Continuation of chronic antiplatelet therapy is not associated with increased need for transfusions: a cohort study in critically ill septic patients.

Background: The decision to maintain or halt antiplatelet medication in septic patients admitted to intensive care units presents a clinical dilemma. This is due to the necessity to balance the benefits of preventing thromboembolic incidents and leveraging anti-inflammatory properties against the increased risk of bleeding.

Methods: This study involves a secondary analysis of data from a prospective cohort study focusing on patients diagnosed with severe sepsis or septic shock.

Liberal transfusion strategy to prevent mortality and anaemia-associated, ischaemic events in elderly non-cardiac surgical patients - the study design of the LIBERAL-Trial.

Background: Perioperative anaemia leads to impaired oxygen supply with a risk of vital organ ischaemia. In healthy and fit individuals, anaemia can be compensated by several mechanisms. Elderly patients, however, have less compensatory mechanisms because of multiple co-morbidities and age-related decline of functional reserves.

American Society of Hematology 2018 guidelines for management of venous thromboembolism: heparin-induced thrombocytopenia.

Background: Heparin-induced thrombocytopenia (HIT) is an adverse drug reaction mediated by platelet-activating antibodies that target complexes of platelet factor 4 and heparin. Patients are at markedly increased risk of thromboembolism.

Objective: These evidence-based guidelines of the American Society of Hematology (ASH) are intended to support patients, clinicians, and other health care professionals in their decisions about diagnosis and management of HIT.

Emergency transfusion of patients with unknown blood type with blood group O Rhesus D positive red blood cell concentrates: a prospective, single-centre, observational study.

Background: Emergency patients with unknown blood type usually receive O Rhesus D negative (RhD-) red blood cell concentrates until their blood group is determined to prevent RhD+ related adverse transfusion reactions. As 85% of individuals are RhD+, this consumption of O RhD- red blood cell concentrates contributes to shortages of O RhD- red blood cell concentrates, sometimes forcing transfusion of known RhD- patients with RhD+ red blood cell concentrates. Here we report the outcome of this transfusion policy transfusing all emergency patients with unknown blood type with O RhD+ red blood cell concentrates.

How I evaluate and treat thrombocytopenia in the intensive care unit patient.

Multiple causes (pseudothrombocytopenia, hemodilution, increased consumption, decreased production, increased sequestration, and immune-mediated destruction of platelets) alone or in combination make thrombocytopenia very common in intensive care unit (ICU) patients. Persisting thrombocytopenia in critically ill patients is associated with, but not causative of, increased mortality. Identification of the underlying cause is key for management decisions in individual patients.

Heparin-induced thrombocytopenia in cardiac surgery and critically ill patients.

Thrombocytopenia as well as anti-platelet factor 4/heparin (PF4/H) antibodies are common in cardiac surgery patients and those treated in the intensive care unit. In contrast, heparin-induced thrombocytopenia (HIT) is uncommon in these populations (~1 % and ~0.5 %, respectively).

Further insights into the anti-PF4/heparin IgM immune response.

Anti-platelet factor 4 (PF4)/heparin antibodies are not only the cause of heparin-induced thrombocytopenia but might also play a role in the antibacterial host defence. Recently, marginal zone (MZ) B cells were identified to be crucial for anti-PF4/heparin IgG antibody production in mice. Combining human studies and a murine model of polymicrobial sepsis we further characterised the far less investigated anti-PF4/heparin IgM immune response.

Discrepant post filter ionized calcium concentrations by common blood gas analyzers in CRRT using regional citrate anticoagulation.

Introduction: Ionized calcium (iCa) concentration is often used in critical care and measured using blood gas analyzers at the point of care. Controlling and adjusting regional citrate anticoagulation (RCA) for continuous renal replacement therapy (CRRT) involves measuring the iCa concentration in two samples: systemic with physiological iCa concentrations and post filter samples with very low iCa concentrations. However, modern blood gas analyzers are optimized for physiological iCa concentrations which might make them less suitable for measuring low iCa in blood with a high concentration of citrate.

Prevalence and clinical implications of anti-PF4/heparin antibodies in intensive care patients: a prospective observational study.

Data on the frequency of anti-platelet factor 4/heparin (PF4/H) antibodies and their association with outcomes in intensive care unit (ICU) patients are sparse. In this prospective, observational study we screened 320 consecutive surgical/medical ICU patients for anti-PF4/H antibodies by enzyme-immunoassay (EIA) for immunoglobulin (Ig)G/A/M separately and heparin-induced platelet activation assay (HIPA) at ICU admission (=baseline), day 6, and day 10. HIPA-positive patients were additionally tested by serotonin-release assay (SRA).

Thrombocytopenia in the intensive care unit-diagnostic approach and management.

Thrombocytopenia often complicates critical illness and is associated with increased morbidity and mortality. Approaching thrombocytopenia is challenging in the intensive care unit (ICU) because of the multifactorial pathogenesis of this disorder. Interpretation of the platelet count course after ICU admission is helpful to narrow down the cause of thrombocytopenia.

Heparin-induced thrombocytopenia.

Heparin-induced thrombocytopenia (HIT) is caused by platelet-activating immunoglobulin (Ig) G antibodies that recognize multimolecular complexes of platelet factor 4 (PF4) bound to heparin or other polyanions. Most laboratory assays for HIT have a high sensitivity for anti-PF4/heparin antibodies and a negative test generally excludes HIT (high negative predictive value), especially in a setting of a low pretest probability. The magnitude of a positive test result correlates with greater likelihood of HIT.

Anti-protamine-heparin antibodies: incidence, clinical relevance, and pathogenesis.

