Hits

Distribution by Scientific Domains
Distribution within Medical Sciences

Kinds of Hits

  • being hit
  • second hit

  • Terms modified by Hits

  • hit antibody
  • hit rate
  • hit ratio

  • Selected Abstracts


    Emergency Department Information System Adoption in the United States

    ACADEMIC EMERGENCY MEDICINE, Issue 5 2010
    Adam B. Landman MD
    Abstract Objectives:, The American Recovery and Reinvestment Act of 2009 incentivizes adoption of health care information technology (HIT) based on support for specific standards, policies, and features. Limited data have been published on national emergency department information systems (EDIS) adoption, and to our knowledge, no prior studies have considered functionality measures. This study determined current national estimates of EDIS adoption using both single-response rates of EDIS adoption and a novel feature-based definition and also identified emergency department (ED) characteristics associated with EDIS use. Methods:, The 2006 National Hospital Ambulatory Medical Care Survey, a nationally representative sample of ED visits that also surveyed participating EDs on EDIS, was used to estimate EDIS adoption. EDIS adoption rates were calculated using two definitions: 1) single-response,response to a single survey question as to whether the EDIS was complete, partial, or none; and 2) feature-based,based on the reported features supported by the EDIS, systems were categorized as fully functional, basic, other, or none. The relationship of EDIS adoption to specific ED characteristics such as facility type and location was also examined. Results:, Using the single-response classification, 16.1% of EDs had a complete EDIS, while 30.4% had a partial EDIS, and 53.5% had none. In contrast, using a feature-based categorization, 1.7% EDs had a fully functional EDIS, 12.3% had basic, 32.1% had other, and 53.9% had none. In multivariable analysis, urban EDs were significantly more likely to have a fully functional or basic EDIS than were rural EDs. Pediatric EDs were significantly more likely than general EDs to have other EDIS. Conclusions:, Despite more optimistic single-response estimates, fewer than 2% of our nation's EDs have a fully functional EDIS. EDs in urban areas and those specializing in the care of pediatric patients are more likely to support EDIS. Accurate and consistent EDIS adoption estimates are dependent on whether there are standardized EDIS definitions and classifications of features. To realize the potential value of EDIS for improved emergency care, we need to better understand the extent and correlates of the diffusion of this technology and increase emergency medicine engagement in national HIT policy-making. Academic Emergency Medicine 2010; 17:536,544 © 2010 by the Society for Academic Emergency Medicine [source]


    Should patients be informed about the risk of heparin-induced thrombocytopenia before prolonged low-molecular-weight heparin thromboprophylaxis post-trauma/orthopedic surgery?

    EUROPEAN JOURNAL OF HAEMATOLOGY, Issue 3 2007
    Norbert Lubenow
    Abstract Objectives:, Heparin-induced thrombocytopenia (HIT) is an immune-mediated prothrombotic adverse drug effect that occurs less frequently with low-molecular-weight heparin (LMWH) than with unfractionated heparin (UFH) in post-trauma/orthopedic surgery patients. The life-threatening nature of HIT raises the question whether informed consent for this treatment-induced adverse effect should be obtained, particularly as LMWH is often continued during the outpatient period when clinical and platelet count monitoring become problematic. Paradoxically, refusal of thromboprophylaxis as a result of seeking informed consent could increase risk for thrombosis. Methods:, We evaluated in patients undergoing routine LMWH thromboprophylaxis post-trauma/orthopedic surgery the feasibility of obtaining informed consent, using a standardized questionnaire to determine patient preferences. We also identified the proportion of HIT patients in our laboratory comprised of trauma/orthopedic surgery patients from 1995,1997 and 2002,2004 (time periods characterized, respectively, by UFH and LMWH thromboprophylaxis for this patient population). Results:, None of 460 patients in whom informed consent was administered rejected LMWH thromboprophylaxis. The patients' perception of the informed consent process and the written information provided about the risk of HIT and its risk due to clinical consequences were highly favorable. From 1995,1997 to 2002,2004, the proportion of HIT identified among trauma/orthopedic surgery patients declined from 30.3% to 1.2% (P < 0.0001). Conclusions:, Obtaining informed consent about HIT is feasible in written form and does not cause refusal of LMWH thromboprophylaxis. Despite the uncommon occurrence of HIT during LMWH thromboprophylaxis, informed consent increases patient's awareness of this potentially life-threatening adverse drug effect, an outcome that could increase outpatient recognition of the diagnosis. [source]


    Etiology of thrombocytopenia in all patients treated with heparin products

    EUROPEAN JOURNAL OF HAEMATOLOGY, Issue 2 2005
    Damian A. Laber
    Abstract:,Purpose:,To characterize the cause of thrombocytopenia in all patients treated with heparin products, to determine the incidence of heparin-induced thrombocytopenia (HIT) in unselected hospitalized patients, and to have modern data of the magnitude of this problem. Methods:,Retrospective hospital-based cohort study. During a random 2-month period, we reviewed the medical records of all patients treated with heparin agents, screened them for thrombocytopenia, and determined the cause of it. Results:,Out of 674 patients who received heparin products, 110 (16%) had thrombocytopenia. The most common causes included cancer chemotherapy, surgery, sepsis, and medications. Three patients met the clinical criteria for HIT. One had antibodies for heparin-platelet factor-4, and received a direct thrombin inhibitor. The other two individuals had a clinical syndrome that resembled immune HIT, but were not tested for HIT antibodies. One suffered a thrombotic episode that led to the death of her fetus. The other died of a possible thromboembolism. Conclusions:,This study provides evidence-based data for the differential diagnosis of thrombocytopenia after treatment with heparin products. Our findings suggest that increased awareness of the HIT syndrome might reduce morbidity and mortality. Patients exposed to heparin products, who develop thrombocytopenia, should not be overlooked. [source]


    Acute signalling responses to intense endurance training commenced with low or normal muscle glycogen

