Guide Platelet Transfusion Research Articles

Point-of-care, goal-directed management of bleeding in trauma patients.

The purpose of this review is to consider the clinical value of point-of-care (POC) testing in coagulopathic trauma patients with traumatic brain injury (TBI) and trauma-induced coagulopathy (TIC). Patients suffering from severe TBI or TIC are at risk of developing pronounced haemostatic disorders. Standard coagulation tests (SCTs) are insufficient to reflect the complexity of these coagulopathies. Recent evidence has shown that viscoelastic tests (VETs) identify haemostatic disorders more rapidly and in more detail than SCTs. Moreover, VET results can guide coagulation therapy, allowing individualised treatment, which decreases transfusion requirements. However, the impact of VET on mortality remains uncertain. In contrast to VETs, the clinical impact of POC platelet function testing is still unproven. POC SCTs are not able to characterise the complexity of trauma-associated coagulopathy. VETs provide a rapid estimation of underlying haemostatic disorders, thereby providing guidance for haemostatic therapy, which impacts allogenic blood transfusion requirements. The value of POC platelet function testing to identify platelet dysfunction and guide platelet transfusion is still uncertain.

Immature Platelet Counts and Thrombopoietin Plasma Concentrations in Thrombocytopenic and Non-thrombocytopenic Preterm Infants.

Objective: Immature platelet counts (IPC) may prove useful in guiding platelet transfusion management in preterm neonates. However, the relationship between IPCs and thrombopoietin (Tpo) concentrations has not been evaluated in preterm neonates.Methods: Prospective cohort study in thrombocytopenic (n = 31) and non-thrombocytopenic very low birth weight (VLBW) infants (n = 38), and healthy term neonates (controls; n = 41). Absolute platelet counts (APCs), IPCs, and Tpo concentrations were assessed by a fully-automated hematological analyzer (IPC, APC) and by ELISA (Tpo concentrations) in parallel on day 1 of life (d1), d3, and d7.Results: In healthy term neonates, APCs remained stable between d1 and d3. In non-thrombocytopenic VLBW infants, APCs increased from d1 to d7, while in the thrombocytopenia group, APCs declined from d1 to d3, before they slightly increased again by d7. Median IPCs were similar in healthy term vs. non-thrombocytopenic VLBW infants and remained stable between d1 and d3 (p > 0.05). Notably, IPCs significantly increased between d3 and d7 in both non-thrombocytopenic and thrombocytopenic VLBW infants. However, in thrombocytopenic VLBW infants, IPC values were significantly lower at each time point as compared to non-thrombocytopenic VLBWs (p < 0.001). In each subgroup, Tpo concentrations increased from d1 to d3. The median Tpo concentrations were significantly higher in thrombocytopenic as compared to non-thrombocytopenic VLBW infants at d3 (p = 0.01) and d7 (p = 0.002).Discussion: Term infants, thrombocytopenic, and non-thrombocytopenic preterm infants display similar developmental changes in indices of megakaryopoietic activity. In thrombocytopenic preterm infants, however, the responsive increases in Tpo and immature platelets appear to be developmentally limited.

Platelet Reactivity Testing for Aspirin Patients Who Sustain Traumatic Intracranial Hemorrhage

BackgroundPatients who take aspirin and sustain traumatic intracranial hemorrhage (tICH) are often transfused platelets in an effort to prevent bleeding progression. The efficacy of platelet transfusion is questionable, however, and some medical societies recommend that platelet reactivity testing (PRT) should guide transfusion decisions. The study hypothesis was that utilization of PRT to guide platelet transfusion for tICH patients suspected of taking aspirin would safely identify patients who did not require platelet transfusion. MethodsThis was a retrospective study of patients with blunt tICH who received PRT for known or suspected aspirin use between June 2014 and December 2017 at a level I trauma center. Chart abstraction was conducted to determine home aspirin status, and PRT values were used to classify patients as therapeutic or nontherapeutic on aspirin. Differences were assessed with Kruskal-Wallis and chi-square tests. Results157 patients met study inclusion criteria, and 118 (75%) patients had documented prior aspirin use. PRT results were available approximately 1.7 h (IQR: 0.9, 3.2) after arrival. Upon initial PRT, 70% of patients were considered inhibited and 88% of those patients had aspirin documented as a home medication. Conversely, 18% of patients with home aspirin use had normal platelet reactivity. Clinically significant worsening of the tICH did not significantly differ when comparing those who received platelet transfusion with those who did not (8% versus 7%, P = 0.87). ConclusionsPlatelet reactivity testing can detect platelet inhibition related to aspirin and should guide transfusion decisions for head injured patients in the initial hours after trauma.