Protamine, which is routinely used after cardiac surgery to reverse the anticoagulant effects of heparin, is known to be immunogenic. Observing patients with an otherwise unexplained rapid decrease in platelet count directly after protamine administration, we determined the incidence and clinical relevance of protamine-reactive antibodies in patients undergoing cardiac-surgery. In vitro, these antibodies activated washed platelets in a FcγRIIa-dependent fashion.

Heparin-induced thrombocytopenia: further evidence for a unique immune response.

Cardiopulmonary bypass surgery (CPB) is associated with a high incidence of IgG Abs against platelet factor 4/heparin (PF4/H) complexes by day 6 after surgery. These Abs are associated with an immune-mediated adverse drug reaction, heparin-induced thrombocytopenia. Although the early onset of the anti-PF4/H IgG response is compatible with a secondary immune response, the rapid decline of Ab titers thereafter is not.

The diagnostic value of the anti-PF4/heparin immunoassay high-dose heparin confirmatory test in cardiac surgery patients.

There are limited and conflicting data on how a confirmatory step using high-dose heparin can improve diagnostic specificity of the antiplatelet factor 4/heparin enzyme immunoassay for heparin-induced thrombocytopenia (HIT). We investigated sera from a recently published study on cardiac surgery patients and found that only half of the sera that were heparin-induced platelet activation assay positive could be inhibited (optical density <40%) by high-dose heparin (100 IU/mL) in the enzyme immunoassay. More importantly, only 2 of the 3 patients with definite HIT were confirmatory test positive.

Incidence and clinical relevance of anti-platelet factor 4/heparin antibodies before cardiac surgery.

Background: Heparin-induced thrombocytopenia (HIT) is caused by anti-platelet factor 4/heparin (PF4/H) immunoglobulin (Ig) G antibodies, which activate platelets. In some patients, anti-PF4/H antibodies are already detectable before cardiac surgery. Whether preoperative presence of antibodies confers adverse prognosis and which particular antibody classes (IgG, IgA, IgM) might be implicated are unknown.

Perioperative thrombocytopenia in cardiac surgical patients - incidence of heparin-induced thrombocytopenia, morbidities and mortality.

Objectives: Heparin-induced thrombocytopenia (HIT) is a life-threatening complication of heparin therapy. At our institution, postoperative cardiac surgical patients are screened for HIT antibodies, when platelet counts persist to be less than 50% of the baseline level or less than 50000 nl(-1). In the present study, we compared the outcomes in HIT-antibody-positive and HIT-antibody-negative patients.

Studies of the anti-platelet factor 4/heparin immune response: adapting the enzyme-linked immunosorbent spot assay for detection of memory B cells against complex antigens.

Background: The anti-platelet factor 4 (PF4)/heparin immune response, which underlies heparin-induced thrombocytopenia (HIT), has several atypical features: relatively rapid onset even without previous heparin exposure, lack of immune anamnesis, and transience of antibody production.

Study Design And Methods: We modified the enzyme-linked immunosorbent spot (ELISPOT) assay to investigate for PF4/heparin-specific memory B cells in cardiac surgery patients, in whom the high anti-PF4/heparin immunization rate made a prospective study feasible. The PF4-containing antigen complexes were attached to microtiter plates via a spacer, rather than using nitrocellulose, and the final reaction enzyme substrate was added in melted agarose which, after rapid hardening, localized color development of enzyme-tagged anti-immunoglobulin G (IgG) probes to single PF4/heparin-specific B cells.

Heparin-induced thrombocytopenia in intensive care patients.

Heparin-induced thrombocytopenia (HIT) is a serious, prothrombotic, immune-mediated complication of heparin therapy that can cause limb- and life-threatening thromboembolic events. Prompt diagnosis and therapeutic dose anticoagulation by an alternative anticoagulant are crucial to improve clinical outcome. In critically ill patients, the diagnosis of HIT is difficult due to the high incidence of thrombocytopenia, often caused by reasons other than HIT, and the high incidence of clinically irrelevant, non-platelet-activating anti-PF4-heparin antibodies.

Management of anticoagulation in patients with subacute heparin-induced thrombocytopenia scheduled for heart transplantation.

Anticoagulation management of patients with recent heparin-induced thrombocytopenia (HIT) requiring cardiopulmonary bypass (CPB) surgery is a serious challenge, and especially difficult in patients requiring urgent heart transplantation. As nonheparin anticoagulants during CPB bear a high risk of major bleeding, these patients are at risk of being taken off the transplant list. Short-term use of unfractionated heparin (UFH) for CPB, with restriction of UFH to the surgery itself, is safe and effective in patients with a history of HIT who test negative for antiplatelet factor 4 (PF4)/heparin antibodies.

Immune heparin-induced thrombocytopenia can occur in patients receiving clopidogrel and aspirin.

Platelet adenosine diphosphate (ADP) receptors may play a role in potentiating platelet activation induced by IgG from patients with immune heparin-induced thrombocytopenia (HIT), as shown by previous studies using the ADP receptor antagonists AR-C66096 and ticlopidine. Consistent with these observations, we found that platelet activation by HIT sera is also significantly reduced in patients receiving clopidogrel, an ADP receptor antagonist prodrug now in wide clinical use. Despite these in vitro and ex vivo findings, we observed two patients develop acute HIT while receiving both clopidogrel and aspirin: both patients' sera tested strongly positive in a heparin-dependent washed platelet activation assay (100% serotonin release) and PF4/heparin-enzyme-immunoassay (2.

Heparin-induced thrombocytopenia and cardiopulmonary bypass: perioperative argatroban use.

Heparin-induced thrombocytopenia (HIT), a serious complication of heparin therapy, mandates heparin cessation and alternative anticoagulation. We report a patient with a history of HIT who successfully underwent cardiopulmonary bypass (CPB) using short-term reexposure to heparin and perioperative therapy with argatroban. No bleeding complications or HIT-related problems occurred.