or superior efficacy and safety to warfarin in randomised trials. They also have the added benefits of fewer food, and/or pharmaceutical interactions, shorter plasma half-life, and an improved safety and efficacy profile.3 NOACs have a predictable effect and do not require International Normalised Ratio (INR) testing.4 Recently, the NOACs were subsidised by the Pharmaceutical Benefits Scheme for the prevention of stroke or systemic embolism in people with non-valvular AF. Assessment of stroke risk The CHADS2 risk score is the most commonly used model to evaluate risk factors for embolisation in non-valvular AF. The CHA2DS2-VASc model is a more detailed model which emphasises the importance of age over 74 years.4 It includes vascular disease, age 65 to 74 years, and female sex as risk factors, all of which are absent from the simpler CHADS2 model.4 This model is used for patients with a CHADS2 score of 0 or 1.4 Patients with a CHADS2 score of 2 or higher are at relatively high risk of stroke (at least 4% per year).3,4 Therefore, oral anticoagulant therapy is strongly recommended for the majority of patients with a CHADS2 score of 2 or higher. There is less evidence in regards to the benefit to risk ratio from oral anticoagulation in patients at a low risk of thromboembolic events, for example those with a CHADS2 score of 0 or a CHA2DS2-VASc score of 1.3 Dabigatran Dabigatran is a competitive and reversible direct thrombin (Factor IIa) inhibitor (Fig. 1).5 In major clinical trials, dabigatran only showed more favourable results compared to warfarin for reducing the incidence of stroke or systemic embolism in patients whose INR was not well controlled on warfarin.5 Dabigatran has twice daily dosing, which may potentially reduce patient compliance. The halflife of dabigatran is prolonged in patients with renal impairment (a creatinine clearance (ClCr) of 30 to 50 mL/minute), consequently dose reductions are necessary.5 In addition, the dose of dabigatran may need to be reduced in individuals over 75 years and those with a higher risk of bleeding.5 Rifampin, carbamazepine, phenytoin and St John’s Wort may decrease the effects of dabigatran due to induction of P-glycoprotein, which reduces systemic absorption of dabigatran from the gastrointestinal tract.4 In patients with normal renal function, dose adjustments are not required with ketoconazole, amiodarone, verapamil, clarithromycin, and quinidine (P-glycoprotein inhibitors), however, it is recommended that dabigatran be given ≥ 2 hours before these drugs.4 In patients with reduced renal function, inhibitors of P-glycoprotein may increase dabigatran concentrations, making dose reductions necessary.4 Adverse gastrointestinal effects include dyspepsia, gastritis and bleeds within the first couple of months.5 Rivaroxaban Rivaroxaban is a direct factor Xa inhibitor (Fig. 1) which potently inhibits the activity of prothrombinase, a complex of factors Xa and V that convert Prothrombin to active Thrombin.1,3 Studies have shown that rivaroxaban is well tolerated in healthy human subjects, with a rapid onset of action.6

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Dose adjustments are required for rivaroxaban in patients with reduced renal function (ClCr 30 to 49mL/min).1 A low propensity for clinically relevant drugdrug and food-drug interactions has been observed with rivaroxaban,6 and it has no effect on the QTc interval.1 Apixaban Apixaban is a direct factor Xa inhibitor that is a highly selective and potent inhibitor of free factor Xa and prothrombinase activity (Fig. 1).1 Clinical studies have shown a high oral bioavailability, low metabolic clearance and multiple pathways of elimination, including renal (25%) and intestinal excretion (75%).7 Food does not affect absorption and the drug is not altered by pH changes.7 In the ARISTOTLE trial, apixaban showed superior results to warfarin for reducing the incidence of stroke in AF in patients with intermediate risk of clinical thromboembolism stroke,8 but this advantage was not demonstrated in patients from centres with the best INR control.9 Inhibitors of CYP3A4, such as azole antifungals, macrolide antibiotics and protease inhibitors, may increase apixaban levels and these combinations should be used with caution.7 Bleeding Risk There is a well-documented association between warfarin therapy and increased bleeding risk, with high rates of bleeding in older patients.2,10 Intracranial haemorrhage is the most serious bleeding complication with warfarin (and other oral anticoagulants), as the likelihood of mortality or subsequent major disability is significantly greater than bleeding at other sites.4 Major risk factors for bleeding with warfarin therapy include uncontrolled anticoagulation, recent haemorrhage, binge drinking, liver and kidney disease, uncontrolled hypertension, the concomitant use of aspirin and non-steroidal anti-inflammatory agents and concomitant bleeding tendency.2,10 NOACs showed small absolute risk reductions in incidence of intracranial haemorrhage and fatal bleeding when compared with warfarin.5,9 However, dabigatran and rivaroxaban showed an increased risk of major gastrointestinal