Combined Use of Rotational Thromboelastometry (Rotem) and Platelet Impedance Aggregometry (Multiplate Analyzer) in Cyanotic and Acyanotic Infants and Children Undergoing Cardiac Surgery With Cardiopulmonary Bypass: Subgroup Analysis of a Randomized Clinical Trial

Few studies have investigated the Multiplate platelet function analyzer in pediatrics. The authors evaluated Multiplate combined with Rotem in terms of guiding platelet transfusion after pediatric cardiac surgery with cardiopulmonary bypass (CPB). The authors further compared coagulation parameters between cyanotic and acyanotic patients. Subgroup analysis of a randomized clinical trial. Tertiary hospital. Patients weighing between seven and 15 kg. None. Rotem and Multiplate tests were performed (1) after anesthesia induction, (2) upon CPB separation, and (3) upon intensive care unit arrival. Among a total of 59 subjects, 9 patients required platelet transfusion. In multivariate linear regression, analysis EXTEM maximum clot firmness upon CPB separation was associated with the volume of transfused platelets (regression coefficient = -0.348 [95% confidence interval -1.006 to -0.028]; p = 0.039). No such association was found for the Multiplate test. Acyanotic and cyanotic heart disease were present in 32 and 27 children, respectively. There were no significant differences between these two groups in terms of platelet count and function. Postoperative blood loss was significantly higher in the cyanotic group compared with the acyanotic arm (p = 0.015; difference [95% confidence interval -2.40 {-4.20 to -0.60}]). There were no differences between groups regarding transfusion of allogeneic blood products. This study showed that Rotem, but not Multiplate results, were associated with platelet transfusion in pediatric cardiac surgery with no intake of platelet inhibitors. The usefulness of combining these tests in platelet transfusion decision-making needs to be evaluated in larger populations.

Impedance Aggregometry Reveals Increased Platelet Aggregation during Liver Transplantation.

In patients presenting for liver transplantation, increased platelet aggregation as well as thrombocytopenia have been demonstrated, but bedside assays have not been investigated. We compared platelet aggregation in liver transplantation patients and control surgical patients using impedance aggregometry. We hypothesized that platelet activity is not altered during liver transplantation. After the allowance of the ethics committee, platelet aggregation was determined using impedance aggregometry with the activators ristocetin, adenosine diphosphate (ADP), arachidonic acid, collagen, and thrombin receptor-activating peptide (TRAP) in liver transplantation patients at four time points (start of surgery, anhepatic phase, reperfusion, end of surgery) and in control surgical patients. Moreover, platelet count was determined using a Coulter counter. To compensate for the thrombocytopenia often present in patients presenting for liver transplantation, the ratio between impedance aggregometry finding and platelet count was used. For statistical evaluation, the t-test or the Mann–Whitney U-test were used, as appropriate. Platelet aggregation ratio showed a 3.1-fold increase in liver transplantation patients (n = 37) in comparison to control surgical patients (n = 10) when ristocetin was used as the activator (p = 0.001). Moreover, an approximately twofold increase of ADP-, arachidonic acid-, collagen-, and TRAP-induced platelet aggregation ratio was determined. Platelet aggregation normalized at the end of the transplantation procedure. Impedance aggregometry revealed a markedly increased platelet aggregation in some liver transplantation patients and might be suitable to guide platelet transfusion and antiplatelet therapy.

Platelet Transfusion Thresholds: How Low Can We Go in Respect to Platelet Counting?

