Implementation and evaluation of a team-based pharmacy practice model in a community health system.

PURPOSE: The development and implementation of a team-based pharmacy practice model is described. METHODS: In January 2016 a transition from a staff-specialist to a team-based pharmacy practice model was implemented. The overall goal of the model change was to enhance the pharmacist's clinical roles and further integrate pharmacists into the healthcare team. Before implementation of the new staffing model, a formalized metric evaluation process was created. The aim of this metric evaluation was to gauge model success, determine areas of model revision, and objectively communicate pharmacist impact. Objective metrics were evaluated before implementation and 1 year after implementation. In addition, surveys were distributed to pharmacists, physicians, nursing and hospital administration before and after model implementation. RESULTS: At 1-year postimplementation, the pharmacist:patient bed ratio decreased from 1:87 to 1:47, the number of rounds/huddles with pharmacist attendance increased by 63% to 80 per week, and the number of clinical interventions and new clinical consultations increased from 57 to 62 and from 12 to 16 per day, respectively. Nonformulary medication use also decreased from 1.77 to 0.623 per 1000 patient days, and compliance with therapeutic initiatives increased from 77%to 91%. Overall, 72% of pharmacist survey responses indicated satisfaction with the model change. CONCLUSION: A team-based pharmacy practice model was designed and successfully implemented over a 3-year period. Data analysis revealed improvements in clinical and operational endpoints and enhanced pharmacist, physician, and nursing satisfaction.

Bicalutamide-associated fulminant hepatotoxicity.

Abstract Bicalutamide is a nonsteroidal antiandrogen used extensively during the start of androgen deprivation therapy with a luteinizing hormone-releasing hormone agonist to reduce occurrence of the symptoms of tumor flare in patients with metastatic prostate carcinoma. The most common adverse effects of bicalutamide are induced by its pharmacologic property of competitive androgen receptor blockade and include gynecomastia, hot flashes, fatigue, and decreased libido. Although not as common, increases in liver function test results are also seen with bicalutamide therapy. These elevations are typically transient, and patients remain asymptomatic. We describe a 59-year-old man with metastatic prostate carcinoma treated with bicalutamide as part of androgen deprivation therapy before starting chemotherapy. At baseline, his liver function test results and serum creatinine concentration were within normal limits, and an abdominal computed tomographic scan did not demonstrate liver metastasis. After 4 days of bicalutamide therapy, the patient came to the emergency department with complaints of abdominal pain, distension, and tenderness. His liver function tests were abnormal, and bicalutamide was discontinued. After 2 days of increasing liver function tests and symptoms of hepatotoxicity, the patient developed tachycardia and hypotension that was resistant to fluid resuscitation. Multiorgan damage was manifested by an alanine aminotransferase level greater than 40 times the upper limit of normal, serum creatinine concentration of 4.2 mg/dl, and troponin I level of 18 ng/ml. The patient died 8 days after bicalutamide therapy was begun secondary to multiorgan failure, most likely as a result of fulminant hepatotoxicity. The Naranjo adverse drug reaction probability scale showed a probable (score of 5) causal relationship between bicalutamide and fulminant hepatotoxicity. Fulminant hepatotoxicity is a rare but potentially fatal adverse effect of bicalutamide. Liver function tests should be monitored before and during bicalutamide therapy, even for patients who have previously completed a course of this therapy with no signs or symptoms of toxicity.

Should beta-blockers be used in the treatment of cocaine-associated acute coronary syndrome?

OBJECTIVE: To critically evaluate the 30 year debate of beta-blocker use in cocaine-induced acute coronary syndrome (CIACS). DATA SOURCES: An Ovid MEDLINE In-Process and Other Non-Indexed Citations, Ovid MEDLINE Daily, and Ovid MEDLINE (1966-August 21, 2007) search of the medical literature was conducted using the key terms cocaine, myocardial infarction, acute coronary syndrome, and adrenergic beta-antagonists. STUDY SELECTION AND DATA EXTRACTION: All clinical trials, case reports, national cardiovascular guidelines, and reviews published in English were evaluated. Case reports were included based on whether (1) acute coronary syndrome was suspected, (2) a beta-blocker was used during the treatment course, and (3) objective and subjective patient-specific information was documented. DATA SYNTHESIS: Three case reports and 2 placebo-controlled trials were identified that used 4 beta-blockers (atenolol, labetalol, metoprolol, propranolol). Three national guidelines addressed beta-blocker use. Although published data are limited, propranolol and labetalol exert minimal to no effect on alleviating cocaine-induced coronary vasoconstriction. None of the evaluated national guidelines recommends beta-blockers as first-line agents in CIACS management. CONCLUSION: Beta-blockers should not be considered first-line agents for controlling chest pain in patients with documented CIACS. If long-term beta-blockade is warranted, its benefits should be weighed against recurrent use of cocaine and possible exacerbation of acute coronary syndrome. Given that carvedilol exhibits ancillary pharmacologic proprieties beneficial in CIACS, and post-myocardial infarction mortality data are available regarding its use, this agent could be considered to be appropriate therapy.