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Objective

The objective was to describe the implementation, work flow, and differences in outcomes between a pharmacist‐managed clinic for the outpatient treatment of venous thromboembolism (VTE) using a non‐vitamin K oral anticoagulant versus care by a primary care provider (PCP).

Methods

Patients in the studied health system that are diagnosed with low‐risk VTE in the emergency department are often discharged without hospital admission. These patients are treated with a non‐vitamin K oral anticoagulant and follow‐up either in a pharmacist‐managed VTE clinic or with their PCP. Pharmacists in the VTE clinic work independently under a collaborative practice agreement (CPA). An evaluation of 34 patients, 17 in each treatment arm, was conducted to compare the differences in treatment‐related outcomes of rivaroxaban when managed by a pharmacist versus a PCP.

Results

The primary endpoint was a 6‐month composite of anticoagulation treatment‐related complications that included a diagnosis of major bleeding, recurrent thromboembolism, or fatality due to either major bleeding or recurrent thromboembolism. Secondary endpoints included number of hospitalizations, adverse events, and medication adherence. There was no difference in the primary endpoint between groups with one occurrence of the composite endpoint in each treatment arm (p = 1.000), both of which were recurrent thromboembolic events. Medication adherence assessment was formally performed in eight patients in the pharmacist group versus no patients in the control group. No differences were seen among other secondary endpoints.

Conclusions

The pharmacist‐managed clinic is a novel expansion of clinical pharmacy services that treats patients with low‐risk VTEs with rivaroxaban in the outpatient setting. The evaluation of outcomes provides support that pharmacist‐managed care utilizing standardized protocols under a CPA may be as safe as care by a PCP.
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Background: The solubility of inorganic calcium and phosphate in parenteral solutions can be complicated in pediatrics due to the dosing of calcium and phosphorus at the saturation point. The purpose of this study was to test the solubility of sodium glycerophosphate (NaGP) with calcium gluconate in pediatric parenteral nutrition (PN) solutions. Methods: Five PN solutions were compounded by adding calcium gluconate at 10, 20, 30, 40, and 50 mEq/L and corresponding concentrations of NaGP at 10, 20, 30, 40, and 50 mmol/L. Each of the 5 solutions was compounded using 1.5% and 4% amino acids, cysteines, and lipids. Compatibility was evaluated by visual inspection (precipitation, haze, and color change). Solutions were evaluated microscopically for any microcrystals and measured by a turbidimeter for changes in turbidity. Solutions were further analyzed using United States Pharmacopeia 788 standards. Six hundred seventy‐one PN solutions were compounded at various concentrations and evaluated for visual stability. Results: Compatibility testing showed no changes in the PN solution in any of the concentrations tested. Microscopically, no microcrystals were detected. The turbidimeter measurements had changes of ≤0.14 nephelometric turbidity units for all test solutions. There were no visual changes in any of the 671 PN solutions. Conclusion: It is recommended that NaGP replace sodium phosphate in PN solutions. This would eliminate the concern of calcium and phosphorus precipitation and the need of any saturation curves.  相似文献   
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Study objective: We sought to characterize the ECG changes associated with symptomatic β-blocker overdose. Methods: The study population consisted of a prospective cohort of patients reporting to 2 regional poison centers with β-blocker overdose. Each patient received an ECG on presentation and a structured follow-up. The inclusion criteria for symptomatic overdose included heart rate of less than 60 beats/min or systolic blood pressure of less than 90 mm Hg; symptoms consistent with decreased end-organ perfusion; therapeutic intervention with cardioactive medication; and corroboration by 2 of the authors that this was a clear-cut case of symptomatic β-blocker overdose with cardiovascular toxicity. Exclusion criteria included cardioactive coingestants, age younger than 6 years, and no available ECG. Results: Of 167 patients, 13 were determined to have symptomatic exposures. First-degree heart block (>200 ms) was the most common ECG finding (10/12) and also had the greatest likelihood ratio (5.31) when comparing those with symptomatic exposures with those with asymptomatic exposures. Comparing the asymptomatic with the symptomatic groups, the mean PR interval was 167 ms (95% confidence interval [CI] 162 to 171 ms) versus 216 ms (95% CI 193 to 238 ms), the mean QRS interval was 89 ms (95% CI 87 to 91 ms) versus 112 ms (95% CI 92 to 132 ms), the mean QTc interval was 422 ms (95% CI 417 to 428) versus 462 ms (95% CI 434 to 490 ms), and the mean heart rate was 72 beats/min (95% CI 69 to 74 beats/min) versus 66 beats/min (95% CI 59 to 73 beats/min). Two cases of symptomatic acebutolol exposure appeared unique by demonstrating disproportionate prolongation of the QTc interval, an RaVR height of 3 mm or greater, and associated ventricular tachydysrhythmia. Conclusion: The majority of clinically significant β-blocker intoxications demonstrate negative dromotropic effects on ECG. Several ECG differences in acebutolol intoxication might reflect unique pathophysiologic processes relative to other β-blockers. [Ann Emerg Med. 2002;40:603-610.]  相似文献   
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