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PubMed2005

The effect of clonidine on perioperative blood coagulation.

STUDY OBJECTIVE: To evaluate the influence of perioperative stress protection by clonidine on blood coagulation. DESIGN: Prospective, randomized, double-blinded, placebo-controlled clinical trial. SETTING: University hospital. PATIENTS: 50 patients scheduled for elective gynecoabdominal surgery. INTERVENTIONS AND MEASUREMENTS: Patients were randomly assigned to control (placebo) or clonidine group (single intravenous clonidine dose; 4 microg/kg(-1) or 3 microg/kg(-1) for age >65 years). Three measurement time points were defined: before administration of placebo/clonidine and anesthesia induction, (t1; baseline measurement); after surgery, before emergence of anesthesia (t2); and at the first postoperative day, 24 hours after anesthesia induction (t3). Blood coagulation was analyzed at all time points measuring international normalized ratio, platelets, thrombin-antithrombin complex, von Willebrand factor, soluble thrombomodulin, d-dimers, plasminogen activator inhibitor 1, and Thrombelastograph analysis. MAIN RESULTS: In the postoperative period (t2, t3), hypercoagulability was present in all patients compared with baseline measurements (t1) but without differences between the control and clonidine group. Regarding hematologic, laboratory blood coagulation, and Thrombelastograph parameters, there was no statistically and clinically relevant difference throughout the study period between the 2 groups. No hemodynamic adverse events of clonidine were observed in the perioperative period. Until day of discharge, no thrombotic or thromboembolic events were reported in both groups. CONCLUSIONS: Preoperative administration of a single dose of clonidine has no effect on perioperative blood coagulation.

Abdomen↗
PubMed2004

Changes in blood coagulability as it traverses the ischemic limb.

OBJECTIVE: We undertook this study to determine whether changes in blood coagulability associated with peripheral arterial occlusive disease are due to contact with the atherosclerotic arterial wall or passage through distal ischemic tissue. METHODS: Thirty patients with peripheral arterial occlusive disease undergoing angiography participated in the study. Ankle-brachial pressure index was recorded before intervention. Blood samples taken from the aorta, common femoral artery, and common femoral vein were analyzed at thromboelastography. Angiograms were scored for stenotic disease by a radiologist blinded to the other results. RESULTS: When femoral artery samples were compared with aortic samples there was a decrease in reaction time (R; P <.05), an increase in maximum amplitude (MA; P <.05), and an increase in coagulation index (CI; P <.002), indicating an increase in coagulability as blood flowed down the iliac segment. These changes also correlated (DeltaR, r = 0.442, P <.05; DeltaMA, r = 0.379, P <.05; DeltaCI, r = 0.429, P <.05) with the severity of disease in the ipsilateral iliac segment. Significant differences in R (P <.05), angle (P <.05), MA (P <.005), and CI (P <.001) between common femoral arterial and venous samples confirmed that venous samples were more coagulable in this group of patients. This difference in Thromboelastography parameters across the arteriovenous segment correlated inversely with the degree of ischemia (represented by ankle-brachial pressure index; DeltaCI, r = -0.427, P <.05; DeltaMA, r = -0.370, P <.05) in the puncture side limb. CONCLUSION: Passage of blood down an atherosclerotic artery leads to an increase in coagulability proportional to the degree of stenosis in that vessel. Passage of blood through ischemic tissue may also contribute to increased coagulability in peripheral arterial occlusive disease.

Aged↗
PubMed2004

A novel modification of the Thrombelastograph assay, isolating platelet function, correlates with optical platelet aggregation.

Flow cytometry, singlet platelet counting, and optical aggregation have been used to monitor clopidogrel and glycoprotein IIb/IIIa (GPIIb/IIIa) platelet antagonists. Optical aggregation is considered the gold standard, but neither it nor flow cytometry is convenient in larger-scale clinical studies or point-of-care systems. Singlet platelet counting, a point-of-care assay correlated with optical platelet aggregation, only provides a measurement of platelet function at a single point in time. The Thrombelastograph is used to assay whole blood for thrombin-generated maximal clot-shear elasticity, referred to as the maximal amplitude (MA). Although platelet dysfunction, thrombocytopenia, and the in vitro effect of strong inhibitors such as IIb/IIIa antagonists can be observed, with thrombin generation milder platelet inhibitors cannot be assessed. We modified the Thromboelastograph assay, using reptilase and factor XIIIa, to form a clot, without thrombin generation, in heparinized whole blood. The resulting clot MA is dependent on added platelet agonists such as ADP or arachidonic acid, is sensitive to platelet antagonists, and provides a continuous measure of platelet function more analogous and better correlated with optical aggregation. This novel modification of the Thromboelastograph assay should prove to be a useful point-of-care whole-blood assay with which to monitor the effects of GPIIb/IIIa, ADP, and thromboxane A(2)-receptor-inhibiting drugs in patients.

