SEARCH · Search PubMed

Results for “Thrombelastography”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

PubMed1997

Hypercoagulability in patients with primary biliary cirrhosis and primary sclerosing cholangitis evaluated by thrombelastography.

BACKGROUND/AIMS: Patients with primary biliary cirrhosis and primary sclerosing cholangitis survive variceal bleeding better than patients with alcoholic cirrhosis and have less bleeding at liver transplantation. Recently, patients with primary biliary cirrhosis have been found to have a higher incidence of thrombosis in the portal venous tree. We hypothesized that primary biliary cirrhosis and primary sclerosing cholangitis patients may be hypercoagulable. METHODS: We used thrombelastography, which is a simple technique for evaluating whole blood clotting and fibrinolysis, to establish if hypercoagulability was present, defined by thrombelastography values greater than 2SD over controls: r<19 mm (this reflects plasma clotting factors), maximum amplitude (ma) >60 mm, and alpha angle >43 degrees (these reflect platelets and fibrinogen levels). We evaluated 47 primary biliary cirrhosis and 21 primary sclerosing cholangitis patients, 40 with non-cholestatic cirrhosis and 40 healthy subjects as control groups with thrombelastography, full blood count, prothrombin time, partial thromboplastin time and, fibrinogen concentrations. In those with hypercoagulability we evaluated protein S, C, anti-thrombin III levels and activated protein C phenotype. RESULTS: All three thrombelastography abnormalities present together defined hypercoagulability: these were found in 13 of 47 (28%) primary biliary cirrhosis and in nine of 21 (43%) primary sclerosing cholangitis patients independent of cirrhosis, and bilirubin concentration, but in only 2 of 40 (5%) patients with noncholestatic cirrhosis and in none of the healthy controls (p<0.03 and p<0.0002, respectively). There was no correlation between the fibrinogen concentration (which was normal in all patients) or platelet count and the thrombelastography parameters. Only six of the 22 hypercoagulable patients had lower than normal values of protein S, C or antithrombin III. Activated protein C phenotype was normal in all. CONCLUSIONS: This diffference between biliary and parenchymal liver disease may have clinical implications, which need to be defined.

Adolescent↗

PubMed2006

Thrombelastography for the monitoring of lipopolysaccharide induced activation of coagulation.

During Gram-negative sepsis, lipopolysaccharide (LPS) activates toll-like receptor (TLR) 4 and induces complex responses of immune system and haemostasis. In the present study we investigated whether thrombelastography is suitable to monitor the LPS-induced activation of coagulation. Whole blood samples from healthy volunteers were incubated with LPS for various incubation periods (0-5 hrs), thereafter rotation thrombelastography was performed. Incubation of whole blood (>or=3 h) with LPS markedly reduced clotting time; after 5 hrs the variable was reduced from 459+/-39 sec to 80+/-20 sec while the other thrombelastography variables (angle alpha, clot formation time, maximal clot formation) remained unaltered. EC(50) of the LPS effect on whole blood clotting time was 18 microg/ml. In isolated leukocytes, diluted in platelet poor plasma, far lower LPS-concentrations were effective: 10 ng/ml LPS reduced clotting time from 439+/-68 sec to 200+/-56 sec. Experiments with the protein synthesis inhibitor cycloheximide and active site-inhibited factor VIIa revealed that LPS exerts its effects via the synthesis of tissue factor. Addition of tissue factor to whole blood samples revealed that a concentration of 100 fmol/l can be detected using thrombelastography. In whole blood samples the tissue factor concentration induced by LPS amounted up to 12 pmol/l. In summary, thrombelastography proved to be a sensitive and reliable tool for the determination of LPS-induced tissue factor mediated activation of haemostasis in whole blood samples.

Blood Coagulation↗

PubMedDate not supplied

Coagulation status during aortic aneurysm surgery: comparison of thrombelastography with standard tests.

