Kerry Wilbur

Incidence, severity and preventability of medication-related visits to the emergency department: a prospective study

Background: Medication-related visits to the emergency department are an important but poorly understood phenomenon. We sought to evaluate the frequency, severity and preventability of drug-related visits to the emergency department. Methods: We performed a prospective observational study of randomly selected adults presenting to the emergency department over a 12-week period. Emergency department visits were identified as drug-related on the basis of assessment by a pharmacist research assistant and an emergency physician; discrepancies were adjudicated by 2 independent reviewers. Results: Among the 1017 patients included in the study, the emergency department visit was identified as drug-related for 122 patients (12.0%, 95% confidence interval [CI] 10.1%–14.2%); of these, 83 visits (68.0%, 95% CI 59.0%–76.2%) were deemed preventable. Severity was classified as mild in 15.6% of the 122 cases, moderate in 74.6% and severe in 9.8%. The most common reasons for drug-related visits were adverse drug reactions (39.3%), nonadherence (27.9%) and use of the wrong or suboptimal drug (11.5%). The probability of admission was significantly higher among patients who had a drug-related visit than among those whose visit was not drug-related (OR 2.18, 95% CI 1.46–3.27, p < 0.001), and among those admitted, the median length of stay was longer (8.0 [interquartile range 23.5] v. 5.5 [interquartile range 10.0] days, p = 0.06). Interpretation: More than 1 in 9 emergency department visits are due to drug-related adverse events, a potentially preventable problem in our health care system.

Drug‐Related Hospitalizations in a Tertiary Care Internal Medicine Service of a Canadian Hospital: A Prospective Study

Study Objectives. To determine the frequency, severity, preventability and classification of adverse drug events resulting in hospitalization, and to identify any patient, prescriber, drug, and system factors associated with these events.

Colchicine Myotoxicity: Case Reports and Literature Review

Two of our patients experienced myotoxicity associated with colchicine administration. The first was a 54‐year‐old woman who was receiving dialysis and came to the emergency department with progressive generalized weakness and vomiting. She recently had taken colchicine for the treatment of gout. Physical examination revealed proximal muscle weakness and tenderness on palpation. Her creatine kinase (CK), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) levels were elevated at 7185, 563, and 541 U/L, respectively. Drug‐induced myopathy was suspected and colchicine was discontinued. The patient was discharged after symptom resolution 1 week later. The second patient was an 83‐year‐old woman with chronic renal insufficiency who came to the hospital with anorexia, diarrhea, and inability to get out of bed due to progressive weakness. Her colchicine dosage recently had been increased for gout management. Physical examination revealed generalized muscle weakness and tenderness on palpation. Her CK, ALT, and AST levels were elevated at 1797, 147, and 172 U/L, respectively. Electromyographic results were consistent with colchicine myopathy. The patient was discharged with minimal residual muscle weakness 1 week after discontinuation of colchicine. A literature search identified 82 documented cases of colchicine‐induced myotoxicity. Most patients had a history of proximal weakness and pain with elevated CK, ALT, and AST levels. Onset of symptoms generally occurred days to weeks after initial administration of colchicine at the usual dosage in patients with renal impairment or a change in underlying disease state in those receiving long‐term therapy. Muscle toxicity was not necessarily accompanied by gastrointestinal symptoms. Concomitantly administered drugs often were cyclosporine or corticosteroids. Diagnosis may be confirmed by electromyography or muscle biopsy. Colchicine‐induced myotoxicity is a rare adverse effect but is well described in the literature. Clinicians should recognize that renal impairment is the primary risk factor for development of colchicine‐induced myotoxicity, and that dosage adjustment or alternative therapy may be required.

Pharmacokinetic Drug Interactions Between Oral Contraceptives and Second-Generation Anticonvulsants

Drug interactions between oral contraceptives (OCs) and traditional anticonvulsants have been well described. However, in the past decade, a number of new anticonvulsants have been developed, as well as modifications made in the composition of the OC preparations themselves. Additionally, anticonvulsants are increasingly employed in the therapy of nonseizure-related disorders, placing more women at risk of potential drug interactions that may lead to contraceptive failure.Second-generation anticonvulsants include felbamate, gabapentin, lamotrigine, oxcarbazepine, tiagabine, topiramate, vigabatrin and zonisamide. Most have been approved for adjunctive management of seizures refractory to therapy with traditional anticonvulsants. On the basis of available study data in women receiving concomitant OC preparations, gabapentin, lamotrigine, tiagabine and vigabatrin may be administered without significant pharmacokinetic interactions that potentially diminish contraceptive efficacy. However, additional or alternative contraceptive measures, including using OCs with higher estrogen content, are recommended when using felbamate, oxcarbazepine and topiramate, as these agents have demonstrated enzyme-inducing activity leading to reduced plasma steroid concentrations. The effects of zonisamide in women receiving OCs have yet to be reported.It is important to characterise the properties [e.g. substrate and enzyme activity (particularly cytochrome P450 3A4 induction)] of new anticonvulsants and recognise their potential to interfere with OCs. However, a pharmacokinetic interaction does not in itself indicate loss of OC efficacy. Contraceptive failure should be measured by changes in ovarian hormone concentrations, maturation of ovarian follicle(s) or ovulation.