    EXPERIMENTAL PHYSIOLOGY, Issue 2 2010
    Wee Kian Yeo
    We have previously demonstrated that well-trained subjects who completed a 3 week training programme in which selected high-intensity interval training (HIT) sessions were commenced with low muscle glycogen content increased the maximal activities of several oxidative enzymes that promote endurance adaptations to a greater extent than subjects who began all training sessions with normal glycogen levels. The aim of the present study was to investigate acute skeletal muscle signalling responses to a single bout of HIT commenced with low or normal muscle glycogen stores in an attempt to elucidate potential mechanism(s) that might underlie our previous observations. Six endurance-trained cyclists/triathletes performed a 100 min ride at ,70% peak O2 uptake (AT) on day 1 and HIT (8 × 5 min work bouts at maximal self-selected effort with 1 min rest) 24 h later (HIGH). Another six subjects, matched for fitness and training history, performed AT on day 1 then 1,2 h later, HIT (LOW). Muscle biopsies were taken before and after HIT. Muscle glycogen concentration was higher in HIGH versus LOW before the HIT (390 ± 28 versus 256 ± 67 ,mol (g dry wt),1). After HIT, glycogen levels were reduced in both groups (P < 0.05) but HIGH was elevated compared with LOW (229 ± 29 versus 124 ± 41 ,mol (g dry wt),1; P < 0.05). Phosphorylation of 5,AMP-activated protein kinase (AMPK) increased after HIT, but the magnitude of increase was greater in LOW (P < 0.05). Despite the augmented AMPK response in LOW after HIT, selected downstream AMPK substrates were similar between groups. Phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK) was unchanged for both groups before and after the HIT training sessions. We conclude that despite a greater activation AMPK phosphorylation when HIT was commenced with low compared with normal muscle glycogen availability, the localization and phosphorylation state of selected downstream targets of AMPK were similar in response to the two interventions. [source]


    An evaluation of monitoring possibilities of argatroban using rotational thromboelastometry and activated partial thromboplastin time

    ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 1 2010
    M. ENGSTRÖM
    Background: Rotational thrombelastometry/thrombelastography with ROTEM® and TEG® is becoming available bedside in an increasing number of intensive care units, where many patients with heparin-induced thrombocytopenia (HIT) are treated. The study has been performed in an effort to find out whether ROTEM® could be an alternative to activated partial thromboplastin time (aPTT) when argatroban is used for anticoagulation. Methods: Argatroban was added in vitro to a series of citrated whole-blood samples from 10 healthy volunteers to obtain whole-blood concentrations of 0, 0.125, 0.25, 0.5, 1.0, 2.0, 4.0 and 8.0 mg/l. ROTEM® and whole-blood aPTT analyses were performed at each argatroban concentration. Correlation analyses were performed using the Spearman correlation analysis. Results: There was a significant and strong correlation between argatroban concentrations and clotting time (CT in ROTEM® analysis with INTEM) (P<0.0001 and r=0.98). Also, the ROTEM® time to maximum clot formation velocity (MAXV-t) appeared to have a very strong and highly significant correlation to argatroban concentrations (P<0.0001 and r=0.95). When we studied the correlation between aPTT and CT, we found a highly significant and strong correlation between these two analyses (P<0.0001 and r=0.97), especially so in the clinically relevant therapeutic range up to 100 s aPTT prolongation for HIT patients. Conclusion: A significant and strong correlation was found between argatroban concentrations and several ROTEM® parameters. Rotational thrombelastometry/thrombelastography has a potential role in increasing the safety of argatroban anticoagulation in critically ill patients. [source]


    Hypothermic cardiopulmonary bypass as a determinant of late thrombocytopenia following cardiac operations in pediatric patients

    ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 8 2009
    M. RANUCCI
    Background: Thrombocytopenia after cardiac operations is a common event in both adult and pediatric patients. Late thrombocytopenia (LTCP) is a less common event that is still without a well-recognized cause. This study explores the role of heparin-induced thrombocytopenia (HIT) and other factors (complexity of the operation, temperature management, and drug use) in determining LTCP. Methods: We conducted an observational study of 63 consecutive patients aged <36 months operated with or without cardiopulmonary bypass (CPB). LTCP was defined as a platelet count <100,000 cells/,l or <50% of the pre-operative count at any point in time between post-operative days 5 and 10. A diagnostic test for heparin-platelet factor 4 (PF4) antibodies was performed in patients with LTCP. Other pre- and post-operative factors were investigated for their association with LTCP. Results: LTCP occurred in 15 (24%) patients. No patient had positive heparin-PF4 antibodies. The lowest temperature on CPB was an independent predictor of LTCP, with a cut-off value at 29 °C (sensitivity 80%, specificity 70%). Other factors associated with LTCP were prolonged post-operative use of unfractionated heparin and milrinone. LTCP was associated with increased post-operative morbidity. Conclusion: LTCP was related to a combination of factors (operation severity, degree of hypothermia during CPB, prolonged use of unfractionated heparin, and milrinone). The individual contribution of each factor seems difficult to establish. However, the degree of hypothermia during CPB and drug-associated effects were identified. HIT could be excluded in all cases. [source]


    Prevalence of heparin-induced antibodies in patients with chronic renal failure undergoing hemodialysis