INITIATION

bleeds.5,9 Of these NOACs, apixaban was the only medication that reduced the incidence of major bleeding compared with warfarin, when warfarin was well-controlled.8 Management of patients undergoing surgery Temporary discontinuation of any of the newer oral anticoagulants, for bleeding, planned surgery or invasive procedures, results in an increased risk of thromboembolism after the period of effective anticoagulation has ended.11 Cessation of dabigatran prior to invasive or surgical procedures is dependent on the patient’s creatinine clearance. For those with a creatinine clearance of ≼50mL/minute, dabigatran should be discontinued one to two days before the procedure.11 For those with a lower creatinine clearance, this agent should be discontinued three to five days prior to the procedure.11 Longer periods than the above should be considered for those undergoing major surgery, spinal puncture and placement of a spinal or epidural catheter or port.11 Rivaroxaban and apixaban are less dependent on renal clearance, therefore, these drugs should typically be stopped one to two days prior to the procedure.11 The NOACs should be resumed postoperatively when haemostasis has been achieved. Since these agents have a rapid onset of action, with peak effects occurring two to three hours after intake, caution should be used when resuming these drugs, especially in patients who have had major surgery or other procedures associated with a high bleeding risk.11 In general, the rapid offset and onset of the NOACs eliminates the need for bridging anticoagulation with heparin or low molecular weight heparin (LMWH) .12 Reversal of anticoagulant effect There is a significant concern about the use of oral direct thrombin and factor Xa inhibitors (unlike warfarin), as there is no known antidote to immediately reverse their anticoagulant effect and strategies for anticoagulation reversal are limited. One promising study in 12 healthy subjects showed an immediate and complete reversal of the anticoagulant effect after the infusion of a warfarin antidote, prothrombin complex concentrate (PCC), a combination of clotting factors II, VII, IX and X, as well as protein C and S.13 However, this effect was only

DAMAGED SURFACE

TRAUMA W W Vll

Kininogen Kallikrein XIIa

XII

PROPAGATION (Platelet Activation)

Vlla Tissue Factor (III) Xla

XI

Tissue Factor (III)

Tenase Complex W IXa

IX W

Vlla

X W Prothrombin (II)

FIBRIN FORMATION

RA Xa Va

Direct Xa inhibitors: Rivaroxaban Apixaban

TRAUMA

W X

Vitamin K antagonist: Warfarin

Prothrombinase Complex

D Thrombin (IIa)

Fibrin (Ia)

Direct thrombin inhibitor: dabigatran

Fibrinogen (I)

Clot Formation

Figure 1. Inhibitory action of the new oral anticoagulants within the coagulation cascade (Adapted from 14).

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demonstrated in rivaroxaban and was not seen with dabigatran.13 While data is currently lacking, it may be expected that apixaban would respond to reversal agents in a similar way to rivaroxaban.15 Haemodialysis has been suggested as a method of removing dabigatran and may be useful in emergency situations for patients with excessive anticoagulation.4,5

glucuronidation, with little involvement of CYP450, thus reducing the likelihood of pharmacokinetic drug-drug interactions.3,4 The remaining drug is excreted unchanged (3%), along with its inactive metabolites, via urine. Dose adjustment is not required for patients with mild-to-moderate renal impairment or patients with mild hepatic impairment.