Adenosine Diphosphate↗
PubMed2005

Comparison of modified Thrombelastograph and Plateletworks whole blood assays to optical platelet aggregation for monitoring reversal of clopidogrel inhibition in elective surgery patients.

Clinically monitoring recovery from clopidogrel and nonsteroidal anti-inflammatory drug (NSAID) inhibition requires whole blood assays corresponding to a standard methodology such as platelet-rich plasma aggregation monitored optically (OPA). We compared OPA, using an ED 50 dose of adenosine diphosphate activation, with 2 whole blood assays, Plateletworks (PWA) and modified Thrombelastograph (TEG). Two sets of assays were performed on 43 surgery patients while on clopidogrel and off clopidogrel to determine the reversal of absolute and relative inhibition. The modified TEG had Spearman correlations with OPA for absolute (rho = .424; P = .006) and relative inhibition (rho = .742; P < .0001). PWA correlations with OPA gave absolute (rho = .28; P = .08) and relative inhibition (rho = .46; P = .004) values. Bland-Altman analysis indicated agreement of both tests with OPA, showing constant biases of about 18% and some dependency on mean magnitude error. Cohen effect size thresholds defined nonresponders as < 7.7% clopidogrel inhibition relative to baseline recovery of full platelet function. Apparent nonresponse to clopidogrel or lack of platelet recovery did not correlate with statin or NSAID therapies. These PWA and modified TEG whole blood assays could prove useful for monitoring the reversal of clopidogrel and NSAID inhibition before surgery. More important, these assays done at baseline and after beginning clopidogrel therapy could monitor the effectiveness for the individual patients with cardiovascular disease and help identify the need for alternative therapies.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2005

A Thrombelastograph whole blood assay for clinical monitoring of NSAID-insensitive transcellular platelet activation by arachidonic acid.

Optical platelet aggregation (OPA) with platelet-rich plasma (PRP) was compared with a Thrombelastograph (TEG) whole blood assay for monitoring arachidonic acid (AA)-induced platelet activation. Assays were performed on 47 interventional cardiology and 24 general surgery patients receiving aspirin therapy for cardiovascular disease, as well as 48 volunteers asked to take nonsteroidal anti-inflammatory drugs (NSAIDs) or 12 volunteers on chronic NSAID therapy unrelated to diagnosed cardiovascular disease. Whole blood TEG monitoring of NSAID inhibition detected NSAID-insensitive AA activation of platelets in a significantly higher number of cardiology (23%) and surgery (25%) patients and normal volunteers on chronic NSAID (25%) therapy relative to normal subjects not on chronic NSAID therapy (0%). Whole blood NSAID insensitivity was observed with cyclooxygenase-I inhibitors, such as aspirin and ibuprofen; was not affected by Celebrex, a cyclooxygenase-II inhibitor; but was completely inhibited by thromboxane-receptor antagonists. This was not due to platelet NSAID insensitivity, because complete inhibition of AA-activation responses in PRP was observed with either TEG or OPA assays. We confirmed that thromboxane B(2) formation in PRP from NSAID-insensitive subjects was completely inhibited by NSAIDs. However, significant amounts were formed in whole blood from NSAID-insensitive subjects, but not in whole blood from NSAID-sensitive subjects. Thromboxane formation after AA addition was not found in washed blood cells with 90% reduced platelet counts or in leukocyte-rich buffy coat fractions, but could be restored by addition of PRP. NSAID-insensitive activation was inhibited by nordihydroguaiaretic acid, with an IC(50) of 30 micromol, implicating 12- and/or 15-lipoxygenases in this transcellular pathway.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2007

The effects of hypothermia on fibrinogen metabolism and coagulation function in swine.