A prospective comparison of thrombelastography to standard coagulation tests was undertaken in ten patients undergoing routine, uncomplicated abdominal aortic aneurysm surgery in order to explore potential clinical utility and establish normal patterns of change. Thrombelastograph k values increased (7.1 vs 5.4 min baseline, P < or = .01), and alpha angle (43 vs 52 degrees baseline, P < or = .001) and ma (39 vs 52 mm baseline, P < or = .01) values decreased following graft placement, while r values remained unaffected (6.4 vs 7.5 min baseline, P > .05). Weak correlations were observed between alpha angle and fibrinogen, prothrombin time, and partial thromboplastin time (aPTT), as well as between k and aPTT (0.70 < r < 0.79 for all). Systemic fibrinolysis was suggested by thrombelastography in 25% of samples, although euglobulin lysis times were abnormal in only 5% (chi 2 = 4.80, P < or = .05). Fibrin degradation product detection increased through the fifth postoperative day in all patients. Variations in thrombelastographic parameters and their correlation to standard coagulation tests in patients undergoing uncomplicated abdominal aortic aneurysm repair were documented. In such a setting, no clear advantages to thrombelastography were defined. Further observations will be necessary to establish the role for thrombelastography in the management of patients experiencing clinically significant perioperative coagulation disorders.

Aged↗

PubMed1987

Effects of progressive blood loss on coagulation as measured by thrombelastography.

The effects of progressive blood loss on coagulation were studied in 87 adults (age 23-66 yr) undergoing a variety of operations under general anesthesia. None had preoperative alterations in coagulation or liver function and none were receiving anticoagulant or antiplatelet medication. Whole blood coagulation status was quantitated using thrombelastography (TEG). Blood samples for TEG were obtained 5 min before and 15 min after induction of anesthesia, after each increment of blood loss (EBL) equalling 5% of estimated blood volume (EBV), at the end of surgery, and 2 hr post-operatively. Patients with EBL exceeding 0.15 EBV were given packed red cells and crystalloid solution. Patients with EBL less than 0.15 EBV received only crystalloid. Thrombelastography analysis showed a trend toward increased coagulability with progressive blood loss. Two of four patients with 80% loss of EBV maintained normal to enhanced coagulation status, although the other two developed clinical and thrombelastographic evidence of coagulopathy. Thrombelastography allowed rapid intraoperative diagnosis and specific treatment of loss of platelet activity in the latter two patients. We conclude that during moderate to massive blood loss, use of supplemental fresh frozen plasma and/or platelets should be reserved for patients with documented defects in coagulation. Thrombelastography is useful for the detection and management of coagulation defects associated with intraoperative blood loss.

Adult↗

PubMed2001

Influence of blood coagulation factor XIII and FXIII Val34Leu on plasma clot formation measured by thrombelastography.

Blood coagulation factor XIII (FXIII) plays an important role in the final stage of the blood coagulation process. Thrombelastography (TEG) enables global assessment of the hemostatic function. The present study tested for the first time the specificity and sensitivity of the rotation thrombelastography (ROTEG: rotation thrombelastography) method for the influence of FXIII and the FXIIIVal34Leu polymorphism on thrombelastograms measured in citrated plasma. Three thrombelastographic parameters were determined in (a) citrated pool plasma, (b) FXIII-deficient plasma, (c) different mixtures of both, and (d) in 60 plasma samples genotyped for FXIIIVal34Leu. Thrombelastograms from FXIII-deficient plasma were significantly smaller than those from pool plasma (8 mm vs. 20.9 mm). Increasing amounts of pool plasma added to FXIII-deficient plasma led to an increase in maximum clot firmness (MCF). FXIIIVal34Leu showed an influence on clot formation time (CFT) values, which decreased with increasing number of Leu alleles. The difference between the wild type and the homozygote mutant genotype was statistically significant (median 185.3 vs. 86.0 s, P=.031). ROTEG is a simple but effective method for the investigation of FXIII function in plasma. The ROTEG method has shown to be not only specific for the FXIII influence, as effects exclusively dependent on FXIII could be observed, but also sensitive, as already smallest amounts of FXIII could be detected. Additionally, the impact of a common genetic polymorphism on ROTEG could be shown for the first time.