    JOURNAL OF CLINICAL LABORATORY ANALYSIS, Issue 5 2005
    Iván Palomo
    Abstract Heparin-induced thrombocytopenia (HIT) type II is a serious complication of heparin therapy. It presents initially as thrombocytopenia, and is associated with thrombosis in 20,50% of the cases. HIT is related to the presence of heparin-induced antibodies (HIA), which show specificity for the PF4-heparin (PF4-H) complex. The Fc,RIIa receptor has been suggested to participate in the pathogenic mechanism of HIA. Since patients undergoing chronic hemodialysis (HD) are exposed repeatedly to heparin, we studied the prevalence of HIA and their eventual relationship with thrombocytopenia and/or thrombosis, and the possible participation of the Fc,RIIa polymorphism. We studied 207 patients with chronic renal failure (CRF) undergoing HD. As a control we included 130 blood donors and 28 patients with CRF without HD. The HIA patients were studied with the use of a PF4-H ELISA. Additionally, in some positive cases for the previous test, a 14C- serotonin release assay (14C-SRA) was performed. The polymorphism Fc,RIIa H/R131 was studied by polymerase chain reaction (PCR) with allele-specific primers. Thirty-seven patients (17.9%) undergoing HD presented with HIA. The majority of these antibodies were IgG, IgM, and IgA. The HIA investigated presented specificity against the PF4-H complex, but not against PF4 alone (P<0.001). Twelve out of 22 (54.5%) PF4-H antibodies were positive when tested with the 14C-SRA. The distribution of the Fc,RIIa polymorphism in patients and healthy controls was 42.6% and 41.6% for H/H131, 41% and 48.9% for the H/R131 isoform, and 16.4% and 9.5% for the R/R131 isoform, respectively. No statistically significant difference in the Fc,RIIa isoform distribution was found. Twenty-nine out of 156 patients (18.5%) presented thrombocytopenia, and 21/207 (12.4%) had thrombosis of the native vein arterio-venous fistula (AVF). We did not find any statistically significant between HIA and thrombocytopenia or thrombosis. An important proportion of patients with CRF undergoing HD developed HIA, but these cases were not associated with thrombocytopenia or thrombosis of AVF. The frequency of the Fc,RIIa polymorphism did not statistically differ between HIT type II and normal controls. J. Clin. Lab. Anal. 19:189,195, 2005. © 2005 Wiley-Liss, Inc. [source]


    BIOGENIC AMINE CONTENT OF SOME TURKISH CHEESES

    JOURNAL OF FOOD PROCESSING AND PRESERVATION, Issue 4 2002
    FÜGEN DURLU-ÖZKAYA
    Biogenic amines in ten samples of Ka,ar (aged), five samples of Ka,ar (fresh), four samples of Mihaliç, nine samples of Van Otlu (herbed), nine samples of Örgü, nine samples of Urfa and six samples of Civil cheeses were obtained from local supermarkets of Ankara. Tryptamine (TRY), phenylethylamine (PHA), putrescine (PUT), cadaverine (CAD), histamine (HIT), tyramine (TYA), spermine (SPM) and spermidine (SPD) contents of Turkish cheese samples were screened by high performance liquid chromatography (HPLC). PUT, CAD, HIT, TYA and SPD were the predominant biogenic amines in maturated Ka,ar (aged), vacuum-packed Ka,ar (fresh), Mihaliç, Otlu (herbed) and Örgü cheeses. PHA, CAD, TYA and SPD were the predominant biogenic amines in Urfa cheese samples. Civil cheeses were found to contain the highest HIT and TYA content with an average of 94.76 mg/100 g and 138.16 mg/100 g, respectively, much higher than the toxic dose. HIT level of Mihaliç cheeses were also higher than the accepted limit. The concentration of amines in all other cheeses was much lower than the toxic dose limits. [source]


    Thrombocytopenia in Patients Treated with Heparin, Combination Antiplatelet Therapy, and Intra-Aortic Balloon Pump Counterpulsation

    JOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 4 2008
    B.C.P.S., HEATHER R. BREAM-ROUWENHORST Pharm D.
    Objectives:Determine the incidence and timing of intra-aortic balloon pump (IABP)-associated thrombocytopenia, if concomitant antiplatelet agents increase the incidence of thrombocytopenia, and the incidence of heparin-induced thrombocytopenia (HIT) in a contemporary IABP population. Background:Previous studies predate the current practice of treating acute coronary syndrome patients with heparin and aspirin plus thienopyridines and glycoprotein IIb/IIIa receptor antagonists such that data are unavailable to determine if their co-administration worsens IABP-associated thrombocytopenia. Methods:A retrospective cohort study of adult IABP patients (n = 107) from 2002 to 2006 was performed to determine the indication for and duration of counterpulsation, platelet counts during and for 7 days postcounterpulsation, medications potentially contributing to thrombocytopenia, and HIT antibody results if obtained. Results:Thrombocytopenia, defined as platelets <150,000/mL or >50% decrease from baseline, occurred in 57.9% of patients. Overall, platelets declined to 60.2 ± 22.8% of baseline with the mean (± standard deviation) nadir on day 2.8 ± 2.0. Comparing patients who received heparin, aspirin, thienopyridines, and glycoprotein IIb/IIIa antagonists (n = 44) versus heparinized patients ± aspirin (n = 45), platelet nadirs were 62.7 ± 20.9% versus 58.3 ± 23.9% of baseline levels, respectively (P = 0.42). The incidence of HIT was 2.8% in the entire cohort. Conclusions:IABP-associated thrombocytopenia occurred in 57.9% of this cohort. HIT was diagnosed in 2.8% and should be considered as a diagnosis if platelet counts do not stabilize or continue to fall after 3,4 days of counterpulsation. Increased use of antiplatelet therapy does not impact the degree of thrombocytopenia although the current practice of prompt IABP removal may offset this effect. [source]


    Early-onset and persisting thrombocytopenia in post-cardiac surgery patients is rarely due to heparin-induced thrombocytopenia, even when antibody tests are positive

    JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 1 2010
    S. SELLENG
    See also Gruel Y, Pouplard C. Post-operative platelet count profile: the most reliable tool for identifying patients with true heparin-induced thrombocypenia after cardiac surgery. This issue, pp 27,29. Summary.,Background:,The high frequency of thrombocytopenia in post-cardiac surgery patients makes it challenging to diagnose heparin-induced thrombocytopenia (HIT). Two platelet count profiles are reported as indicating possible HIT in these patients: profile 1 describes a platelet count fall that begins between postoperative days 5 and 10, whereas profile 2 denotes early-onset thrombocytopenia that persists beyond day 5. Objectives: To examine how these platelet count profiles correlate with antibody status and HIT post-cardiac surgery. Methods: We prospectively screened 581 cardiac surgery patients for heparin-dependent antibodies by platelet factor 4 (PF4),heparin immunoassay and platelet-activation test, and performed daily platelet counts (until day 10) with 30-day follow-up. Results: All three patients with platelet count profile 1 tested positive for platelet-activating anti-PF4,heparin IgG antibodies [odds ratio (OR) 521.7, 95% confidence interval (CI) 3.9,34 000, P = 0.002], and were judged to have HIT. In contrast, none of 25 patients with early-onset and persisting thrombocytopenia (profile 2) was judged to have HIT, including five patients testing positive for platelet-activating anti-PF4,heparin IgG antibodies. In these patients, the frequency of heparin-dependent antibodies did not differ from that in non-thrombocytopenic controls, either for anti-PF4,heparin IgG (OR 1.7, 95% CI 0.7,4.1, P = 0.31) or for platelet-activating antibodies (OR 1.9, 95% CI 0.6,5.7, P = 0.20). Multivariate analysis revealed that type of cardiac surgery, but not HIT antibody status, predicted early-onset and persisting thrombocytopenia. Together, these findings show that HIT was uncommon in this study population [overall frequency, 3/581 (0.5%), 95% CI 0.1,1.5%]. Conclusions: Thrombocytopenia that begins between 5 and 10 days post-cardiac surgery is highly predictive for HIT. In contrast, early-onset and persisting thrombocytopenia is usually caused by non-HIT factors with coinciding heparin-dependent antibody seroconversion. [source]


