Reducing Unnecessary Phlebotomy Testing Using a Clinical Decision Support System

Overuse of phlebotomy testing offers little to improve patient outcomes but may subject patients to additional morbidity. Low-cost, high-frequency tests are ordered recurrently, unnecessarily, and contribute to the high cost of health care. Reducing unnecessary phlebotomy tests can cut costs without compromising quality. Type and screen tests are active for three days from the date the specimen is collected, yet our blood bank laboratory observed type and screen tests were often unnecessarily ordered in our organization. We set out to determine the effectiveness of a clinical decision support system (CDSS) on reducing unnecessary type and screen tests, estimate the cost saved by the CDSS implementation, and describe the unnecessary ordering practices by provider type. Adoption of CDSSs has been successful in reducing unnecessary radiologic imaging, overutilization of antibiotics, and Clostridium dificile testing. Our value improvement initiative was a separate-sample pretest posttest design at a mid-Atlantic academic health system. A CDSS was embedded in our computerized order entry (COPE) system to promote appropriate test ordering. The CDSS appears when a type and screen is ordered informing the provider of the date and time the current test expires. Our study demonstrated that CDSSs impacted a variety of provider types, reduced unnecessary phlebotomy tests, and achieved yearly cost savings. Unnecessary testing continues in health care and contributes to excessive health spending without adding value. Phlebotomy testing is one example of how providers can reduce waste and control healthcare costs for low-cost, high-frequency tests. To further improve test ordering practices of all provider types, we recommend additional interventions such as organizational support, education, audits, and feedback. In this era of precision medicine, ordering the right test, at the right time, for the right reason can reduce cost, reduce waste, and improve quality, outcomes, and satisfaction for patients. Until the establishment of national quality measures aimed to control the number of low-cost, high-frequency tests, health systems must find a way to reduce unnecessary health services. CPOE is widely used in a variety of health care settings and can incorporate CDSS to guide all provider types to make judicious decisions at the time of care

Hypercoagulability progresses to hypocoagulability during evolution of acetaminophen-induced acute liver injury in pigs

Increases in prothrombin time (PT) and international normalised ratio (INR) characterise acute liver injury (ALI) and failure (ALF), yet a wide heterogeneity in clotting abnormalities exists. This study defines evolution of coagulopathy in 10 pigs with acetaminophen (APAP)-induced ALI compared to 3 Controls. APAP administration began at 0 h and continued to ‘ALF’, defined as INR >3. In APAP pigs, INR was 1.05 ± 0.02 at 0 h, 2.15 ± 0.43 at 16 h and > 3 at 18 ± 1 h. At 12 h thromboelastography (TEG) demonstrated increased clot formation rate, associated with portal vein platelet aggregates and reductions in protein C, protein S, antithrombin and A Disintegrin and Metalloprotease with Thrombospondin type 1 repeats–13 (ADAMTS-13) to 60%, 24%, 47% and 32% normal respectively. At 18 ± 1 h, INR > 3 was associated with: hypocoagulable TEG profile with heparin-like effect; falls in thrombin generation, Factor V and Factor VIII to 52%, 19% and 17% normal respectively; further decline in anticoagulants; thrombocytopenia; neutrophilia and endotoxemia. Multivariate analysis, found that ADAMTS-13 was an independent predictor of a hypercoagulable TEG profile and platelet count, endotoxin, Protein C and fibrinogen were independent predictors of a hypocoagulable TEG profile. INR remained normal in Controls. Dynamic changes in coagulation occur with progression of ALI: a pro-thrombotic state progresses to hypocoagulability

Troponin elevation in acute ischemic stroke (TRELAS) - protocol of a prospective observational trial

<p>Abstract</p> <p>Background</p> <p>Levels of the cardiac muscle regulatory protein troponin T (cTnT) are frequently elevated in patients with acute ischemic stroke and elevated cTnT predicts poor outcome and mortality. The pathomechanism of troponin release may relate to co-morbid coronary artery disease and myocardial ischemia or, alternatively, to neurogenic cardiac damage due to autonomic activation after acute ischemic stroke. Therefore, there is uncertainty about how acute ischemic stroke patients with increased cTnT levels should be managed regarding diagnostic and therapeutic workup.</p> <p>Methods/Design</p> <p>The primary objective of the prospective observational trial TRELAS (TRoponin ELevation in Acute ischemic Stroke) is to investigate the frequency and underlying pathomechanism of cTnT elevation in acute ischemic stroke patients in order to give guidance for clinical practice. All consecutive patients with acute ischemic stroke admitted within 72 hours after symptom onset to the Department of Neurology at the Campus Benjamin Franklin of the University Hospital Charité will be screened for cTnT elevations (i.e. >= 0.05 μg/l) on admission and again on the following day. Patients with increased cTnT will undergo coronary angiography within 72 hours. Diagnostic findings of coronary angiograms will be compared with age- and gender-matched patients presenting with Non-ST-Elevation myocardial infarction to the Department of Cardiology. The primary endpoint of the study will be the occurrence of culprit lesions in the coronary angiogram indicating underlying co-morbid obstructive coronary artery disease. Secondary endpoints will be the localization of stroke in the cerebral imaging and left ventriculographic findings of wall motion abnormalities suggestive of stroke-induced global cardiac dysfunction.</p> <p>Discussion</p> <p>TRELAS will prospectively determine the frequency and possible etiology of troponin elevation in a large cohort of ischemic stroke patients. The findings are expected to contribute to clarify pathophysiologic concepts of co-morbid cardiac damage in ischemic stroke patients and also to provide a basis for clinical recommendations for cardiac workup of such patients.</p> <p>Trial registration</p> <p>clinicaltrials.gov <a href="http://www.clinicaltrials.gov/ct2/show/NCT01263964">NCT01263964</a></p