Is propofol an optimal agent for procedural sedation and rapid sequence intubation in the emergency department

OBJECTIVE We conducted a qualitative systematic review to evaluate the efficacy and safety of propofol for direct current cardioversion (DCC), rapid sequence intubation (RSI) and procedural sedation in adult emergency department (ED) patients. DATA SOURCE MEDLINE (1966 to September 2000), PubMed (to September 2000), EMBASE (1988 to September 2000), Database of Systematic Reviews (to September 2000), Best Evidence (1991 to September 2000) and Current Contents (1996 to September 2000) databases. STUDY SELECTION English-language, randomized, comparative evaluations of propofol for procedures routinely conducted in adults (>18 years) were included. Direct current cardioversion, RSI and procedural sedation were considered. DATA EXTRACTION Efficacy and safety endpoints were evaluated for all trials. For DCC and procedural sedation trials, efficacy measures included induction and recovery times, as well as the association for successful procedure. For the RSI trials, optimal intubating conditions were evaluated as the primary efficacy endpoint. Safety measures included hemodynamic changes, apnea rates and adverse effects. DATA SYNTHESIS In the setting of DCC, efficacy and safety outcomes were similar for propofol, thiopental, etomidate and methohexital. All of these agents provided markedly shorter induction and recovery times than midazolam. Patients who were pre-medicated with fentanyl exhibited prolonged recovery times and greater decreases in blood pressure. When used for RSI, propofol administration was associated with satisfactory intubating conditions that were comparable to those seen with thiopental and etomidate. Blood pressure reductions were seen in both DCC and RSI studies. Apneic episodes (>30 seconds) occurred in 23% of propofol recipients, 28% of thiopental recipients and 7% of etomidate and midazolam recipients. Apart from the DCC studies described, no procedural sedation studies met our predefined review eligibility criteria. CONCLUSION The body of literature evaluating propofol for DCC and RSI in the ED is limited. There is evidence to support the use of propofol for DCC and RSI, but this evidence comes from stable patients in non-ED settings. Further ED-based randomized comparative trials should be conducted before propofol is adopted for widespread use in the ED.

Myocardial Infarction Associated with Intravenous Immune Globulin

OBJECTIVE To report a case of acute myocardial infarction (MI) experienced by a patient receiving intravenous immune globulin (IVIG) and review other published cases of MI associated with IVIG. CASE SUMMARY An 81-year-old Vietnamese man was prescribed IVIG for treatment of toxic epidermal necrolysis secondary to allopurinol. Thirty minutes following the start of the IVIG infusion, the patient developed crushing retrosternal chest pain and shortness of breath. The pain improved upon discontinuation of IVIG infusion but recurred when IVIG was restarted. The troponin level reached 140 μg/L, and a persantine sestamibi stress test (MIBI) indicated anterolateral ischemia. The patient was diagnosed with non–ST-elevation MI. An objective causality assessment using the Naranjo probability scale revealed a probable association between this adverse reaction and IVIG treatment. DISCUSSION Although an association between IVIG administration and MI has not been demonstrated in clinical trials, accumulating clinical experience suggests that a relationship between IVIG and myocardial ischemia exists. Twenty published case reports were identified. Risk of acute MI seems to be increased with use of high-dose IVIG and in older individuals, especially those with at least one cardiovascular risk factor, such as ischemic heart disease or hypertension. CONCLUSIONS Case reports suggest a causal relationship between the use of IVIG and MI and other thrombotic events. While cardiovascular disease is not considered an absolute contraindication to therapy, expanding indications and subsequent use of IVIG merit that clinicians be aware of patient characteristics that may increase the risk for adverse reactions and recognize early signs of infarction.

Phenytoin–Diazepam Interaction:

