Incidence and risk factors for PTT prolongation in patients receiving low-dose unfractionated heparin thromboprophylaxis.

Low-dose unfractionated heparin (LDUH) prophylaxis decreases the incidence of venous thromboembolism (VTE) in hospitalized patients, but increases the risk of bleeding events. Patients who develop a prolonged activated partial thromboplastin time (aPTT) while on LDUH may be at higher risk for bleeding complications. To determine the incidence and risk factors for aPTT prolongation in hospitalized patients receiving LDUH thromboprophylaxis, we performed a retrospective pharmacoepidemiologic cohort study of adult patients admitted to an academic medical center from September 2013 through September 2015. Among 3857 patients with at least one aPTT checked within 24 h of LDUH administration, aPTT prolongation > 1.5 times the upper limit of normal occurred in 131 (3.4%). Age 68-78 years (OR 1.6, 95% CI 1.01-2.4), age > 78 years (OR 1.9, 95% CI 1.3-2.9), female gender (OR 1.9, 95% CI 1.4-2.5), black race (OR 1.6, 95% CI 1.1-2.3), low BMI (OR 1.8, 95% CI 1.3-2.5), being admitted to a surgical service (OR 0.5, 95% CI 0.3-0.8), and receipt of high-dose (> 10,000 units in a day) unfractionated heparin prophylaxis (OR 1.4, 95% CI 1.003-2.0), were independently associated with aPTT prolongation after LDUH exposure. LDUH VTE prophylaxis is associated with aPTT prolongation in 3.4% of general hospitalized patients. We demonstrated several factors independently associated with aPTT prolongation. Monitoring aPTT levels may be indicated for select patients on LDUH thromboprophylaxis who are at high risk or consequence of bleeding and for aPTT prolongation.

Improving appropriateness of acid-suppressive medication use via computerized clinical decision support.

As part of the Choosing Wisely Campaign, the Society of Hospital Medicine identified reducing inappropriate use of acid-suppressive medication for stress ulcer prophylaxis as 1 of 5 key opportunities to improve the value of care for hospitalized patients. We designed a computerized clinical decision support intervention to reduce use of acid-suppressive medication for stress ulcer prophylaxis in hospitalized patients outside of the intensive care unit at an academic medical center. Using quasiexperimental interrupted time series analysis, we found that the decision support intervention resulted in a significant reduction in use of acid-suppressive medication with stress ulcer prophylaxis selected as the only indication, a nonsignificant reduction in overall use, and no change in use on discharge. We found low rates of use of acid-suppressive medication for the purpose of stress ulcer prophylaxis even before the intervention, and continuing preadmission medication was the most commonly selected indication throughout the study. Our results suggest that attention should be focused on both the inpatient and outpatient settings when designing future initiatives to improve the appropriateness of acid-suppressive medication use.

Periprocedural management of antithrombotic therapy in hospitalized patients.

The management of antithrombotic medications in patients requiring invasive procedures is a common problem in hospital medicine, for which there is limited evidence to guide clinical decision making. Existing guidelines do not address many hospital-based procedures and have not kept pace with the introduction of newer antiplatelet and anticoagulant medications. This article provides a conceptual framework for the periprocedural management of antithrombotic therapy, with a focus on the procedures that hospitalists are most likely to perform and the pharmacology of the common and newer antithrombotic medications.

Risk factors for nosocomial gastrointestinal bleeding and use of acid-suppressive medication in non-critically ill patients.

BACKGROUND: It is unknown whether there exist certain subsets of patients outside of the intensive care unit in whom the risk of nosocomial gastrointestinal bleeding is high enough that prophylactic use of acid-suppressive medication may be warranted. OBJECTIVE: To identify risk factors for nosocomial gastrointestinal bleeding in a cohort of non-critically ill hospitalized patients, develop a risk scoring system, and use this system to identify patients most likely to benefit from acid suppression. DESIGN: Cohort study. PATIENTS: Adult patients admitted to an academic medical center from 2004 through 2007. Admissions with a principal diagnosis of gastrointestinal bleeding or a principal procedure code for cardiac catheterization were excluded. MAIN MEASURES: Medication, laboratory, and other clinical data were obtained through electronic data repositories maintained at the medical center. The main outcome measure-nosocomial gastrointestinal bleeding occurring outside of the intensive care unit-was ascertained via ICD-9-CM coding and confirmed by chart review. KEY RESULTS: Of 75,723 admissions (median age = 56 years; 40 % men), nosocomial gastrointestinal bleeding occurred in 203 (0.27 %). Independent risk factors for bleeding included age > 60 years, male sex, liver disease, acute renal failure, sepsis, being on a medicine service, prophylactic anticoagulants, and coagulopathy. Risk of bleeding increased as clinical risk score derived from these factors increased. Acid-suppressive medication was utilized in > 50 % of patients in each risk stratum. Our risk scoring system identified a high risk group in whom the number-needed-to-treat with acid-suppressive medication to prevent one bleeding event was < 100. CONCLUSIONS: In this large cohort of non-critically ill hospitalized patients, we identified several independent risk factors for nosocomial gastrointestinal bleeding. With further validation at other medical centers, the risk model derived from these factors may help clinicians to direct acid-suppressive medication to those most likely to benefit.

Assessment of hemostatic risk factors in predicting arterial thrombotic events.

Arterial thrombosis results from endovascular injury and, to a lesser extent, alterations in hemostatic equilibrium. Although multiple hereditary and acquired hemostatic risk factors have been described in the pathophysiology of venous thrombosis, the degree and type of abnormalities that contribute to arterial thrombosis are less well understood. Endothelial cell injury with the elaboration of proinflammatory mediators stimulates the process of arterial thrombosis. Although this is most often the result of endovascular injury attributable to atherosclerotic disease, other disease states can elicit a similar response as well. Similarly, once thrombosis has been initiated, variations in the activity of coagulation proteins and endogenous anticoagulants, as well as the kinetics of platelet aggregation, may alter the effectiveness of thrombus formation. Epidemiological studies have identified several acquired or inherited states that may result in endothelial damage or altered hemostatic equilibrium, thereby predisposing patients to arterial thrombosis. These include hyperhomocysteinemia, elevated C-reactive protein, antiphospholipid antibodies, elevated fibrinogen, Factor VII, plasminogen activator inhibitor-1 (PAI-1), hereditary thrombophilias, and platelet hyper-reactivity. This review explores our present understanding of these risk factors in the development of arterial thrombotic events. At present, the literature supports a role for hyperhomocysteinemia, elevated C-reactive protein, and elevated fibrinogen as risk factors for arterial thrombosis. Similarly, the literature suggests that lupus anticoagulants and, to a lesser extent, elevated titers of cardiolipin IgG antibodies predispose to arterial vascular events. In certain subsets of patients, including those with concomitant cardiac risk factors, <55 years of age, and women, hereditary thrombophilias such as carriership of the factor V Leiden and the prothrombin G20210A mutations may confer a higher risk of arterial thrombosis. However, the data on Factor VII, PAI-1, and platelet receptor polymorphisms are contradictory or lacking.