Platelet transfusion is conventionally used to prevent or treat bleeding in patients with low platelet counts or impaired platelet function. The identification of accurate thresholds of platelet count for guiding platelet transfusion practices is a crucial aspect in health care to prevent adverse events, side effects, unwarranted costs for the health care service, and deprivation of supplies. This article is therefore aimed at providing a narrative overview on current guidelines and recommendations for platelet transfusion across many clinical settings, including platelet function disorders, and critically analyzing the available platelet transfusion thresholds according to the current analytical performance of platelet counting with automated hematological analyzers. Overall, universal agreement on the definition of platelet transfusion thresholds has not been reached. The degree of accuracy and imprecision of many fully automated hematological analyzers appears also unsatisfactory, especially at the lower thrombocytopenic range, and this may thus jeopardize the managed care of patients who are candidates for platelet transfusions. Potential solutions to overcome the current shortcomings of automated platelet counting are also discussed, encompassing the use of alternative tests for guiding platelet transfusion (e.g., thrombin generation assays or thromboelastography) along with innovative approaches for platelet enumeration (e.g., fluorescent labeling and flow cytometry).

Flow cytometry for near-patient testing in premature neonates reveals variation in platelet function: a novel approach to guide platelet transfusion

BackgroundNeonatal haemorrhaging is often co-observed with thrombocytopenia; however, no evidence of a causal relationship with low platelet count has been reported. Regardless, the administration of a platelet transfusion is often based upon this parameter. Accurate measurement of platelet function in small volumes of adult blood samples by flow cytometry is well established and we propose that the use of the same technology could provide complementary information to guide the administration of platelet transfusions in premature neonates.MethodsIn 28 neonates born at 27–41 weeks gestation, platelet function after stimulation agonists was measured using fibrinogen binding and P-selectin expression (a marker of degranulation).ResultsPlatelets of neonates with gestation of ≤36 weeks (n = 20) showed reduced fibrinogen binding and degranulation with ADP, and reduced degranulation with CRP-XL. Degranulation Scores of 7837 ± 5548, 22,408 ± 5301 and 53,131 ± 12,102 (mean ± SEM) identified significant differences between three groups: <29, 29–36 and >36 weeks gestation). Fibrinogen binding and degranulation responses to ADP were significantly reduced in suspected septic neonates (n = 6) and the Fibrinogen Binding scores clearly separated the septic and healthy group (88.2 ± 10.3 vs 38.6 ± 12.2, P = 0.03).ConclusionsFlow cytometric measurement of platelet function identified clinically different neonatal groups and may eventually contribute to assessment of neonates requiring platelet transfusion.

Transfusion Practice Following Intracranial Hemorrhage in Acute Leukemia: An Institutional Review