Amino Acid Substitution↗

PubMed1999

Use of abciximab-modified thrombelastography in patients undergoing cardiac surgery.

UNLABELLED: Thrombelastography (TEG) is a reliable coagulation monitoring system that can guide blood product transfusion in cardiac surgery. The maximum amplitude (MA) of TEG measures clot strength, which is dependent on both fibrinogen level and platelet function. Inhibition of platelet function with abciximab-fab is suggested to permit quantitative assessment of the contribution of fibrinogen to clot strength. We hypothesized that abciximab-modified TEG permits prediction of plasma fibrinogen levels and that the difference of standard MA and abciximab-modified MA (deltaMA) is a correlate for platelet function. We correlated abciximab-modified MA with plasma fibrinogen levels and deltaMA with platelet count in patients undergoing coronary revascularization. Correlation between plasma fibrinogen levels and abciximab-modified MA was significant (adjusted r2: 0.8; P < 0.0001). Correlation of deltaMA with platelet count was not significant when calculated in millimeters (adjusted r2: 0.04; P = 0.73). However, when deltaMA was calculated in dynes per square centimeter (deltaGMA), it correlated significantly with platelet count (adjusted r2: 0.51; P < 0.0001). We conclude that abciximab-modified TEG may therefore help to discriminate between hypofibrinogenemia and platelet dysfunction as a cause of decreased MA. IMPLICATIONS: We examined the use of abciximab-modified thrombelastography in patients undergoing cardiac surgery. Modification of thrombelastography with abciximab-fab allows prediction of fibrinogen levels, despite coagulation altered by cardiac surgery. The difference of standard maximum amplitude and abciximab-modified maximum amplitude correlates with platelet function when expressed in dynes per square centimeter.

Abciximab↗

PubMed2005

Tailoring haemostatic treatment to patient requirements - an update on monitoring haemostatic response using thrombelastography.

Currently, there is no single haemostasis laboratory test that has the capacity to accurately illustrate the clinical effects of procoagulant or anticoagulant interventions. Although the time course of thrombin generation in plasma and the endogenous thrombin potential (ETP) may be useful coagulation parameters, clotting involves components other than thrombin (e.g. platelets, fibrinogen). The continuous coagulation profiles of thrombelastography may provide a more accurate reflection of in vivo biology, covering initiation, development and final clot strength during whole blood clot formation. This method has helped to clarify the mechanism of action of whole blood clot formation, demonstrating the differences from clotting in plasma, and the importance of platelets and tissue factor titrations. It has also been used to investigate hypocoagulation (in haemophilia A, rare coagulation disorders, anticoagulant therapy and dilutional coagulopathy), hypercoagulation and the ex vivo testing of haemostatic interventions. Thrombelastography has been shown to reflect the clinical efficacy of activated prothrombin complex concentrate (aPCC) and recombinant activated factor VII (rFVIIa) in patients with haemophilia A with inhibitors and in patients with acquired haemophilia. Overall, tailoring laboratory assays to illustrate and correlate with clinical phenotypes is essential for effective coagulation monitoring. Applying an algorithm of preoperative, perioperative and postoperative tests, including thrombelastography, may enable physicians to achieve this.

Algorithms↗

PubMed2005

Effects of coagulation factor deficiency on plasma coagulation kinetics determined via thrombelastography: critical roles of fibrinogen and factors II, VII, X and XII.

