A human factors approach to improving electronic performance measurement of venous thromboembolism prophylaxis.

OBJECTIVE: In 2011, our institution developed a venous thromboembolism (VTE) prophylaxis order set to monitor prophylaxis management through physician-generated risk assessment orders. Prophylaxis rates obtained using the risk assessment orders were falsely low compared with chart review. Our goal was to redesign the order set to increase the percentage of VTE risk assessments ordered, both to improve care and to better reflect performance. DESIGN: Quality Improvement Project. SETTING: Veterans Health Administration. PARTICIPANTS: Patients admitted to acute care and intensive care medical units. INTERVENTIONS: Process analysis was used to identify systems failures limiting use of the original order set. The order set was redesigned using a human factors approach. MAIN OUTCOME MEASURE: VTE risk assessment orders. RESULTS: The order set was redesigned to reduce complexity and improve integration into provider workflow. The rate of risk assessment orders placed within 24 h increased from 48.6 to 80.4% (P < 0.001). There was no difference in the actual use of prophylaxis. However, for patients on prophylaxis, the rates of having a documented 'moderate' or 'high' risk assessment within 24 h increased from 66.7 to 95.7% (P < 0.001). CONCLUSIONS: Using human factor principles to redesign an order set led to a significant increase in the percentage of patients with a risk assessment order placed within 24 h of admission. Although the risk assessments using the redesigned order set better reflected physician performance, it remained an imperfect measure for VTE prophylaxis. New technology used to measure human performance must be evaluated following implementation to assess accuracy.

Clostridium difficile: recent epidemiologic findings and advances in therapy.

Clostridium difficile-associated disease (CDAD) has become an important public health problem. The causative organism is acquired by the oral route from an environmental source or by contact with an infected person or a health care worker who serves as a vector. Disruption of the bowel microflora, generally by antibiotics, creates an environment that allows C. difficile to proliferate. Organisms produce toxins A and B, which cause intense inflammation of the colonic mucosa. The syndrome that results includes severe diarrhea, fever, abdominal pain, and leukocytosis. A new strain of C. difficile has become prevalent in the United States, Canada, and the United Kingdom. Identified by pulsed-field gel electrophoresis (PFGE), this strain is called North America PFGE type 1, abbreviated as NAP-1. Clostridium difficile NAP-1 characteristically generates large amounts of toxins A and B, as well as an additional binary toxin and is associated with enhanced morbidity and a poor response to antibiotic therapy. Mild cases of CDAD may respond to cessation of antibiotic therapy, perhaps related to antibody production by the infected person, but most infected persons require antimicrobial therapy. Vancomycin has been approved by the United States Food and Drug Administration for treatment of CDAD, but reluctance to use this antibiotic in the hospital setting has led to reliance on metronidazole as first-line therapy. Recent studies show a high rate of failure, due either to infection by NAP-1 or to the presence, in hospitals, of older and sicker adults who have been treated with many broad-spectrum antibiotics. Nitazoxanide, bacitracin, teicoplanin, and fusidic acid are additional agents that have published efficacy for this indication in humans. Rifaximin and PAR-101 are under investigation. Other therapies, including polymers that bind C. difficile toxin and monoclonal antibodies to toxins, and preventive measures such as toxoid vaccines are also under study.