    The costs of heparin-induced thrombocytopenia: a patient-based cost of illness analysis

    JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 5 2009
    T. WILKE
    Summary.,Background and objectives:,Due to the complexity of heparin-induced thrombocytopenia (HIT), currently available cost analyses are rough estimates. The objectives of this study were quantification of costs involved in HIT and identification of main cost drivers based on a patient-oriented approach. Methods:,Patients diagnosed with HIT (1995,2004, University-hospital Greifswald, Germany) based on a positive functional assay (HIPA test) were retrieved from the laboratory records and scored (4T-score) by two medical experts using the patient file. For cost of illness analysis, predefined HIT-relevant cost parameters (medication costs, prolonged in-hospital stay, diagnostic and therapeutic interventions, laboratory tests, blood transfusions) were retrieved from the patient files. The data were analysed by linear regression estimates with the log of costs and a gamma regression model. Mean length of stay data of non-HIT patients were obtained from the German Federal Statistical Office, adjusted for patient characteristics, comorbidities and year of treatment. Hospital costs were provided by the controlling department. Results and conclusions:,One hundred and thirty HIT cases with a 4T-score ,4 and a positive HIPA test were analyzed. Mean additional costs of a HIT case were 9008 ,. The main cost drivers were prolonged in-hospital stay (70.3%) and costs of alternative anticoagulants (19.7%). HIT was more costly in surgical patients compared with medical patients and in patients with thrombosis. Early start of alternative anticoagulation did not increase HIT costs despite the high medication costs indicating prevention of costly complications. An HIT cost calculator is provided, allowing online calculation of HIT costs based on local cost structures and different currencies. [source]


    Quantitative interpretation of optical density measurements using PF4-dependent enzyme-immunoassays

    JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 8 2008
    T. E. WARKENTIN
    Summary.,Background:,Many laboratories test for heparin-induced thrombocytopenia (HIT) using a PF4-dependent enzyme-immunoassay (EIA). An advantage of the EIA is its simplicity; a disadvantage is that it only indirectly detects heparin-dependent, platelet-activating antibodies (,HIT antibodies'). Objectives:,To determine whether the magnitude of a positive EIA result, expressed in optical density (OD) units, predicts risk of HIT antibodies, defined as a strong-positive platelet serotonin-release assay (SRA) result (,50% serotonin release). Patients/methods:,We determined the risk of a strong-positive SRA result for five categories of OD reactivity (<0.40, 0.40,<1.00, 1.00,<1.40, 1.40,<2.00, and ,2.00 OD units) using two EIAs (commercial anti-PF4/polyanion IgG/A/M and in-house anti-PF4/heparin,IgG). Results:,For patient sera investigated for HIT antibodies, a weak-positive result (0.40,<1.00 OD units) in either EIA indicated a low probability (,5%) of a strong-positive SRA; the risk increased to ,90% with an OD , 2.00 units. Quantifying the EIA,SRA relationship for 1553 referred patient sera, we found that for every increase of 0.50 OD units in the EIA,IgG, the risk of a strong-positive SRA result increased by OR = 6.39 [95% confidence interval (CI), 5.13, 7.95; P < 0.0001]. For every increase of 1.00 OD units in the EIA,IgG, the risk increased by OR = 40.81 (95% CI, 26.35, 63.20; P < 0.0001). Conclusions:,The probability of HIT antibodies (strong-positive SRA result) inferred by a positive PF4-dependent EIA varies considerably in relation to the magnitude of the EIA result, expressed as OD values. In our laboratory, the probability of HIT antibodies being present reached ,50% only when the OD level was ,1.40 units. [source]


    Heparin-induced thrombocytopenia: a prospective study on the incidence, platelet-activating capacity and clinical significance of antiplatelet factor 4/heparin antibodies of the IgG, IgM, and IgA classes

    JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 8 2007
    A. GREINACHER
    Summary.,Introduction:,Platelet-activating antiplatelet factor 4/heparin (anti-PF4/heparin) antibodies are the major cause of heparin-induced thrombocytopenia (HIT). However, the relative utility of functional (platelet activation) vs. antigen [enzyme-immunoassay (EIA)] assays, and the significance of assay discrepancies remain unresolved.Methods:,Consecutive patient sera (n = 1650) referred for diagnostic HIT testing were screened prospectively by both the heparin-induced platelet activation (HIPA) test and anti-PF4/heparin EIA , including individual classes (IgG, IgA, IgM) , with clinical correlations studied. Platelet microparticle and annexin-V-binding properties of the sera were also investigated.Results:,Only 205 (12.4%) sera tested positive in either the HIPA and/or EIA: 95 (46.3%) were positive in both, 109 (53.1%) were only EIA-positive, and, notably, only one serum was HIPA-positive/EIA-negative. Of 185 EIA-positive sera, only 17.6% had detectable IgM and/or IgA without detectable IgG. Among sera positive for EIA IgG, optical density values were higher when the sera were HIPA-positive (1.117 vs. 0.768; P < 0.0001), with widely overlapping values. Two HIPA-positive but EIA-IgG-negative sera became HIPA-negative following IgG depletion, suggesting platelet-activating antibodies against non-PF4-dependent antigens. Clinical correlations showed that HIPA-negative/EIA-positive patients did not develop thrombosis and had reasons other than HIT to explain thrombocytopenia. IgM/A antibodies did not increase microparticle penetration, but increased annexin-V binding.Conclusions:,The anti-PF4/heparin EIA has high (,99%) sensitivity for HIT. However, only about half of EIA-positive patients are likely to have HIT. Anti-PF4/heparin antibodies of IgM/A class and non-PF4-dependent antigens have only a minor role in HIT. [source]