BACKGROUND: Thrombelastography (TEG) is used to assess coagulopathy. However, a comprehensive characterization of the effects of specific coagulation factor deficiencies and mode of activation on TEG data does not exist. METHODS: Thrombelastography was performed for 15 min with control plasma and plasmas deficient (<1% activity) in Factors II, V, VII, VIII, IX, X, XI, XII, or XIII activated with celite (0.28 mg ml(-1)) or tissue factor (TF, 0.1%) (n = 6 per condition). Additional fibrinogen concentration activity (75-345 mg dl(-1)) and Factor II, VII, X and XII activity-response relationships (1%, 6.25%, 12.5%, 25%, 50% and 100% activity) were obtained (n = 8 per condition). Thrombelastography parameters included reaction time (R), angle (alpha), and clot strength (A, amplitude; G, elastic modulus). RESULTS: Celite activation of FXII-deficient plasma, TF activation of FVII-deficient and FX-deficient plasma, and celite or TF activation of FII-deficient plasma resulted in an almost undetectable clot. Compared to control values, celite activation of plasmas deficient in FXI, FIX and FVIII resulted in prolonged R and decreased alpha values, whereas TF activation resulted in decreased alpha values. Celite and TF activation of FV-deficient plasma resulted in prolonged R and decreased alpha values, whereas FXIII-deficient plasma had decreased alpha, A and G-values compared to control values. CONCLUSIONS: The fundamental finding of this study is that coagulation factor deficiencies affect TEG parameters in both a factor-dependent and activation-dependent fashion. Utilizing both celite and TF activation improves the diagnostic power of TEG. Based on such TEG data, more targeted administration of blood products could potentially help improve perioperative hemostatic outcomes.

Blood Coagulation↗

PubMed2006

Effects of aprotinin on plasma coagulation kinetics determined by thrombelastography: role of Factor XI.

BACKGROUND: Aprotinin is commonly administered in settings involving cardiopulmonary bypass and liver transplantation to decrease peri-operative bleeding. Thrombelastography has been utilized to monitor coagulation in these settings, and aprotinin delays clot initiation, presumably by inhibiting kallikrein; however, aprotinin also inhibits Factor XI (FXI), a contact system protein. Thus, it was hypothesized that celite-activated thrombelastography coagulation kin-etics would be decreased via aprotinin-mediated FXI inhibition. METHODS: Citrated normal plasma and prekallikrein-deficient (<1% normal activity) plasma were exposed to 0, 200, 400 or 800 kallikrein inhibitory units (KIU)/ml (n = 6 per condition). Samples were recalcified and celite-activated in a thrombelastograph, with clot initiation (R, s) determined. To confirm contact system specificity, additional prekallikrein-deficient samples with 0 or 800 KIU/ml aprotinin were activated with tissue factor (n = 4 per condition). RESULTS: Exposure of celite-activated, normal plasma to aprotinin 0, 200, 400 or 800 KIU/ml resulted in R values of 167 +/- 14, 253 +/- 10, 293 +/- 22 and 349 +/- 21 s, respectively, which were significantly different from one another (P < 0.05). Exposure of celite-activated, prekallikrein-deficient plasma to aprotinin 0, 200, 400 or 800 KIU/ml resulted in R values of 366 +/- 15, 630 +/- 64, 698 +/- 46 and 850 +/- 47 s, respectively, which were significantly different from one another (P < 0.05). There were no significant differences in R values between tissue factor-activated, prekallikrein-deficient plasma samples with 0 or 800 KIU/ml aprotinin. CONCLUSIONS: These data support a role for the inhibition of FXI as the mechanism for aprotinin-mediated delayed contact system clot initiation determined by thrombelastography.

Aprotinin↗

PubMed2006

Validation of rotation thrombelastography in a model of systemic activation of fibrinolysis and coagulation in humans.