▪Background: Intracranial hemorrhage (ICH) is a common complication in acute leukemia that is associated with significant morbidity and mortality. While evidence supports prophylactic platelet transfusions at a threshold < 10 x 109/L to reduce the risk of bleeding in acute leukemia, there is little data to guide platelet transfusion practice in patients following ICH. The objectives of this study were to characterize the clinical features and outcomes of acute leukemia patients with ICH and to understand current platelet transfusion practice following ICH.Methods: This was a retrospective study conducted at a large, quaternary, academic cancer centre. We included all adult patients with a diagnosis of acute leukemia who had a documented ICH at our centre between January 1, 2009 and December 31, 2016. We assessed demographics, medications, infection and bleeding history in the week preceding ICH, characteristics of ICH including site of bleed, acute management, transfusion practice in the first 90 days, and clinical outcomes. Radiologic scans were re-assessed by neuroradiology to determine if the ICH was stable or if new or progressive bleeding had developed. Transfusion practice following the ICH was compared between the two groups with longitudinal data analysis using platelet counts as outcome. Kaplan-Meier product limit method was used to estimate overall survival (OS) rates as well as to obtain median survival; log-rank test was used to compare OS among those without new or progressive ICH vs. those with progression.Results: During the study period, of 2576 patients diagnosed with acute leukemia, 101 suffered from ICH and were included in the study. Most patients (94) had AML, of which 9 had APL, 6 had ALL, and 1 had MPAL. At the time of ICH, 61 patients were newly diagnosed or receiving induction chemotherapy, 33 had relapsed disease and 7 were in complete remission. Spontaneous ICH occurred in 76 patients. Within the week preceding ICH, 7 patients were on medications known to increase bleeding risk and 39 were on tranexamic acid. Sixty-four patients had clinical evidence of bleeding elsewhere and 22 had evidence of infection.On the day of ICH, the median platelet count was 16 x 109/L (range 0- 433 x109/L). Thirty-one patients had a platelet count < 10 x 109/L and 10 of these patients received a platelet transfusion prior to the bleed. Seventy patients had a platelet count ≥10 x109/L and 17 of these received a platelet transfusion prior to the bleed. Six patients (6%) exhibited evidence of platelet transfusion refractoriness.In the 90 days following ICH, 21% of platelet transfusions were given for a platelet count < 10 x 109/L, 55% were given with a platelet count between 10-29 x109/L, and 24% were given with a platelet count ≥ 30 x 109/L. New or progressive ICH occurred in 28 patients. The median platelet transfusion threshold was 19 x 109/L (range 0-114 x 109/L) for those without new or progressive ICH and 21 x 109/L (range 0-93 x 109/L) for those with progression (p=0.04; Figure 1). Of the 101 study patients, 79 have died. Median OS was 5.6 months for those without new or progressive ICH and 2.9 months for those with progression (p=0.002) (Figure 2). Cause of death was attributed to non-ICH causes in the majority of patients 65/79 (82%).Conclusions: In this retrospective study, we evaluated the outcomes of 101 patients with acute leukemia and ICH. At the time of the bleed, the majority of patients had active disease and more than two thirds had platelet counts of 10 x 109/L or higher. During 90 days of follow-up, nearly one third of patients developed new or progressive ICH. Platelet transfusion practice was variable and the median threshold was, in fact, higher in those who subsequently developed new or progressive bleeding. The reasons for this were unclear from our chart review, but we hypothesize that these patients may have had additional risk factors, e.g. fever, infection. The outcomes of patients with acute leukemia and ICH are poor. Factors other than platelet transfusion threshold likely contribute to secondary ICH events and the overall poor prognosis. DisclosuresMaze:Novartis: Consultancy, Honoraria.

The application of point-of-care platelet function assay in guiding platelet transfusion in aspirin-users with intracranial haemorrhages

BackgroundAn increasing number of patients with intracranial haemorrhages are aspirin-users. Neurosurgeons commonly attempt to minimize the risk of re-bleeding by withholding the medication and giving platelet transfusion. However, recent studies raised safety concerns and showed poorer outcome with platelet transfusion when the latter was not guided by changes in platelet function. Aim of studyTo study the temporal pattern and degree of changes in platelet activities following a fixed dose of platelet transfusion in aspirin-users with intracranial haemorrhages. MethodsAspirin-users with intracranial haemorrhages underwent baseline aspirin response units (ARU) using the VerifyNow® assay. Those who showed abnormal platelet activity received a single dose of 4 units of platelet concentrate. ARU were then repeated at 4 h, 24 h and 48 h post-transfusion. Patients were classified according to their responses to transfusion. ResultsTwenty patients were recruited. At 4 h after transfusion, 11 (55%) patients had normalised platelet activities while the rest may show delayed or absent of normalization. Overall, eight (40%) patients were ‘early and persistent transfusion responders’, five ‘delayed transfusion responders’, and five (25%) had persistently abnormal platelet function. Two (10%) patients who initially responded to transfusion failed to maintain normalized platelet activity. ConclusionPlatelet activities in aspirin-users showed considerable heterogeneity up to 48 h following a blanket approach of platelet transfusion. The need for repeated transfusion or alternative therapy strongly argues for a guided practice for transfusion based on point-of-care platelet function assay. Future research should also adopt this approach to re-examine the safety and effectiveness of platelet transfusion in these patients.

