A prospective, randomized trial to assess the cost impact of pharmacist-initiated interventions.

BACKGROUND: Hospital pharmacists make many recommendations that improve patients' quality of care and/or reduce drug costs. While the impact of quality-of-care interventions is difficult to quantify, those limited to cost savings could be assessed in a prospective, randomized fashion. OBJECTIVE: To assess the impact of pharmacist-initiated interventions on cost savings. METHODS: Six pharmacists at a large university hospital recorded patient-specific recommendations for 30 days. All quality-of-care interventions were completed by the pharmacists, but those strictly aimed at reducing costs were stratified by drug class and randomized to an intervention or control group. Pharmacists contacted physicians with cost-saving recommendations in the intervention group, while control group patients were simply observed. MAIN OUTCOME MEASURE: Drug costs after randomization. RESULTS: Most (n=967 [79%]) of the 1226 interventions recorded were aimed at improving quality of care. The remaining 259 (21%) provided equivalent quality of care, but at less expense. These cost-saving interventions typically involved streamlining therapy to less expensive agents (39%), discontinuing an unnecessary medication (25%), or modifying the route of administration (24%). The group randomized to receive a pharmacist's intervention had drug costs that were 41% lower than those in the control group (mean, $73.75 vs $43.40; P<.001). Interventions involving anti-infective agents had the greatest cost savings (mean, $104.08 vs $58.45; P<.001). For our institution, this extrapolates to an annual savings of approximately $394,000 (95% confidence interval, $46,000-$742,000). As expected, these interventions had no impact on length of hospital stay, in-hospital mortality, 30-day readmissions, or the need to readminister the targeted medication or restart intravenous therapy. CONCLUSIONS: While interventions solely aimed at reducing costs represent a small portion of a pharmacist's activities, they can result in significant savings for an institution.

Enoxaparin-associated dermal necrosis: a consequence of cross-reactivity with heparin-mediated antibodies.

OBJECTIVE: To describe a patient with enoxaparin-induced dermal necrosis and to review previously reported cases of skin manifestations associated with low-molecular-weight heparins. CASE SUMMARY: A 43-year-old white woman with adult respiratory distress syndrome developed localized dermal necrosis and thrombocytopenia secondary to subcutaneous administration of unfractionated heparin. Upper extremity thrombi that had developed after administration of subcutaneous heparin at an outside hospital were treated with subcutaneous enoxaparin. Although platelet counts remained stable during enoxaparin therapy, dermal necrosis developed at the injection site. Parenteral anticoagulant therapy was discontinued and the necrotic lesions secondary to enoxaparin resolved with minimal local care. DISCUSSION: Numerous cases of dermal necrosis secondary to heparin administration have been reported while this reaction secondary to enoxaparin use has been reported only briefly. It has been postulated that dermal necrosis secondary to heparin is associated with heparin-induced thrombocytopenia and is a result of heparin-mediated thrombosis in the microvasculature. Antibodies to heparin have cross-reactivity with enoxaparin; therefore, dermal necrosis secondary to enoxaparin may occur by a similar mechanism. CONCLUSIONS: Although enoxaparin-associated dermal necrosis appears to be a rare occurrence, we advise against the use of enoxaparin or other low-molecular-weight heparins in patients with a previous history of heparin-associated thrombocytopenia or heparin-induced dermal necrosis.