    IgG classification of anti-PF4/heparin antibodies to identify patients with heparin-induced thrombocytopenia during mechanical circulatory support

    JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 2 2007
    S. SCHENK
    Summary., Commercial immunoassays frequently detect anti-PF4/heparin antibodies during mechanical circulatory support (MCS), but only a small minority of patients develops heparin-induced thrombocytopenia (HIT). Whereas platelet functional tests can distinguish between platelet-activating and non-platelet-activating antibodies, commercial PF4-dependent immunoassays do not. Between 2003 and 2004, 113 patients were placed on MCS. Blood samples were obtained on postimplant day 5,7 for analyses by antibody assays and the functional heparin-induced platelet activation (HIPA) assay. Three distinct groups of patient sera were identified: platelet-activating anti-PF4/heparin antibodies (n = 10), non-platelet-activating anti-PF4/heparin antibodies (n = 53), and anti-PF4/heparin antibody negative (n = 50). Patients with platelet-activating antibodies had the highest risk for thromboembolic events (P < 0.005), whereas those with non-platelet-activating antibodies did not differ from antibody negative patients (P = 0.369). The enzyme-immunoassay and column agglutination assays, which cover all immunoglobulin classes, demonstrated adequate sensitivity and negative predictive value; yet, both lacked specificity with respect to the platelet-activating antibodies. If all antibody positive patients were further classified by an IgG-specific anti-PF4/heparin enzyme-immuno assay, specificity for platelet-activating antibodies increased. Whereas IgG-specific optical density (OD) values below 1.0 were likely for non-platelet-activating anti-PF4/heparin antibodies, higher values were progressively predictive for pathogenic platelet activation. The probability of the development of clinical HIT also increased steeply. In conclusion, platelet-activating anti-PF4/heparin antibodies are relatively common (about 9%) in patients on MCS and are associated with significantly higher thrombotic event rates. Low IgG-specific OD values (< 1.0) in the enzyme-immunoassay indicate low likelihood for the presence of platelet-activating antibodies. These results justify further validation so that anticoagulation during MCS becomes safer and adequate. [source]


    IN FOCUS: Activation of platelets by heparin-induced thrombocytopenia antibodies in the serotonin release assay is not dependent on the presence of heparin

    JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 10 2005
    M. M. PRECHEL
    Summary., The serotonin release assay (SRA) tests for antibodies responsible for heparin-induced thrombocytopenia (HIT). By definition, SRA-positive antibodies cause platelet serotonin release in vitro, in the presence of low concentrations of heparin, but not with excess heparin. Many SRA-positive sera activate platelets in the presence of saline without drug, either as a result of residual heparin in the specimen, or because of intrinsic features of the HIT antibodies. The present experiments show that neither exhaustive heparinase treatment, nor chromatographic removal of heparin abrogates the spontaneous platelet activation caused by these HIT antibodies. This is the first study to systematically demonstrate that in vitro activity of HIT antibodies can be independent of heparin. In addition, T-gel chromatography demonstrated differences among fractions of enzyme-linked-immunosorbent assay (ELISA)-positive HIT antibodies within individual specimens. Certain ELISA-positive fractions had SRA activity while others did not, and the SRA activity was not proportional to HIT antibody ELISA titer. These data suggest that antibodies formed as a result of heparin treatment are heterogeneous, and that some can contribute to the pathogenesis of HIT even when heparin is no longer present. [source]


    Diagnostic score for heparin-induced thrombocytopenia after cardiopulmonary bypass

    JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 11 2004
    A. Lillo-Le Louet
    Summary. Heparin-induced thrombocytopenia (HIT) occurs in nearly 3% of patients treated with heparin after cardiopulmonary bypass (CPB). HIT carries a risk of severe thrombotic complications, and must be diagnosed rapidly. To identify simple criteria for estimating the probability of HIT after CPB, we retrospectively analyzed the files of 84 patients with suspected HIT after CPB and we analyzed the usefulness of several variables collected at the time of HIT suspicion to estimate HIT probability. HIT was confirmed in 35 cases and ruled out in 49 cases, on the basis of a platelet increment after heparin withdrawal, detection of heparin-dependent antibodies, and absence of other clear cause of thrombocytopenia. A biphasic platelet count from CPB to the first day of suspected HIT, an interval of ,,5 days from CPB to the first day of suspected HIT, and a CPB duration of ,,118 min were independent risk factors for HIT. These variables were combined to create a post-CPB HIT probability score. The score correctly identified 34/35 HIT patients and 28/49-non-HIT patients. This score, which can be applied as soon as HIT is suspected after CPB, has very good negative predictive value (97%). Prospective studies are required to confirm these findings. [source]


    Heparin-induced thrombocytopenia: Current status and diagnostic challenges,

    AMERICAN JOURNAL OF HEMATOLOGY, Issue 9 2010
    Stavroula A Otis
    Heparin-induced thrombocytopenia (HIT) is a fairly common and potentially catastrophic complication of heparin therapy. Diagnosing HIT remains a challenge, as the patients at risk often have other reasons for thrombocytopenia and/or thrombosis. HIT is considered a clinicopathologic disorder whose diagnosis is generally made on the basis of both clinical criteria and the presence of "HIT antibodies" in the patient's serum or plasma. There are two basic laboratory approaches to detect HIT antibodies. The immunoassays detect antibodies based on their binding properties, whereas the functional assays detect antibodies based on their platelet-activating properties. Prompt and accurate diagnosis of HIT is imperative, as overdiagnosis exposes patients to alternative anticoagulants and their associated bleeding risks, whereas under- or delayed diagnosis leaves patients vulnerable to the thromboembolic sequelae of HIT, which can be life threatening. A critical interpretation of laboratory results by the clinician is an essential component of diagnosing HIT. This requires a keen understanding of the current concepts in the pathophysiologic mechanisms of the disease, and the application of these concepts when interpreting the results of both the functional and immunoassays. Equally important is an awareness of the strengths and weaknesses, as well as the current lack of standardization and proficiency testing, of these assays. Am. J. Hematol., 2010. © 2010 Wiley-Liss, Inc. [source]