BACKGROUND: Thrombelastography (TEG) is a whole blood assay to evaluate the viscoelastic properties during blood clot formation and clot lysis. Rotation thrombelastography (e.g. ROTEM) has overcome some of the limitations of classical TEG and is used as a point-of-care device in several clinical settings of coagulation disorders. Endotoxemia leads to systemic activation of the coagulation system and fibrinolysis in humans. OBJECTIVES: We validated whether ROTEM is sensitive to endotoxin induced, tissue factor-triggered coagulation and fibrinolysis and if its measures correlate with biohumoral markers of coagulation and fibrinolysis. PATIENTS AND METHODS: Twenty healthy male volunteers participated in this randomized placebo-controlled trial. Volunteers received either 2 ng kg(-1) National Reference Endotoxin or saline. RESULTS: Endotoxemia significantly shortened ROTEM clotting time (CT) by 36% (CI 0.26-0.46; P < 0.05) with a strong inverse correlation with the peak plasma levels of prothrombin fragments (F(1 + 2)) (r = -0.83, P < 0.05). Additionally, endotoxin infusion enhanced maximal lysis (ML) 3.9-fold (CI: 2.5-5.2) compared with placebo or baseline after 2 h (P < 0.05). Peak ML and peak tissue plasminogen activator (t-PA) values correlated excellently (r = 0.82, P < 0.05). ROTEM parameters clot formation time and maximal clot firmness were not affected by LPS infusion, whereas platelet function analyzer (PFA-100) closure times decreased. CONCLUSIONS: Rotation thrombelastography (ROTEM) detects systemic changes of in vivo coagulation activation, and importantly it is a point of care device, which is sensitive to changes in fibrinolysis in humans. The ex vivo measures CT and ML correlate very well with established in vivo markers of coagulation activation (F(1 + 2)) and fibrinolysis (t-PA), respectively.

Adult↗

PubMed2006

The effect of excess protamine on thrombelastography in vitro.

The aim of the current study was to assess the direct effect of protamine on conventional thrombelastography in vitro. Protamine was added to blood samples collected from 25 adult cardiac surgical patients prior to the induction of anaesthesia and after separation from cardiopulmonary bypass. The final protamine concentrations were 0 (control), 0.05 mg/ml, 0.1 mg/ml and 0.2 mg/ml (i.e. sufficient to reverse heparin 0, 5, 10 and 20 IU/ml respectively, assuming a 1:1 reversal ratio). In the pre-induction samples, protamine was associated with increases in r time and reductions in maximum amplitude (P<0.01). After bypass, the control samples demonstrated a heparin effect as expected, which was corrected by the addition of protamine 0.05 mg/ml. However, the higher concentrations of protamine were again associated with increases in r time and reductions in maximum amplitude (P<0.01). The results indicate that protamine has a direct anticoagulant effect on conventional thrombelastography in vitro. This effect occurs whether protamine is present alone, or whether protamine is present in excess after neutralization of heparin. Unless this effect is taken into account, excess protamine may confound the interpretation of conventional thrombelastography in cardiac surgical patients.

Adult↗

PubMed2004

Thrombelastography monitoring of platelet substitution therapy and rFVIIa administration in haemato-oncological patients with severe thrombocytopenia.

Thrombocytopenic patients refractory to platelet concentrates (PC) could be treated during bleeding episodes with the recombinant activated FVII (rFVIIa). However, monitoring of administration of the rFVIIa or a response to platelet substitution therapy in thrombocytopenia patients is not well documented so far. Using of whole blood ROTEG analysis we monitored the changes in haemostatic parameters following in vivo platelet concentrate administration compared to ex vivo rFVIIa administration in patients with a severe to mild thrombocytopenia secondary to haemato-oncological disease. We use non-activated thrombelastography (NATEG) and a mild intrinsic activation thrombelastography (INTEG). NATEG analysis was sufficiently sensitive to monitor changes following PC and rFVIIa administration. Both, platelet infusion and rFVIIa treatment induced significant shortening of clotting time (CT) and clot formation time (CFT) parameters (p<0.05). When we compared the effect of platelet vs. rFVIIa treated whole blood by NATEG analysis we did not found any significant difference. Analysis with INTEG system was less sensitive and changes in CT and CFT were not significant. The monitoring with thrombelastography could enable efficient application of platelet concentrate and furthermore the using of rFVIIa as an alternative treatment of patients refractory to platelet infusion or with allergic reactions.