Clinical coagulopathy frequently occurs in the presence of hypothermia. The primary purpose of this study was to investigate the effects of hypothermia on clotting protein fibrinogen metabolism and on coagulation function in a swine model. Twelve pigs were randomly allocated into control and hypothermia groups. Hypothermia of 32 degrees C was induced using a blanket with circulating water at 4 degrees C. Fibrinogen synthesis and breakdown were quantified using a 6-hour stable isotope infusion with subsequent gas chromatograph and mass spectrometry analysis. Clotting enzyme thrombin generation kinetics was quantified at baseline and at the end of the infusion. Changes in fibrinogen metabolism and thrombin generation were correlated with coagulation function assessed by thromboelastography (TEG). Hypothermia decreased fibrinogen synthesis from the control value of 2.6 +/- 0.4 to 1.2 +/- 0.2 mg kg(-1) h(-1) (P < .05), with no effect on fibrinogen breakdown. Thrombin generation at the initiation phase was delayed by hypothermia, but there were no changes at the propagation phase. In thromboelastography measurements, the initial clotting time (R time) was prolonged from the baseline value of 3.01 +/- 0.13 to 4.30 +/- 0.24 minutes (P < .05) and clotting rapidity (angle alpha) was decreased from the baseline value of 72.30 +/- 0.90 to 65.34 +/- 1.07 (P < .05). Hypothermia caused no significant changes in clot strength (maximum amplitude) and clot lysis (LY(60)). We concluded that hypothermia caused a potential deficit in fibrinogen availability and a delay in thrombin generation, consequently inhibiting coagulation function. Our data support the current practices of rewarming and prescribing recombinant factor VIIa for hypothermic patients with coagulation defects.

Animals↗
PubMed2004

The effect of hypertonic saline dextran on whole blood coagulation.

Hypertonic saline dextran (RescueFlow) is being promoted for resuscitation from hypovolaemia following injury. We studied the in vitro effect on coagulation of serial dilutions of blood with this fluid. There was a mild procoagulant effect up to a dilution of 11% and an anticoagulant effect above this level, which rapidly increased so that coagulation was grossly deranged at a 15% dilution. Although the clinical significance of these findings is not yet known, it may suggest that for hypertonic saline dextran there is little to separate the top of the therapeutic window from the threshold of potentially serious adverse effects.

Anticoagulants↗
PubMed2004

Evaluation of a novel kallikrein inhibitor on hemostatic activation in vitro.

BACKGROUND: DX-88 is a potent kallikrein inhibitor that is being studied for the treatment of hereditary angioedema (HAE) and represents a potential alternative to aprotinin in cardiac surgical patients. The current study was designed to evaluate in vitro effects of DX-88 on coagulation in comparison with aprotinin. METHODS: Blood samples were obtained from consented 12 healthy volunteers. DX-88 or aprotinin was added to blood at 200 and 800 kallikrein inhibitory units (KIU) per milliliter for aprotinin, and at 1.1, 2.2, or 8.8 microg/ml for DX-88. Thromboelastography (TEG) was performed using celite, kaolin, or tissue factor (TF) activation. Kaolin-based activated clotting times (ACTs) were measured at different heparin levels. The whole blood prothrombin time (PT)/PTT values were also measured. The endogenous thrombin generation was assessed with a fluorogenic assay using platelet-poor plasma (PPP). RESULTS: With celite and kaolin activation of TEG, the reaction time was prolonged with DX-88 and aprotinin. With tissue factor activation, TEG parameters were not affected. DX-88 caused dose-dependent kaolin-ACT prolongation that was augmented by increasing doses of heparin. DX-88 or aprotinin had no significant effects on the PT values, but PTT values were dose-dependently prolonged. Both agents delayed the onset of thrombin generation when PTT reagent was used as a trigger, whereas no change was observed when tissue factor was used. CONCLUSION: We found that DX-88 delayed contact activator induced coagulation without affecting tissue factor mediated coagulation. For evaluation of coagulation during DX-88 therapy, the use of PT or tissue factor-activated TEG may be preferable.

Aprotinin↗
PubMed2004

Coagulation status and complications of pregnancy.