Platelet dysfunction in the perioperative and critical care setting

Achieving haemostasis and, simultaneously, preventing venous thromboembolism (VTE) in the perioperative and critical care setting is challenging. Although the traditional coagulation parameters, including international normalised ratio (INR), activated partial thromboplastin time (aPTT) and platelet count, are important, evidence suggests that far more subtle aspects of platelet dysfunction may occur without antiplatelet therapy, and play a pivotal role both in critical bleeding and the pathogenesis of VTE. With advances in our ability to measure platelet activity and function beyond platelet count alone, we are making substantial progress in our understanding of how and when platelets interact and cross-talk with coagulation factors to achieve haemostasis and, conversely, contribute to the development of VTE after major surgery or trauma. With the ability to quantify the ability of platelets to aggregate, it is clear that platelet function tests have the potential to assist prediction of bleeding after cardiac surgery, especially for those who are treated with P 2 Y 12 -blockers. In addition, unregulated platelet activation or, conversely, platelet dysfunction in the absence of antiplatelet therapy, is increasingly being recognised as one of the key missing elements in the pathogenesis of VTE or critical bleeding, respectively. Our current understanding of the coagulation system—in particular the significance of platelet dysfunction and activation—may not be adaptive to benefit survival in all patients, especially after traumatic brain injury (TBI). Indeed, cardiolipin release from damaged neuronal mitochondria into the systemic circulation may explain why coagulopathy after TBI is associated with increased VTE instead of bleeding. Similarly, in patients with acquired coagulopathy due to liver disease, sepsis or trauma, excessive platelet activation has been observed explaining why these patients are not immune to developing VTE and, hence, VTE prophylaxis is still needed. While many drugs can inhibit platelet function through one of the three major platelet activation pathways—cyclooxygenase/thromboxane A 2 , P 2 Y 12 -ADP and thrombin—currently we do not have many interventions that can improve platelet function. Recent evidence suggested that an antioxidant polyphenol, resveratrol, may improve platelet function by reducing apoptosis and improving platelet mitochondrial function. We are now entering the exciting stage of precision-medicine in the area of coagulation in perioperative and critical care. Ultimately, we would be able use information beyond abnormal platelet count, INR and aPTT to guide platelet transfusion including withholding unnecessary platelet transfusion, and also avoid omission of VTE prophylaxis in the critically ill.

Platelet adenosine diphosphate receptor inhibition provides no advantage in predicting need for platelet transfusion or massive transfusion

Thrombelastography platelet mapping is a useful assay to assess antiplatelet therapy. Inhibited response to the adenosine diphosphate receptor on platelets occurs early after injury, but recent work suggests this alteration occurs even with minor trauma. However, the utility of thrombelastography platelet mapping, specifically the percent of adenosine diphosphate receptor inhibition, in predicting outcomes and guiding platelet transfusion in trauma-induced coagulopathy remains unknown We assessed the role of percent of adenosine diphosphate-inhibition in predicting survival, requirement for massive transfusion or platelet transfusion in patients at risk for trauma-induced coagulopathy. Thrombelastography platelet mapping was assessed in 303 trauma activation patients from 2014-2016 and in 89 healthy volunteers. Percent of adenosine diphosphate-inhibition is presented as median and interquartile range. We compared the area under the receiver operating characteristic curve of percent of adenosine diphosphate-inhibition, platelet count, and rapid thrombelastography maximum amplitude for in-hospital mortality, massive transfusion (>10 red blood cells or death/6hours), and platelet transfusion (>0 platelet units or death/6hour). Overall, 35 (11.5%) patient died, 27 (8.9%) required massive transfusion and 46, platelet transfusions (15.2%). Median percent of adenosine diphosphate-inhibition was 42.5% (interquartile range: 22.4-69.1%), compared with 4.3 % (interquartile range: 0-13.5%) in healthy volunteers (P<.0001). Patients that died, had a massive transfusion, or platelet transfusion had higher percent of adenosine diphosphate-inhibition than those that did not (P<.05 for all). However, percent of adenosine diphosphate-inhibition did not add significantly to the predictive performance of maximum amplitude or platelet count for any of the 3 outcomes, after adjustment for confounders. Subgroup analyses by severe traumatic brain injury, severe injury and requirement of red blood cells showed similar results. Adenosine diphosphate receptor inhibition did not add predictive value to predicting mortality, massive transfusion, or platelet transfusion. Thus, the role of thrombelastography platelet mapping as a solitary tool to guide platelet transfusions in trauma requires continued refinement.

Utility of the Aspirin and P2Y12 Response Assays to Determine the Effect of Antiplatelet Agents on Platelet Reactivity in Traumatic Brain Injury.