Conclusion Overall, trials of the NOACs demonstrate equal or superior thromboembolism efficacy and major bleeding safety compared to warfarin, but at a higher treatment cost. At present, there are no formal Australian guidelines in regards to the NOACs in patients with non-valvular AF, therefore, strict adherence to approved indications and doses are strongly recommended. According to current European guidelines, NOACs are recommended as broadly preferable to warfarin in a majority of patients for stroke prevention in non-valvular AF.16

Tapentadol has been trialed against placebo and oxycodone for tolerability and effectiveness. They have shown non-inferiority in effectiveness to oxycodone. The most common (≥10%) adverse reactions are nausea, constipation, dizziness, headache, and somnolence. There is a lower incidence of gastrointestinal adverse effects with tapentadol CR compared to Oxycontin®, while CNS adverse effects are comparable or worse for tapentadol.3,6 Tolerance has not been observed in studies of up to 24 months.3 Due to tapentadol’s µ-opioid agonist activity it has the potential for illicit abuse and addiction, thus is restricted as a Schedule 8 drug. Being relatively expensive compared to established opioids at present, its use is best restricted to patients who suffer unacceptable GI adverse effects or fail to obtain satisfactory analgesia.7

References available on request.

New Drug Brief: Tapentadol

References available on request.

Anthony Fico, APHS Pharmacy Murdoch Tapentadol is a new centrally acting synthetic analgesic which combines opioid and non-opioid activity. It acts as a µ-opioid agonist and an inhibitor of synaptic re-uptake of noradrenaline. Unlike tramadol it has no serotonergic effects thus reducing the risk of precipitating serotonin toxicity (there have been postmarketing reports of serotonin syndrome with the concomitant use of tapentadol and serotonergic drugs).1 The synergistic action of tapentadol’s two mechanisms of action may explain why it is approximately 3 times less potent than morphine, despite its 50-fold lower affinity for the µ-opioid receptor.2 Tapentadol is currently available in Australia as a controlled release (CR) tablet formulation (brand name Palexia® SR) in 50mg, 150mg, 200mg and 250mg strengths. It is approved for use in the management of moderate to severe chronic pain unresponsive to non-narcotic analgesics, such as back pain and diabetic neuropathy.3 Further studies are required to establish effectiveness in palliative care and pain due to malignancy, although early reports look promising.

Tapentadol is not subsidised by the PBS and has an approximate patient cost of $76-$204 per month dependent on dose.

circuit If you have any queries regarding Circuit content and authors please contact the APHS Pharmacy Practice Unit by email: circuit.editor@aphs.com.au Every effort has been made to ensure this newsletter is free from error or omission.

The recommended starting dose of tapentadol for opioid naive patients is 50mg twice daily, with dose titration in increments of 50mg twice daily every three days to achieve maintenance (effective tolerable dose). The maximum total daily dose is 500mg.3,4 If rotating from another opioid, the nature, route of administration and mean daily dose of the previous opioid should be taken into account.

Although adequate data is lacking on direct opioid conversion with tapentadol, half of the estimated daily tapentadol requirement should be considered for initial dosing, use Table 1 as a guide to equivalency.1 As no immediate release (IR) formulation is available in Australia an alternate IR opioid should be used for rescue/breakthrough requirements.

Tapentadol Equivalence (Oral) Tapentadol

50mg

Morphine

15mg

Oxycodone

10mg

Table 1. Tapentadol equivalence, based on non-inferiority trial data (extrapolated).1,3,5 An initial drug release of about 20% occurs over the first 30 minutes with ongoing release over the ensuing 12 hour period. Maximum serum concentrations of tapentadol are observed between 3 and 6 hours after administration. Tapentadol is almost completely metabolised in the liver by