    Heparin-induced thrombocytopenia with multiple organized thrombi accompanied by unusual cholesterin deposition: Autopsy case after long-term follow up

    PATHOLOGY INTERNATIONAL, Issue 10 2009
    Masaaki Ichinoe
    Heparin-induced thrombocytopenia (HIT) is characterized by a reduction in the platelet count and systemic thromboembolism during heparin therapy. Herein is reported a case of HIT with characteristic thrombus formation. A 68-year-old man who had been treated for hypertension for 27 years suffered a brain infarction and was treated with heparin. After this treatment, other new infarctions occurred in multiple organs. Because serum antibodies against heparin/PF4 complex were detected, he was diagnosed as having HIT, and warfarin and argatroban were administered instead of heparin. He died, however, 119 days after the first onset. At autopsy infarction due to organized thrombi with cholesterin deposition in multiple organs were found, similar to usual atherosclerotic emboli, but different to them with regard to clinical course and distribution of thrombi. This case in which organization and frequent cholesterin deposition were found in thromboembolized lesions of multiple organs after relatively long-term follow up, is unusual. The findings suggest that HIT accompanied by marked hypercholesterolemia of long duration contributes to a characteristic form of thromboembolism that needs careful management. [source]


    Recurrent acute thrombocytopenia in the hospitalized patient: Sepsis, DIC, HIT, or antibiotic-induced thrombocytopenia,,

    AMERICAN JOURNAL OF HEMATOLOGY, Issue 1 2010
    Talla A. Rousan
    First page of article [source]


    Argatroban and catheter-directed thrombolysis with alteplase for limb- and graft-threatening thromboses in a patient with a history of HIT,

    AMERICAN JOURNAL OF HEMATOLOGY, Issue 4 2009
    Angela Maldonado
    No abstract is available for this article. [source]


    Utility of consecutive repeat HIT ELISA testing for heparin-induced thrombocytopenia

    AMERICAN JOURNAL OF HEMATOLOGY, Issue 3 2008
    Maren Chan
    Heparin-induced thrombocytopenia (HIT) is a serious complication of heparin therapy. Limited data are available regarding repeat HIT antibody testing after an initial negative test. We conducted a retrospective study to determine the utility of repeat testing. Heparin antibodies were detected using the GTI-PF4 enzyme-linked immunoabsorbent assay, ELISA (GTI Diagnostics, Waukesha, WI). Patients (n = 137) were assigned to one of three groups based upon the initial negative test optical density (OD) range of low = 0,0.132, medium = 0.133,0.267, and high = 0.268,0.399. A pretest clinical score was retrospectively determined using the "4T's" (Thrombocytopenia, Timing of platelet fall, Thrombosis, and the absence of oTher causes of thrombocytopenia). A subsequent positive ELISA was found in 16% (22/137) of patients who underwent repeat testing. Most of these patients had a low pretest clinical score (62%). Four patients had an interval change in the pretest score between the initial negative and subsequent positive tests. Only these four patients developed HIT with thrombosis (HITT). Eighty percent of patients with a high initial negative test OD value had a positive ELISA on repeat testing; however, the initial negative test OD value could not predict whether a patient developed HITT. In contrast, an increase in the pretest clinical probability between initial and repeat testing better predicted HITT. Consecutive repeat ELISA testing for heparin antibodies may be warranted in patients with an increase in their pretest clinical score after an initial negative test as an adjunct to confirm the diagnosis of HIT. Am. J. Hematol., 2008. © 2007 Wiley-Liss, Inc. [source]


    Using health information technology to improve drug monitoring: a systematic review

    PHARMACOEPIDEMIOLOGY AND DRUG SAFETY, Issue 12 2009
    Geoffrey L. Hayward MD
    Abstract Purpose To conduct a systematic review of current evidence regarding the use of health information technology (HIT) interventions to improve drug monitoring in ambulatory care. Methods We searched PubMed, CINAHL, the Cochrane Library, and other computerized databases from 1 January 1998 to 30 June 2008 using the key words "drug monitoring," "medical records systems, computerized," "ambulatory care," and "outpatients." We manually reviewed reference lists of articles identified through computer searches and asked experts in the field to review our search strategy and results for completeness. Results Seven relevant studies were identified. Four of these studies assessed real-time interventions that used alerts to physicians at the time of medication ordering to ensure adequate monitoring, only one of which showed an improvement in monitoring. Of three studies using HIT outside the physician encounter, two suggested some improvement in monitoring rates. Methodological limitations were apparent in all studies identified. Conclusions Few studies have assessed the effectiveness of HIT interventions to improve drug monitoring, and among them, there is no clear consensus regarding the most consistently effective approaches to reducing drug monitoring errors. There is a clear need for well designed randomized trials to evaluate possible interventions to reduce drug monitoring errors. Such studies should incorporate health outcomes and detailed cost analyses to further characterize the feasibility of successful interventions. Copyright © 2009 John Wiley & Sons, Ltd. [source]


    Health Care Information Technology in Rural America: Electronic Medical Record Adoption Status in Meeting the National Agenda