Premorbid antithrombotic medication may worsen intracranial injury and outcome after traumatic brain injury (TBI). Routine laboratory tests are insufficient to evaluate platelet activity. To profile the spectrum of platelet inhibition, as measured by aspirin and P2Y12 response unit assays, in a TBI population on antiplatelet therapy. This single-center, prospective cohort study included patients presenting to our institution between November 2010 and January 2015 with a clinical history of TBI. Serum platelet reactivity levels were determined immediately on admission and analyzed using the aspirin and P2Y12 response unit assays; test results were reported as aspirin response units and P2Y12 response units. We report congruence between assay results and clinical history as well as differences in assay results between types of antiplatelet therapy. A sample of 317 patients was available for analysis, of which 87% had experienced mild TBI, 7% moderate, and 6% severe; the mean age was 71.5years. The mean aspirin response units in patients with a history of any aspirin use was 456 ± 67 (range, 350-659), with 88% demonstrating therapeutic platelet inhibition. For clopidogrel, the mean P2Y12 response unit was 191 ± 70 (range, 51-351); 77% showed therapeutic response. Rapid measurement of antiplatelet function using the aspirin and P2Y12 response assays indicated as many as one fourth of patients on antiplatelet therapy do not have platelet dysfunction. Further research is required to develop guidelines for the use of these assays to guide platelet transfusion in the setting of TBI.

Intracerebral hemorrhage after pipeline embolization: Management of antiplatelet agents and the case for point-of-care testing—Case reports and review of literature

The pipeline embolization device (PED) has emerged as a highly efficient treatment modality for a wide range of intracranial aneurysms [3–5,10,14,17–19,27]. In contrast to conventional endovascular techniques, the PED provides a more physiologic approach in the treatment of intracranial aneurysms through a combination of flow diversion and endoluminal vessel reconstruction. The PED has been shown to be safe and effective in several large recent studies [1,10,14,15,18,19,24,28]. One concern with PED therapy, however, is the risk of distal intracerebral hemorrhage (ICH) [8]. This poorly understood complication occurs not uncommonly following flow diversion (1–2% of the cases) and its management is difficult since complete reversal of antiplatelet agents could result in stent thrombosis while continuing the antiplatelet agents could facilitate hemorrhage expansion. At our institution, we have recently implemented a new protocol for management of patients taking clopidogrel who present with spontaneous intraparenchymal hemorrhage and a low P2Y12 reaction units value (PRU). This protocol is used to guide platelet transfusion and antiplatelet therapy in these patients. Specifically,

Platelets in the neonatal period: developmental differences in platelet production, function, and hemostasis and the potential impact of therapies

AbstractThrombocytopenia is a common problem among sick neonates admitted to the neonatal intensive care unit. Frequently, platelet transfusions are given to thrombocytopenic infants in an attempt to decrease the incidence or severity of hemorrhage, which is often intracranial. Whereas there is very limited evidence to guide platelet transfusion practices in this population, preterm infants in the first week of life (the highest risk period for bleeding) are nearly universally transfused at higher platelet counts than older infants or children. To a large extent, this practice has been influenced by the observation that neonatal platelets are hyporeactive in response to multiple agonists in vitro, although full-term infants exhibit normal to increased primary hemostasis. This apparently paradoxical finding is due to factors in the neonatal blood that enhance the platelet-vessel wall interaction and counteract the platelet hyporeactivity. Relatively few studies have evaluated the platelet function and primary hemostasis of preterm infants, the subset of neonates at highest risk of bleeding and those most frequently transfused. Current understanding of platelet production and function in preterm and full-term neonates, how these factors affect their response to thrombocytopenia and their primary hemostasis, and the implications of these developmental differences to transfusion medicine are reviewed herein.

Platelets in the neonatal period: developmental differences in platelet production, function, and hemostasis and the potential impact of therapies.

Thrombocytopenia is a common problem among sick neonates admitted to the neonatal intensive care unit. Frequently, platelet transfusions are given to thrombocytopenic infants in an attempt to decrease the incidence or severity of hemorrhage, which is often intracranial. Whereas there is very limited evidence to guide platelet transfusion practices in this population, preterm infants in the first week of life (the highest risk period for bleeding) are nearly universally transfused at higher platelet counts than older infants or children. To a large extent, this practice has been influenced by the observation that neonatal platelets are hyporeactive in response to multiple agonists in vitro, although full-term infants exhibit normal to increased primary hemostasis. This apparently paradoxical finding is due to factors in the neonatal blood that enhance the platelet-vessel wall interaction and counteract the platelet hyporeactivity. Relatively few studies have evaluated the platelet function and primary hemostasis of preterm infants, the subset of neonates at highest risk of bleeding and those most frequently transfused. Current understanding of platelet production and function in preterm and full-term neonates, how these factors affect their response to thrombocytopenia and their primary hemostasis, and the implications of these developmental differences to transfusion medicine are reviewed herein.