Adult↗

PubMed1987

Thrombelastography of blood from subjects with chronic renal failure.

Blood samples from 23 subjects with chronic renal failure and 19 controls were tested using thrombelastography and other hematologic tests. The uremic subjects were divided into two groups, those who had not yet begun maintenance hemodialysis treatments (12 subjects) and those who had (11 subjects). Compared to those from control subjects, the thrombelastograms from the uremic subjects consistently indicate normal clotting times but significantly elevated amplitudes. The increased amplitudes correlate positively in the dialyzed uremic group with both platelet count and fibrinogen concentration and correlate negatively in both uremic groups with hematocrit. Thrombelastography demonstrates a hypercoagulability in these samples in vitro, despite the prolonged bleeding time that commonly occurs in uremic subjects.

Fibrinogen↗

PubMed1997

Functional maturity of the coagulation system in children: an evaluation using thrombelastography.

There are quantitative deficiencies in the coagulation system for at least the first 6 mo of life. Clinical experience, however, does not indicate an increased risk of excessive bleeding during surgical procedures. Thrombelastography, a test providing a functional evaluation of coagulation, was used to assess the hemostatic system of pediatric patients under 2 yr of age. Thrombelastographic data were obtained from 237 healthy pediatric patients less than 2 yr of age undergoing elective noncardiac surgery. Five groups were distinguished: under 30 days, 1-3 mo, 3-6 mo, 6-12 mo, and 12-24 mo. Thrombelastography revealed no defects in coagulation when these groups were compared to each other or to adults, indicating a functionally intact hemostatic process even in neonates. Indeed, children less than 12 mo of age were found to initiate and develop clot faster than adults, with the coagulation process slowing to adult rates after 1 yr of age. In addition to defining functional integrity, our data represents a set of pediatric control thrombelastographic values that have not been previously reported and that may become important in understanding coagulation changes that accompany disease states and surgery in pediatric patients.

Age Factors↗

PubMed2002

Hemodilution with albumin, but not Hextend, results in hypercoagulability as assessed by Thrombelastography in rabbits: role of heparin-dependent serpins and factor VIII complex.

UNLABELLED: Isovolemic hemodilution (IVHD) has been advocated as an effective method of reducing the need for transfusion but has been associated with hypercoagulability. We tested the hypothesis that IVHD enhances hemostatic function by decreasing circulating antithrombin activity in rabbits. Furthermore, it was determined whether different replacement solutions would affect hemostasis. Sedated rabbits were randomly assigned to groups that underwent IVHD (40% blood volume removed) with 5% human albumin (n = 10) or a 6% hetastarch solution (Hextend). Antithrombin and Factor VIII complex (VIII:C) activities were determined, and thrombelastography(R) was performed with or without platelet inhibition. IVHD resulted in a significant (P < 0.05) decrease in antithrombin (32%-39%) without fluid-specific differences observed. VIII:C did not change in the albumin group, whereas the hetastarch group had a significant (P < 0.05) decrease (43%) in VIII:C that was also significantly (P < 0.05) less than the albumin group. The time to clot initiation was decreased, and the rate of clot formation increased significantly via thrombelastography(R) in albumin animals. No significant change in clot kinetics was observed in hetastarch animals. In rabbits, the primary determinant of hemostasis after IVHD was the interaction of changes in antithrombin activity and VIII:C. These data serve as a rational basis to determine whether IVHD-mediated hypercoagulability encountered clinically may be attenuated or exacerbated by the choice of colloid administered. IMPLICATIONS: Isovolemic hemodilution (IVHD) is associated with hypercoagulability. Rabbits hemodiluted with albumin, but not Hextend, became hypercoagulable secondary to a loss of antithrombin activity with simultaneous maintenance of Factor VIII complex activity (VIII:C). Hextend-treated animals had proportionate decreases in both antithrombin activity and VIII:C. IVHD-mediated hypercoagulability encountered clinically may be attenuated or exacerbated by the choice of colloid administered.