    THE JOURNAL OF RURAL HEALTH, Issue 2 2008
    James A. Bahensky MS
    ABSTRACT:,Continuing is a national political drive for investments in health care information technology (HIT) that will allow the transformation of health care for quality improvement and cost reduction. Despite several initiatives by the federal government to spur this development, HIT implementation has been limited, particularly in the rural market. The status of technology use in the transformation effort is reviewed by examining electronic medical records (EMRs), analyzing the existing rural environment, identifying barriers and factors affecting their development and implementation, and recommending needed steps to make this transformation occur, particularly in rural communities. A review of the literature for HIT in rural settings indicates that very little progress has been made in the adoption and use of HIT in rural America. Financial barriers and a large number of HIT vendors offering different solutions present significant risks to rural health care providers wanting to invest in HIT. Although evidence in the literature has demonstrated benefits of adopting HIT such as EMRs, important technical, policy, organizational, and financial barriers still exist that prevent the implementation of these systems in rural settings. To expedite the spread of HIT in rural America, federal and state governments along with private payers, who are important beneficiaries of HIT, must make difficult decisions as to who pays for the investment in this technology, along with driving standards, simplifying approaches for reductions in risk, and creating a workable operational plan. [source]


    A simple measure to reduce the incidence of heparin induced thrombocytopenia (HIT) in cardiac intensive care patients , a retrospective observational analysis

    ANAESTHESIA, Issue 1 2009
    C. R. Evans
    No abstract is available for this article. [source]


    The Use of Bivalirudin for Cardiopulmonary Bypass Anticoagulation in Pediatric Heparin-Induced Thrombocytopenia Patients

    ARTIFICIAL ORGANS, Issue 8 2010
    Richard Gates
    Abstract Infants with heparin-induced thrombocytopenia (HIT) represent a challenging and high-risk group of patients when they require cardiopulmonary bypass (CPB). Bivalirudin offers many potential pharmacologic advantages over other nonheparin anticoagulants for such patients. We describe our protocol for the use of bivalirudin in a 5-month-old infant undergoing stage 2 Norwood for hypoplastic left heart syndrome. The patient was a 5- month-old, 6-kg infant who developed HIT after a bowel resection complicating initial Norwood stage 1. After sternotomy and dissection had been redone, the child received an initial dose of bivalirudin of 1.0 mg/kg and 0.5 mg/kg 5 min later. The CPB circuit was primed with 50 mg/kg bivalirudn/400 cc volume. With the initiation of CPB, a continuous infusion of 2.5 mg/kg bivalirudin was begun. Activated clotting time (ACT) was targeted for over 400 s, with an examination prior to bypass and each 15 min thereafter. Bivalirudin was discontinued with separation from bypass and during modified ultrafiltration (MUF). The ACT was 286 s after the initial 1 mg/kg bolus and 597 s after the second 0.5 mg/kg bolus and initiation of CPB. At a rate of 2.5 mg/kg/min, ACT ranged between 461 and 597 s. At the completion of MUF, the ACT was 316 s. The ACT was 214 s 20 min after MUF. No clots were noted in the CPB circuit, and good hemostasis was achieved within 10 min after MUF was completed. Incision to closure time was 160 min; time from completion of MUF to sternal closure was 30 min. Post-MUF, 60 cc of processed cell saver blood was reinfused, and no clotting factors were required. Chest tube output was 10, 10, 3, and 4 ccs, respectively, at hours 1,4 post operation. Bivalirudin provides effective anticoagulation in infants requiring CPB in the presence of HIT. Bivalirudin's efficacy is effectively monitored by ACT, and, after CPB, its short half-life and ability to be ultrafiltered facilitate the ability to achieve hemostasis in a timely fashion. [source]


    The Emergency Informatics Transition Course: A Flexible, Online Course in Health Informatics for Emergency Medicine Clinicians and Trainees

    ACADEMIC EMERGENCY MEDICINE, Issue 2009
    Michael Wadman
    Increasing emphasis on health information technology (HIT) as a mechanism to control costs and increase quality in health care is accelerating the diffusion of more advanced health information systems into emergency medicine. This has created an increased demand for informatics-trained emergency physicians to provide clinical input. In response to this need we partnered with the American College of Emergency Physicians (ACEP) to adapt an existing informatics educational program to emergency medicine. The American Medical Informatics Association (AMIA) 10X10 program is an effort to provide formal informatics training to 10,000 clinicians by 2010. Our first AMIA-ACEP 10X10 Emergency Informatics Transition Course matriculated 37 emergency physicians this fall. This 12 week online course is an adaption of the Oregon Health & Science University (OHSU) introductory informatics 10X10 course where students complete weekly assignments and participate in online discussions. At the end of the course they meet face-to-face at the ACEP Scientific Assembly where they present their projects and discuss common themes. The online design of the course proved adaptable for a widely varied enrollment. The first class contained students from the United States and four other countries, both large urban and small rural hospitals, and both new and experienced clinicians. Extensive input from the students will assist us in further refining this annual course to better meet the needs of emergency clinicians. We will demonstrate the design of this course, which we believe offers interested residents and fellows in emergency medicine a flexible opportunity to advance their informatics training. [source]