OBJECTIVE: To report a case of phenytoin toxicity potentially associated with concurrent diazepam therapy. CASE SUMMARY: A 44-year-old First Nations man presented to the emergency department with headache, nystagmus, diplopia, and ataxia. Apart from a long-standing seizure disorder, his past medical history was unremarkable. The antiepileptic drug regimen of phenytoin, phenobarbital, and lamotrigine had been unchanged for almost 5 months. Total phenytoin serum concentration reported 2 weeks prior to hospital admission was 8 μg/L. Two days prior to admission, he was prescribed amoxicillin and diazepam; he denied use of nonprescription or herbal medications. The serum phenytoin concentration drawn in the hospital was 37 μg/mL. Both phenytoin and diazepam were stopped, and the symptoms resolved. His neurologic abnormalities were attributed to phenytoin toxicity caused by an interaction with diazepam. DISCUSSION: The literature documenting a potential interaction between diazepam and phenytoin is conflicting. Case reports and controlled studies have demonstrated both increases and decreases in serum phenytoin concentrations when these agents were administered concomitantly. Phenytoin induces the metabolism of drugs that are substrates of CYP2C, CYP2D, and CYP3A; however, phenytoin is eliminated predominantly by CYP2C9-and CYP2C19-dependent hepatic metabolism. Diazepam is one example of a drug that is extensively metabolized by CYP2C19 and could potentially influence phenytoin elimination by acting as an alternate substrate for this isoenzyme. In our patient, the timing of drug administration, clinical and physical examination findings, and laboratory data suggest that diazepam therapy resulted in phenytoin toxicity. Use of the Naranjo probability scale indicated a probable relationship between the adverse clinical effects observed and phenytoin and diazepam coadministration in this patient. CONCLUSIONS: Phenytoin is a known inducer of drugs metabolized by CYP2C, CYP2D, and CYP3A, but its own metabolism may be altered by drugs influencing CYP2C9 or CYP2C19, such as diazepam. Agents not acting as enzyme inhibitors or inducers, but instead behaving as alternate substrates for enzyme-binding sites, may produce clinically relevant drug interactions through an underrecognized mechanism.

Pharmacy Student and Preceptor Impressions of Faculty Liaison Visits to Experiential Training Sites.

Objective. To characterize preceptor and student views about and experiences with faculty liaison visits to practice sites during clinical internships. Methods. A survey was administered at the conclusion of each of the first 3 academic years of a new postbaccalaureate doctor of pharmacy (PharmD) program. Results. Preceptors were satisfied overall with faculty liaison visits, while students initially were not; however, their perception increased in subsequent years. Students felt development of their patient care skills benefited, but less so their interpersonal communication skills. Each year, almost all preceptors indicated faculty liaison visits were helpful in developing and refining their mentorship skills. Conclusion. Faculty liaison visits provided a valuable opportunity to interact and support preceptors and students during advanced pharmacy internships in a nascent PharmD program.

Lecture-capture: the early Qatar experience.

To the Editor. The recent article by Benavides et al explored the correlation of faculty members’ publication productivity to student-faculty ratios in colleges of pharmacy. These investigators also evaluated the influence of other factors, such as research funding, public vs. private university status, and supportive faculty members on scholarship. While these areas are important topics of investigation where additional insight would be welcomed, I would like to point out 2 potentially serious methodological errors in the study. These authors attempted to compile publication rates of colleges of pharmacy by searching PubMed. While there is insufficient detail in the article about how these searches were performed, it appears that the authors utilized the affiliation field of the MEDLINE database to search for individual schools and colleges. Unfortunately, the problem with this approach is that the MEDLINE database lists only the address of the corresponding author, not all the authors of the paper. So in a multi-university collaborative paper with, for example, 6 authors, only the corresponding author’s address will appear in the MEDLINE record. This is in contrast to a database such as Science Citation Index (Web of Science online) which captures the address of every author on a particular paper. This error would result in a significantly underestimated publication count for some colleges. The second related error is that many authors do not list ‘‘college of pharmacy’’ or ‘‘school or pharmacy’’ in their addresses. If this were part of the search strategy, it also would contribute to a significant underestimation of the true publication count. As an example, a 2007 calendar year PubMed search for just 3 individual basic science faculty members (KM Giacomini, A Sali, and BK Shoichet), all of whom are listed in the AACP Roster for the 2006-2007 academic year from the University of California at San Francisco (UCSF), yielded 43 nonoverlapping publications. Since bibliometric author searches on any database can be contaminated by homologues (ie, authors with the same name who are in different disciplines or institutions), I was able to validate 33 of these papers by searching the Web site of these faculty members at UCSF. The Benavides study lists only 24 total publications for UCSF for this timeframe. A careful inspection of the MEDLINE records for these 3 faculty members reveals that many list ‘‘Department of Biopharmaceutical Sciences’’ at UCSF in the affiliation field without mentioning school of pharmacy. As a result of these possible errors, this study may have seriously underestimated the publication output of some colleges and schools of pharmacy.

Continuing Professional Development and Self-Learning for Pharmacists

Abstract Life-long learning (LLL), continuing education (CE), and (more recently) continuing professional development (CPD) were triggered by a realization of healthcare practitioners’ needs to keep up with the fast pace of change in order to provide care to patients that is appropriate, relevant, and evidence-based. While often considered synonymous, CPD is distinct, as it is intended to be driven by the learners sense of accountability and autonomy, where he or she chooses the subject of need or interest, the content or materials, and the learning space and pace. Today, interest in CPD is seen all over the world, and Ministries of Health, healthcare regulators, and professional bodies advocate CPD as a strategy that leads to better health outcomes. The interest in CPD was soon followed by policies mandating it as prerequisite to licensure and practice. Many forms of CPD and CE programs exist across countries, and there is no one way of applying them. The aim of this chapter is to provide an update on the status of CPD in pharmacy and to describe the crucial elements and requirements of a CPD program. We have also covered aspects related to mandatory accreditation of CPD and the challenges and conditions associated with this.