Animals↗

PubMed2002

The detection of changes in heparin activity in the rabbit: a comparison of anti-xa activity, thrombelastography, activated partial thromboplastin time, and activated coagulation time.

UNLABELLED: Thrombelastography (TEG) has been used to detect both exogenous and endogenous circulating heparin activity in clinical and laboratory settings. Thus, in this study I sought to compare the sensitivity of TEG, activated partial thromboplastin time (aPTT), and activated coagulation time (ACT) values with changes in anti-Xa activity after small-dose heparin administration in rabbits. Conscious rabbits (n = 11) had blood obtained from ear arteries for hematological analyses after the administration of 0, 10, 20, and 30 U/kg of IV heparin. Anti-Xa activities after the administration of 0, 10, 20, and 30 U/kg of heparin were, respectively, 38 +/- 9 mU/mL, 74 +/- 15 mU/mL, 105 +/- 14 mU/mL, and 134 +/- 17 mU/mL; all values were significantly different from each other. TEG variables (R and alpha) significantly (P < 0.05) changed between 0, 10, and 20 U/kg heparin doses, but a difference between 20 and 30 U/kg could not be discerned secondary to loss of a detectable clot. The aPTT was significantly (P < 0.05) different between 0, 20, and 30 U/kg doses. ACT values were significantly different between the 0 U/kg heparin dose and all other doses; however, there were no significant differences between the 10, 20, and 30 U/kg heparin doses. Changes in anti-Xa activity were significantly linearly related to R (r = 0.81, P < 0.0001), alpha (r = -0.85, P < 0.0001), aPTT (r = 0.74, P < 0.0001), and ACT (r = 0.41, P = 0.005). In this model of small-dose heparin administration, TEG variables were more sensitive to changes in heparin activity than aPTT and ACT. IMPLICATIONS: Changes in thrombelastography (TEG) variables more sensitively reflect changes in circulating heparin activity than activated partial thromboplastin time (aPTT) and activated coagulation time (ACT) after small-dose heparin administration in rabbits. Thus, TEG may be more helpful than aPTT and ACT in the detection of heparin in both laboratory and clinical settings wherein heparin may play a role in coagulopathy.

Animals↗

PubMed2006

Monitoring survival and function of transfused platelets in Glanzmann thrombasthenia by flow cytometry and thrombelastography.

Patients with Glanzmann thrombasthenia (GT) may form isoantibodies which induce refractoriness or inhibition of function of transfused platelets. We monitored the survival and function of transfused platelets by flow cytometry and thrombelastography in a patient with GT. Gating on CD42a+ allowed identification of even a few transfused platelets. Only by gating on these CD41+ CD42a+ cells were we able to demonstrate their capability to bind fibrinogen and PAC-1 upon activation. Platelets were rapidly cleared from the circulation as a result of boosted isoantibodies. The contribution of transfused platelets to clot formation was also demonstrated by thrombelastography by blocking their function with abciximab.

Adolescent↗

PubMed2000

Postoperative fibrinolysis diagnosed by thrombelastography.

Thrombelastography is a useful method for the monitoring of bedside coagulation, especially for fibrinolysis. We report a case where thrombelastography facilitated early detection of fibrinolysis with significant clinical bleeding in a patient immediately following hip replacement surgery. The early diagnosis enabled institution of antifibrinolytic therapy and monitoring of the patient's response. It is likely to have led to less blood product transfusion and may possibly have prevented unnecessary surgical re-exploration.

Aged↗