    The management of heparin-induced thrombocytopenia

    BRITISH JOURNAL OF HAEMATOLOGY, Issue 3 2006
    David Keeling
    Abstract The Haemostasis and Thrombosis Task Force of the British Committee for Standards in Haematology has produced a concise practical guideline to highlight the key issues in the management of heparin-induced thrombocytopenia (HIT) for the practicing physician in the UK. The guideline is evidence-based and levels of evidence are included in the body of the article. All patients who are to receive heparin of any sort should have a platelet count on the day of starting treatment. For patients who have been exposed to heparin in the last 100 d, a baseline platelet count and a platelet count 24 h after starting heparin should be obtained. For all patients receiving unfractionated heparin (UFH), alternate day platelet counts should be performed from days 4 to 14. For surgical and medical patients receiving low-molecular-weight heparin (LMWH) platelet counts should be performed every 2,4 d from days 4 to 14. Obstetric patients receiving treatment doses of LMWH should have platelet counts performed every 2,4 d from days 4 to 14. Obstetric patients receiving prophylactic LMWH are at low risk and do not need routine platelet monitoring. If the platelet count falls by 50% or more, or falls below the laboratory normal range and/or the patient develops new thrombosis or skin allergy between days 4 and 14 of heparin administration HIT should be considered and a clinical assessment made. If the pretest probability of HIT is high, heparin should be stopped and an alternative anticoagulant started at full dosage unless there are significant contraindications while laboratory tests are performed. Platelet activation assays using washed platelets have a higher sensitivity than platelet aggregation assays but are technically demanding and their use should be restricted to laboratories experienced in the technique. Non-expert laboratories should use an antigen-based assay of high sensitivity. Only IgG class antibodies need to be measured. Useful information is gained by reporting the actual optical density, inhibition by high concentrations of heparin, and the cut-off value for a positive test rather than simply reporting the test as positive or negative. In making a diagnosis of HIT the clinician's estimate of the pretest probability of HIT together with the type of assay used and its quantitative result (enzyme-linked immunosorbent assay, ELISA, only) should be used to determine the overall probability of HIT. Clinical decisions should be made following consideration of the risks and benefits of treatment with an alternative anticoagulant. For patients with strongly suspected or confirmed HIT, heparin should be stopped and full-dose anticoagulation with an alternative, such as lepirudin or danaparoid, commenced (in the absence of a significant contraindication). Warfarin should not be used until the platelet count has recovered. When introduced in combination with warfarin, an alternative anticoagulant must be continued until the International Normalised Ratio (INR) is therapeutic for two consecutive days. Platelets should not be given for prophylaxis. Lepirudin, at doses adjusted to achieve an activated partial thromboplastin time (APTT) ratio of 1·5,2·5, reduces the risk of reaching the composite endpoint of limb amputation, death or new thrombosis in patients with HIT and HIT with thrombosis (HITT). The risk of major haemorrhage is directly related to the APTT ratio, lepirudin levels and serum creatinine levels. The patient's renal function needs to be taken into careful consideration before treatment with lepirudin is commenced. Severe anaphylaxis occurs rarely in recipients of lepirudin and is more common in previously exposed patients. Danaparoid in a high-dose regimen is equivalent to lepirudin in the treatment of HIT and HITT. Danaparoid at prophylactic doses is not recommended for the treatment of HIT or HITT. Patients with previous HIT who are antibody negative (usually so after >100 d) who require cardiac surgery should receive intraoperative UFH in preference to other anticoagulants that are less validated for this purpose. Pre- and postoperative anticoagulation should be with an anticoagulant other than UFH or LMWH. Patients with recent or active HIT should have the need for surgery reviewed and delayed until the patient is antibody negative if possible. They should then proceed as above. If deemed appropriate early surgery should be carried out with an alternative anticoagulant. We recommend discussion of these complex cases requiring surgery with an experienced centre. The diagnosis must be clearly recorded in the patient's medical record. [source]


    Biological and clinical features of low-molecular-weight heparin-induced thrombocytopenia

    BRITISH JOURNAL OF HAEMATOLOGY, Issue 5 2003
    Yves Gruel
    Summary. Heparin-induced thrombocytopenia (HIT) is a common adverse effect of unfractionated heparin (UFH) therapy. In contrast, only a few patients have been reported with HIT following low-molecular-weight heparin (LMWH) therapy (LMW-HIT). To define the clinical and biological characteristics of LMW-HIT, 180 patients treated for suspected HIT at 15 French centres were investigated. Clinical history was recorded and HIT was confirmed in 59 patients with positive serotonin release assay results: 57 of them had high levels of antibodies (Abs) to heparin,platelet factor 4 complexes (H/PF4) and two had Abs to interleukin 8. Eleven patients were treated exclusively with LMWH (LMW-HIT) and 48 with UFH either alone (UF-HIT, n = 34) or combined with LMWH (UF/LMW-HIT, n = 14). The LMW-HIT and UF-HIT groups were similar with respect to sex, age, platelet count before heparin therapy, frequency of bleeding and occurrence of disseminated intravascular coagulation. The interval to onset of HIT was longer in LMW-HIT patients compared with UF-HIT patients (P = 0·03). Severe thrombocytopenia (platelets <,15 × 109/l) was more frequent in the LMW-HIT group (P = 0·04). Thrombosis occurred in three of 11 LMW-HIT patients, i.e. as frequently as in UF-HIT patients. LMW-HIT is potentially severe and may be observed after longer heparin treatment compared with UF-HIT. It is highly recommended, therefore, that platelet counts be monitored carefully whenever LMWH is administered. [source]


    Heparin-induced thrombocytopenia (HIT) causing pulmonary emboli during coronary intervention,

    CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS, Issue 6 2008
    Ronny S. Jiji MD
    Abstract Thrombotic complications of heparin-induced thrombocytopenia (HIT) can be devastating if not recognized and treated promptly. We describe an unusual case of rapid-onset HIT resulting in massive-bilateral pulmonary emboli in a 70 year-old man who developed chest pain during elective percutaneous coronary intervention (PCI). The diagnosis was made the following day after persistent chest pain and laboratory work demonstrating a new thrombocytopenia, a mildly elevated troponin, and positive DIC panel led to confirmatory imaging tests. HIT-related thrombosis should be considered in the differential diagnosis of chest pain in patients undergoing PCI. © 2008 Wiley-Liss, Inc. [source]


    12 Highly Interactive Teaching: A "HIT" with Residents

    ACADEMIC EMERGENCY MEDICINE, Issue 2008
    Linda Regan
    Covering the core content of emergency medicine during residency training is both a time consuming and challenging endeavor. One of the more significant challenges in graduate medical education is to develop more interactive, less didactic teaching modalities. In an attempt to develop a more interactive educational curriculum, we interspersed weekly sessions titled "Highly Interactive Teaching" (HIT) with standard formal lecture didactics. A primary focus of many educators in emergency medicine is teaching residents how to manage the undifferentiated patient. To this end, we revised our curriculum to include 34 four-hour symptom/chief complaint-based sessions. The first hour is an introductory lecture on the general approach to a patient with the specified complaint. Residents then divide into small groups which rotate through specific case-based sections covering varied diagnoses which might present with the symptom complaint. These faculty-run small groups use a case-based approach, either high or low simulation-based or oral boards-based format. Each faculty then is required to sum up the salient points of their section. The final hour of the day is an evidenced-based review of supporting literature. Residents are required to read and critique selected articles for the audience so that the basis for diagnosis and management decisions can be discussed as a large group discussion. We believe this change in format will help residents not only to become more active learners, but also to become more astute clinicians. [source]