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RESEARCHAT

APHS PHARMACY

In 2013, APHS Pharmacies across Australia conducted a number of research projects to advance Pharmacy Practice in hospital and oncology settings. Of these, 8 projects were submitted and accepted for presentation at the annual Society of Hospital Pharmacists (SHPA) conference, an outstanding result in recognition of the quality of each submission. Two of these won conference awards, recognising their value as innovative, high-standard pharmacy practices. These projects aren’t often shared with our hospital partners, so we have included 4 of the 8 abstracts below to give you some understanding of APHS’ behind-the-scenes innovations. The posters presented at the conference can be viewed at http://www.aphs.com.au/index.php/news/2014/02/aphs-research-in-2013/

TECHNICIAN TRIAGE- ASSISTING CLINICAL PHARMACY SERVICE IN A PRIVATE REGIONAL HOSPITAL

DEVELOPMENT AND IMPLEMENTATION OF AN ONCOLOGY PHARMACY OBSERVATIONAL QUALITY ASSURANCE TOOL

WINNER ORAL PRESENTATION, SHPA ANNUAL CONFERENCE 2013

WINNER INNOVATION AWARD, SHPA ANNUAL CONFERENCE 2013

AIM: To develop, implement and evaluate a triage procedure conducted by pharmacy technicians for a prioritised clinical pharmacy service.

AIM: To develop and implement an oncology pharmacy quality assurance tool which provides a framework for systematically assessing quality and compliance with oncology pharmacy standards of practice.

BACKGROUND: Private regional hospital pharmacies face the challenges of no direct government funding and limited human resources in providing clinical ward pharmacist services, while adhering to SHPA guidelines.

METHOD: A patient assessment triage tool (PATT) was created, incorporating elements from an SHPA publication, How to prioritise clinical pharmacy services, ACQSHC publications and an APHS publication, Medication reconciliation and pharmacy communication tool. Triage was conducted for new admissions and inpatients after medication changes. Technicians were trained and supervised by a pharmacist before implementation. After ward rounds, the technician returned the completed PATT to the pharmacist, with a reason for missed patients noted. The process was piloted in 3 wards with 75 beds, serviced by three technicians and one pharmacist over 4 weeks.

Data collected includes the number of patients triaged, the number of patients referred to the pharmacist and the outcome. Feedback from technicians and pharmacists was also evaluated.

RESULT: Of the 151 patients triaged, 60% were referred to the pharmacist.

Of these referred patients, 20% required no intervention, 60% non-immediate intervention and 20% immediate intervention with no identifiable risk trend. The pharmacy technicians reported increased job satisfaction from participation in screening work and the pharmacist reported satisfaction with a time efficient procedure to prioritise triaged patients.

DISCUSSION: This study was driven by the need to best utilise pharmacist time to provide an efficient clinical pharmacy service. By utilising Cert IV Hospital/Health Services trained pharmacy technicians to triage and collect clinical information, at risk patients were able to be prioritised and assessed in a timely and resource efficient manner.

CONCLUSION: The PATT procedure, prioritising patients for clinical review in a private regional hospital, enabled effective use of technician and pharmacist’s time.

Eve Finn and Kim Proudfoot APHS Pharmacy Lismore

METHOD: A literature review of Australian and international oncology pharmacy practice standards was undertaken. A set of criteria were developed into an observational audit tool. Four domains were created which included: • • • •

Personnel Occupational health and safety Oncology pharmacist responsibilities Cytotoxic transport and storage

Each domain was numerated to enable a scoring system which supported both intra- and inter-site quantitative analysis. A total of 17 oncology pharmacy services were audited. The audits were completed by five senior and experienced oncology staff who received training in application of the audit tool. Auditors were not permitted to undertake audit of sites where they had direct responsibility.

RESULTS: Following review of all 17 sites, organisational wide compliance was 71%. Domains where compliance were greatest were: • • • •

Cytotoxic exposure and extravasation incidents Oncology pharmacist activities Labeling Cytotoxic spill handling

Domains where compliance was lowest were: • Education and training of staff • Medical examinations • Stock and storage of cytotoxics Factors that appear to have contributed to variances between sites include older established sites versus newer sites, historical practices, lack of local guidance, lack of a central quality program and resource availability. Each site has been provided with a follow-up action plan and a re-audit will occur in twelve months.