INTRODUCTION: There is much interest in the relationship between coagulation status and complications of pregnancy. The thrombelastograph (TEG) has been proposed as a useful, inexpensive tool to screen for patients with hypercoagulable states. MATERIALS AND METHODS: We investigated 588 unselected pregnant women at booking, obtaining blood samples for TEG and thrombophilia investigation. Pregnancy outcome data was recorded. RESULTS: We found significant correlations between TEG parameters and the Prothrombin time (PT) and Activated Partial Thromboplastin time (APTT) (p<0.01) and with plasma Antithrombin level (p<0.01). There was no correlation between TEG and other thrombophilic defects (protein C, protein S, Factor V Leiden mutation, Prothrombin G20210A mutation, MTHFR C677T mutation and Lupus Anticoagulant). There was a significant association of TEG parameters with mid-trimester loss (MTL) but not with other adverse pregnancy outcomes. CONCLUSIONS: The correlation between TEG and PT, APTT and antithrombin level supports its value in providing a global measure of haemostasis. Coagulation status at booking is associated with increased risk of MTL but not with complications occurring later in pregnancy.

Adolescent↗
PubMed2005

Purification and characterization of a new anticoagulant protein, PP27, from placenta.

It has long been known that water extracts of placenta hominis (Jahage in Korean) are effective for treating immunological and vascular diseases and is a major constituent of traditional oriental medicines. We report herein on the isolation and purification of a new type of anticoagulant protein, PP27, from human placenta. PP27 ran as a single band on SDS-PAGE with a molecular mass (Mr) of 27 kDa under denaturing conditions and chromatography on a calibrated Sepharose 4B column indicated a molecular mass of 23 kDa, a value that is similar to those of other PP4 enzymes reported to date. The isoelectric point of PP27 was pI 5.2. PP27, at doses higher than 10 microg/ml, inhibited platelet activating factor (PAF)-induced platelet activation in a dose-dependent manner. The protein was found to inhibit the coagulation time in a concentration-dependent manner. PP27, which acts as a vascular anticoagulant of annexin type, inhibits the blood clotting process by virtue of its binding of essential lipids, which is dependent on the presence of Ca2+ ions. In the presence of Ca2+ ions, PP27 combines with platelet membranes and neutralizes their procoagulant effect. Coagulation, triggered by the addition of thromboplastin/lipid mixtures, is extinguished by PP27.

Anticoagulants↗
PubMed2006

The platelet inhibiting effect of a clopidogrel bolus dose in patients on long-term acetylsalicylic acid treatment.

INTRODUCTION: Addition of clopidogrel to patients treated with ASA has been shown to decrease the incidence of in-stent thrombosis after percutaneous coronary interventions. However, it has also been reported that up to 30% of patients do not achieve adequate platelet inhibition from standard dosages of ASA and clopidogrel. There is a demand for reliable methods to measure the individual platelet inhibiting effect of this combination therapy. MATERIALS AND METHODS: The primary aim of the present investigation was to compare three methods for evaluation of the platelet inhibiting effect of a clopidogrel bolus dose in patients on long-term acetylsalicylic acid treatment. Thirty patients presenting for coronary angiography/PCI were included. Two patients were excluded due to technical problems. All patients were on 75-100 mg ASA/day for at least 8 days. Blood samples were analysed before and 16 h after a 300 mg clopidogrel bolus dose. The platelet inhibiting effect was measured with (1) Whole blood flow cytometry (17 patients); (2) a bed-side test, Platelet Mapping assay for the thrombelastograph (28 patients); and (3) PFA (Platelet function analyser) -100 (26 patients). RESULTS: With flow cytometry, the percentage of platelets expressing P-selectin (p=0.03) on their surface decreased significantly after the bolus dose of clopidogrel. There was also a reduction of platelets binding fibrinogen when stimulated with ADP. A significantly (p=0.002) increased platelet inhibition could also be demonstrated with Platelet Mapping. PFA-100 could not measure any significant platelet inhibiting effect of clopidogrel. CONCLUSION: A significant platelet inhibition could be demonstrated with flow cytometry and the Platelet Mapping assay, but not with PFA-100. However, levels of response for the individual patient with these three methods were inconsistent. Further studies are needed to evaluate how the results correlate to the clinical risk of thrombosis and bleeding.

Aged↗
PubMed2006

In vitro testing of platelets using the thromboelastogram, platelet function analyzer, and the clot signature analyzer to predict the bleeding time.