Optimization of thromboelastography-guided platelet transfusion in cardiovascular surgery

Platelet dysfunction is a major cause of bleeding complications in patients undergoing cardiovascular surgery under cardiopulmonary bypass (CPB). Thromboelastography (TEG) can be used to assess post-CPB coagulopathy, but its utility in guiding platelet transfusion (PT) after CPB is unclear. This study assessed the utility of a TEG-guided PT protocol in patients undergoing cardiovascular surgery under CPB. The platelet count and TEG maximum amplitude (MA) was measured in 100 patients undergoing valvular or thoracic aortic surgery under CPB. PTs were guided by an empiric protocol in 50 patients (group C) and by a TEG-guided protocol (MA <35 mm, platelet count <7 × 10(4)/mm(3)) in the other 50 patients (group T). PT was utilized significantly less in group T (11 patients; 22%) than in group C (24 patients; 48%) (P < 0.01). The difference in PT utilization was particularly marked in patients undergoing aortic arch aneurysm repair (20% in group T vs. 100% in group C; P < 0.01), yet there was no difference in bleeding complications between these two groups. Use of a TEG-guided transfusion protocol dramatically reduced PT after CPB, particularly in patients undergoing aortic arch aneurysm repair.

Assessment of platelet transfusion for reversal of aspirin after traumatic brain injury

Platelet transfusion is utilized increasingly for traumatic brain injury (TBI) for the reversal of aspirin (ASA) therapy. Assessment of platelet inhibition and reversal by platelet transfusion after TBI has not been adequately characterized. A retrospective cohort analysis of TBI patients at a level I trauma center (January 2008-December 2009) was performed. The Aspirin Response Test (ART; VerifyNow) was used to assess platelet inhibition in TBI patients and guide platelet transfusion in patients with ASA-induced suppression. A follow-up ART was obtained after platelet administration. Primary endpoints were progression of intracranial hemorrhage on computed tomography, need for craniotomy, and mortality. We analyzed 84 patients (median age, 78 [interquartile range, 64-86)]; 54% male). ASA use was documented in 36 (42%) patients. Initial ART indicated platelet dysfunction in 54 (64%) patients, including 42% of patients without a documented history of ASA use. Of the patients with a documented history of ASA, 2.4% had a normal ART. Of those with an initial ART of <550 ASA response units, 45 received platelets. Repeat ART demonstrated reversal of inhibition in 29 patients (64.4%). Initial responders to transfusion received a greater volume of platelets, suggesting a dose-response relationship. Logistic regression revealed a trend toward higher mortality in nonresponders to transfusion (P = .09). Receiver operating characteristic curve analysis revealed that ART results increased prediction of poor outcome compared with ASA history alone (area under the curve = 0.760 and 0.775, respectively). The ART should be used to better target and guide platelet transfusions in TBI patients with known or suspected ASA use history. Patients with occult platelet dysfunction can be identified, unnecessary platelet transfusions avoided, and the adequate volume of platelets administered to correct drug-induced dysfunction. A dose-response relationship between quantity of platelets transfused and reversal of ASA inhibition was observed.

Quantitative measurement of thromboelastography as a function of platelet count.

T hromboelastography (TEG) analyzes the status of blood coagulation, including abnormalities associated with low platelet count (1). Using TEG to guide platelet transfusion has thus been advocated by several investigators (2–6). However, it is not clear whether TEG variables, assessed from the shape of its tracing, are regulated by platelets quantitatively, because these variables are concurrently under the influence of coagulation factors. We examined the modulation of TEG variables by the amount of platelet, which was controlled by the dilution of platelets into the patient’s plasma without affecting other factors. We also attempted to evaluate the critical platelet counts in coagulation by using this technique.