CONCLUSION: The development and implementation of an oncology pharmacy observational audit tool has provided an objective outcome and set a framework for continual quality improvement. The tool has facilitated the

RESEARCHAT

APHS PHARMACY

identification of support materials required, such as organisation-wide policies and mandatory training plans, which aim to create consistency in practice among oncology sites.

Russell Hill, Louise Keamy and Ellisha Vas APHS Pharmacy Western Australia and John Flynn Pharmacy

IMPLEMENTING A PHARMACY QUALITY AUDIT TOOL WITHIN A NATIONAL ORGANISATION AIM: To implement a sustainable quality assurance framework across a diverse range of private and public hospital pharmacy services in six states and territories.

METHODS: A literature search of pharmacy practice standards, jurisdictional legislation, medication safety standards and supporting materials was conducted. Six domains were established pertaining to: • • • • • •

Pharmacy drug storage Imprest and drug distribution Dispensing Risk management (incident reporting) Clinical information resource availability Clinical pharmacy services (pharmaceutical review)

Criteria within each domain were scored to allow analysis of compliance within and between sites. Denominators were adjusted for elements that were not applicable at certain sites, with scores expressed as percentages.

Twenty-five sites were independently audited by eight senior pharmacy staff without direct management responsibility for the respective sites. Training and support materials were provided to assist auditors with consistency of interpretation and scoring of each criteria.

RESULTS: Organisation-wide compliance averaged 69%. Highest achievements were in the domains of accessibility to clinical information resources and incident reporting. Focus areas for improvement were imprest and clinical pharmacy services. Site performance was influenced by factors including: • • • • •

Time with the organisation Available resources Workspace size and design Jurisdicational requirements Practices of non-pharmacy staff (e.g. prescribers and other hospital staff)

Actions to address issues include local practice change and organisation-wide policy development. Non-pharmacy risk factors affecting medication safety are

to be raised with the hospital’s administration. Each site has been provided with an action plan and will be re-audited in twelve months.

Conclusion The development and implementation of the pharmacy observational audit tool has provided an objective outcome and set a framework for continual quality improvement. The tool has facilitated the identification of support materials required such as organisation-wide policies and mandatory training plans, which aim to create consistency in practice across a diverse range hospital pharmacy sites.

Chris Giles APHS Pharmacy Practice Unit

THE WARFARIN SONG AIM: Collecting data on patients who receive warfarin counselling before discharge is a KPI for the pharmacy. A novel method of using song as a learning tool is investigated. The song is used to inspire people to learn, activate prior knowledge and patient recall.

METHOD: It was found that greater than 90% of patients who commenced on warfarin in hospital received medication counselling, as annotated in the inpatient notes. However, approximately 25% of patients counselled had no recall of the counselling on discharge. Research was conducted into adult learning theories and recall of information, and the finding that music helps to focus a learner’s attention and functions as a mnemonic device led to the development of The Warfarin Song. A rhyme was written about the elements in the pharmacy’s existing warfarin counselling and matched to the tune of Waltzing Matilda. The song was recorded using a professional singer and developed into a short narrated PowerPoint presentation. It was played to patients in the hospital’s cardiac rehabilitation program.

RESULTS: The recall of data was self-reported by the patient group as being increased, with comments made that the use of music also made the medication seem more straightforward. The patient comments indicated that singing the song helped to make the information more personal to their own circumstances.

CONCLUSION: Music can help to focus a learner’s attention and function as a mnemonic device to aid recall of information. Use of music in learning can stimulate creativity and foster a positive attitude towards the data presented. The Warfarin Song has been shown to improve recall in patients, and will be used more widely across the hospital for the provision of warfarin counselling. Using a tablet device with a narrated PowerPoint presentation enabled a personalised presentation to be presented easily at a ward level.

Rachel Taylor APHS Pharmacy Port Macquarie and Kempsey