BACKGROUND: Platelet aggregation, thromboxane A2 production and platelet annexin V binding are in vitro tests used to assess platelet function. This study was done to evaluate the clot signature analyzer (CSA), platelet function analyzer (PFA), and thromboelastogram (TE) as in vitro tests to predict the template bleeding time (BT). STUDY DESIGN AND METHODS: Twelve normal volunteers were studied before and after removal of 2 units of RBC. Seven females were reinfused their RBC and 5 males were not. Samples were collected prior to and at 24, 48, and 72 h and 7 days after the RBC removal whether or not reinfusion of RBC was performed for measurement of TE, CSA, PFA and template BT. RESULTS: BT increased significantly following the removal of 2 units of RBC and BT decreased significantly after the reinfusion of the 2 units of RBC in the 7 female volunteers. BT decreased during the 7-day period in the 5 male volunteers not reinfused their RBC. No significant correlations were observed between BT and platelet hemostatic time (PHT) and clotting time (CT) in the CSA and between the bleeding time and the closure time (CT) in the platelet function analyzer (PFA). Significant correlations were observed between BT and K time, the MA, and the angle recorded in the thromboelastogram. CONCLUSION: In this study in vitro testing using the clot signature analyzer, platelet function analyzer and the thromboelastogram could not be used to predict the template bleeding time.

Annexin A5↗
PubMed2006

Study on biological variation of haemostatic parameters in clinically healthy dogs.

Thromboelastography (TEG) may be a valuable supplement to the coagulation assays activated partial thromboplastin time (aPTT), prothrombin time (PT), thrombin time (TT), fibrinogen, antithrombin (AT) and D-Dimer currently used in most clinical pathology laboratories. Allowable imprecision and bias reference limits for analytical tests can be calculated based on measurements of biological variation. No studies to date have examined the effect of biological variation on these haemostasis parameters in the same group of dogs. Plasma samples were collected after a set protocol once weekly for five consecutive weeks from eight healthy dogs (four males and four females) and stored at -80 degrees C until analysis. Randomized duplicate coagulation tests and TEG analyses were performed on all plasma samples within one run. The data were analyzed for outliers and subsequently subjected to nested analysis of variance to obtain the coefficient of analytical, intra-individual and inter-individual variation. From these objective analytical performance standards for imprecision, critical difference, total error and the index of individuality were calculated to assess the utility of conventional population-based reference ranges. All the clotting times (aPTT, PT and TT), fibrinogen, AT and D-Dimer showed a degree of individuality, which may make the use of population-based reference ranges alone an insensitive interpretation criterion, whereas a population-based reference interval seems to be sensitive for interpreting all TEG parameters. Analytical performance standards for imprecision were only met for one of the coagulation assays, whereas all TEG parameters except the alpha angle, alpha achieved this analytical goal.

Animals↗
PubMed1996

Adverse effects of postoperative infusion of shed mediastinal blood.

BACKGROUND: Postoperative infusion of shed mediastinal blood has been used in an effort to decrease blood usage after cardiac operations. Recent experience has suggested that this practice may actually lead to a delayed increase in bleeding. METHODS: In a prospective, randomized study, 40 patients undergoing coronary artery bypass grafting with shed mediastinal blood collected in a cardiotomy reservoir were divided into two equal groups and studied during their first 4 hours in the intensive care unit. Shed mediastinal blood was directly infused in group I (n = 20), whereas in group II (n = 20), it was not. In group II, if a sufficient volume of red cells was present to allow processing (n = 5), washed red cells were infused. Variables studied before and after infusion were the amount of blood lost and infused, homologous blood transfused, complete blood count and differential, serum fibrinogen, fibrin split products, D-dimers, clotting factors, prothrombin time, activated partial thromboplastin time, thromboelastograms, plasma-free hemoglobin, complement factors C3 and C4, creatine kinase and its MB isoenzyme, and body temperature. RESULTS: After infusion of shed mediastinal blood, elevated levels of fibrin split products and D-dimers were found in significantly more patients in group I. The thromboelastogram index was normal in 76% of patients in group II but in only 12.5% in group I. Group I also had an increase in band neutrophils, a greater number of febrile patients, higher serum levels of creatine kinase, its MB isoenzyme, and plasma-free hemoglobin, and greater blood loss during hours 3, 4, and 5 in the intensive care unit. The volume of red cells in shed mediastinal blood (hematocrit, 9% to 10%) was small, resulting in clinically insignificant autotransfusion when infused directly, and insufficient for cell processing in most patients. CONCLUSIONS: These data support those in previous studies that direct infusion of shed mediastinal blood does not save substantial amounts of autologous red cells and can cause a delayed coagulopathy and other adverse effects that may be harmful to patients postoperatively.

Adult↗
PubMed1998

Hematologic and economic impact of aprotinin in reoperative pediatric cardiac operations.

BACKGROUND: Aprotinin consistently reduces blood loss and transfusion requirements in adults during and after cardiac surgical procedures, but its effectiveness in children is debated. We evaluated the hemostatic and economic effects of aprotinin in children undergoing reoperative cardiac procedures with cardiopulmonary bypass. METHODS: Control, low-dose aprotinin, and high-dose aprotinin groups were established with 15 children per group. Platelet counts, fibrinogen levels, and thromboelastographic values at baseline and after protamine sulfate administration, number of blood product transfusions, and 6-hour and 24-hour chest tube drainage were used to evaluate the effects of aprotinin on postbypass coagulopathies. Time needed for skin closure after protamine administration and lengths of stay in the intensive care unit and the hospital were recorded prospectively to determine the economic impact of aprotinin. RESULTS: Coagulation tests performed after protamine administration rarely demonstrated fibrinolysis but did show significant decreases in platelet and fibrinogen levels and function. The thromboelastographic variables indicated a preservation of platelet function by aprotinin. Decreased blood product transfusions, shortened skin closure times, and shortened durations of intensive care unit and hospital stays were found in the aprotinin groups, most significantly in the high-dose group with a subsequent average reduction of nearly $3,000 in patient charges. CONCLUSIONS: In children undergoing reoperative cardiac surgical procedures, aprotinin is effective in attenuating postbypass coagulopathies, decreasing blood product exposure, improving clinical outcome, and reducing patient charges.

Adolescent↗
PubMed1997

Monitoring platelet glycoprotein IIb/IIIa-fibrin interaction with tissue factor-activated thromboelastography.

Computerized thromboelastography (TEG) was used to study platelet glycoprotein IIb/IIIa function, characterize the consequences of the interaction between polymerizing fibrin and activated platelets, and establish a quantitative assay of platelet function. The ability of platelets to augment the shear elastic modulus of blood clots was measured by TEG under conditions of maximal platelet activation during ex vivo clot formation accelerated by recombinant human tissue factor (TF). Under these conditions, platelets significantly enhance clot strength eightfold (relative to platelet-free fibrin clots). This effect, inhibited by cytochalasin D and c7E3 Fab, appears to be dependent on the transmission of platelet contractile force to fibrin, through glycoprotein IIb/IIIa receptors. The c7E3 Fab dose response of TF-TEG clot strength is identical to results with platelet aggregation induced by the thrombin receptor agonist peptide (50% inhibitory concentration (IC50 = 3.6 microg/ml); adenosine diphosphate-induced aggregation is easier to inhibit (IC50 = 1.2 microg/ml). The results obtained with this system are reproducible (coefficient of variation for clot strength 4%; intraclass correlation coefficient 0.96). As a clinical assay, TF-triggered computerized TEG is easy to perform at the bedside, provides on-line results within 30 minutes, and may offer advantages over conventional measures of platelet function.

Abciximab↗
PubMed1975

Hypercoagulability in childhood cancer.

Thirty-two children with solid tumors (lymphangioma, fibrosarcoma, hepatocarcinoma, osteogenic sarcoma, rhabdomyosarcoma, lymphosarcoma, mesenchymoma, hepatoma, Ewing's sarcoma, reticulum cell sarcoma, neuroblastoma, Hodgkin's disease, and brain tumors) were studied for alterations in coagulation by means of platelet counts, platelet aggregation, thrombelastogram, procoagulant and antigenic factor VIII, fibrin split products, and antithrombin III level. Results indicated hypercoagulability as shown by abnormally short thrombelastograms and elevated factor VIII levels and platelet counts in approximately one-half of the group. With the exception of increased fibrin split products in a third of the patients, little laboratory or clinical evidence for disseminated intravascular coagulation was seen. Hypercoagulability, as noted in adult carcinoma patients, can also occur in childhood sarcoma patients.

Adolescent↗